Program Day 2

• Lipoprotein(a): What Endocrinologists Need to Know
  Kathryn TanHong Kong, China Speaker Lipoprotein(a): What Endocrinologists Need to KnowLipoprotein(a) [Lp(a)] is a cholesterol-rich LDL-like particle with apolipoprotein(a) covalently linked to apolipoprotein B100 via a disulfide bond. Lp(a) is synthesized within the liver and there is a general inverse correlation between Lp(a) isoform size and plasma Lp(a) concentrations. About 90% of plasma Lp(a) concentration is genetically determined and plasma levels can modestly rise after menopause in women, and in conditions like hypothyroidism, nephrotic syndrome. It has been shown that elevated Lp(a) is an independent risk factor for atherosclerotic cardiovascular disease (ASCVD) and calcific aortic valve stenosis. Although Lp(a) concentration does vary with ethnicity, relationships between Lp(a) concentration and ASCVD risk remain similar across different ethnic groups. Elevated Lp(a) is considered a cardiovascular risk-enhancing or amplification factor, and recent guidelines and consensus have increasingly recommended universal screening for Lp(a). There are as yet, no approved therapies for elevated Lp(a). Current management focuses on intensifying control of concurrent risk factors, particularly LDL-C, to reduce ASCVD risk. Amongst existing lipid-lowering drugs, only proprotein convertase subtilisin/kexin type 9 inhibitors can lower Lp(a) levels modestly. Emerging RNA-based and small-molecule therapeutics are under development and are showing promising Lp(a)-lowering effects up to 80-90%. Ongoing phase 3 cardiovascular outcomes trials will determine whether effectively lowering Lp(a) can translate to cardiovascular benefit.
• A Novel Therapeutic Concept for Familial LCAT Deficiency: Long-Term Enzyme Replacement Using Genetically Modified Adipocytes
  Masayuki KurodaJapan Speaker A Novel Therapeutic Concept for Familial LCAT Deficiency: Long-Term Enzyme Replacement Using Genetically Modified AdipocytesFamilial lecithin:cholesterol acyltransferase (LCAT) deficiency is a rare autosomal recessive disorder marked by defective HDL maturation, leading to corneal opacity, hemolytic anemia, and progressive renal dysfunction. No disease-modifying treatment has been established to date. Conventional enzyme replacement requires repeated administration with limited durability. Glybera, the first AAV1-based gene therapy for lipoprotein lipase deficiency, was withdrawn after limited clinical use and modest benefit. More broadly, in vivo AAV gene therapies face challenges including immune responses, hepatotoxicity at high vector doses, and considerable inter-patient variability in transgene expression. Our therapeutic approach originated from studies in diabetic mouse models, where adipocytes were explored as platforms for sustained protein delivery. These cells demonstrated endocrine-like properties and long-term protein secretion in vivo. Adipocytes are particularly suited for this purpose due to their longevity, secretory capacity, and low tumorigenic risk. Building on these findings, we established an ex vivo gene and cell therapy platform using genetically modified adipocytes (GMAC), autologous adipocyte-derived cells engineered to express therapeutic proteins. As its first application, we targeted familial LCAT deficiency. These cells were expected to engraft upon subcutaneous implantation, re-differentiate into functional adipocytes, and provide long-lasting and therapeutically relevant LCAT secretion. In a first-in-human clinical trial conducted under Japan’s regulatory framework for regenerative medicine, mature adipocytes were collected from the patient’s subcutaneous fat, converted into proliferative cells via ceiling culture, and transduced to express therapeutic human LCAT, then administered subcutaneously to the patient. Single administration of LCAT-GMAC was well tolerated with no serious adverse events. Sustained increases in serum LCAT activity were observed, accompanied by improvements in lipoprotein profiles and hemolytic anemia. A marked reduction in proteinuria was noted, and renal function remained stable throughout the follow-up period. Remarkably, serum LCAT activity persisted for over eight years after the single administration, the longest durability ever reported for enzyme replacement. This provides the first clinical evidence that ceiling culture-derived, ex vivo modified adipocytes can achieve lasting correction of systemic enzyme deficiencies. LCAT-GMAC therapy thus offers a potentially curative strategy for familial LCAT deficiency and a new paradigm for treating dyslipidemias and other lifelong plasma protein deficiencies.
• Novel and Future Lipid-Lowering Therapy
  Sung Hee ChoiSouth Korea Speaker Novel and Future Lipid-Lowering TherapyIn this lecture, I want to introduce the mechanism of current developing lipid lowering drugs. Small molecular inhibitors such as bempedoic acid, oral forms of newer drugs, Anti-sense oligonucleotide drugs, and siRNA technique based new lipid lowering drugs and its clinical trials. These agents target diverse pathways such as proprotein convertase subtilisin/kexin type 9 (PCSK9), angiopoietin-like protein 3 (ANGPTL3), apolipoprotein C-III (apoC-III), and Lp(a), achieving potent lipid modulation in different mechanistic approach.

• Clinical Pathways for Obesity Management
  I-Weng YenTaiwan Speaker Clinical Pathways for Obesity Management
• Anti-Obesity Medications: Clinical Use
  Kang-Chih FanTaiwan Speaker AI-Driven Precision Drug Therapy: Tailoring Personalized Treatment for Type 2 Diabetes Type 2 diabetes (T2D) is a highly heterogeneous syndrome where "one-size-fits-all" algorithms often fail to address individual pathophysiological variations. While recent guidelines prioritize cardiorenal protection, the choice between second-line agents—particularly SGLT2 inhibitors versus GLP-1 receptor agonists—remains largely empirical. This "trial-and-error" paradigm frequently results in therapeutic inertia and suboptimal glycemic durability. Artificial Intelligence (AI) and machine learning (ML) offer a paradigm shift from population-based guidelines to precision diabetology. By integrating high-dimensional data from electronic health records (EHR), continuous glucose monitoring (CGM), and routinely available clinical features, AI models can now quantify heterogeneous treatment effects (HTE) at the individual level. In this presentation, I will discuss: 1. Phenotypic Stratification: Moving beyond classic classification to identify data-driven clusters (e.g., severe insulin-resistant vs. age-related clusters) that dictate distinct disease trajectories. 2. Predictive Pharmacotherapy: Reviewing recent evidence where ML algorithms predict individual glycemic response, cardiorenal outcomes, and weight loss outcomes for specific drug classes. We will highlight how AI-driven decision support can optimize the selection between SGLT2 inhibitors and GLP-1 receptor agonists, maximizing efficacy while minimizing adverse events. 3. Real-World Implementation: Discussing the potential of leveraging large-scale longitudinal datasets, such as Taiwan’s National Health Insurance Research Database (NHIRD), to build robust, population-specific prediction models and facilitate the clinical adoption of explainable AI (XAI). Bridging the gap between data science and clinical practice, this session aims to demonstrate how AI can empower clinicians to prescribe the right drug for the right patient at the right time, fundamentally transforming T2D management.Anti-Obesity Medications: Clinical Use Obesity is a chronic, relapsing neurobehavioral disease requiring long-term management. Recent guidelines have shifted the treatment goal from BMI-centric weight loss to a "health-centered" approach, focusing on the remission of weight-related complications. With the advent of nutrient-stimulated hormone-based therapies, we have entered an era where pharmacotherapy can achieve double-digit weight loss comparable to bariatric surgery, offering systemic organ protection. In this session, we will navigate the clinical use of anti-obesity medications (AOMs) through three key dimensions based on the latest evidence: 1. Efficacy and Organ Protection: We will review the landmark trials establishing GLP-1 and dual GIP/GLP-1 receptor agonists as the cornerstone of treatment. Highlights include Semaglutide (STEP, SELECT, ESSENCE) and Tirzepatide (SURMOUNT, SUMMIT, SURMOUNT-OSA), demonstrating not only 15–20% weight loss but also breakthrough benefits in cardiovascular outcomes (MACE), heart failure with preserved ejection fraction (HFpEF), metabolic dysfunction-associated steatohepatitis (MASH), and obstructive sleep apnea (OSA). 2. Comorbidity-Directed Strategy: A practical framework for drug selection will be proposed, distinguishing between "Fat Mass Disease" (e.g., OSA, osteoarthritis), which benefits primarily from mechanical weight reduction, and "Sick Fat Disease" (e.g., T2D, CVD, MASH), which requires correction of adipose dysfunction. We will discuss how to prioritize agents like Semaglutide and Tirzepatide for high-risk profiles, while utilizing Naltrexone/Bupropion for emotional eating or Orlistat for patients requiring non-systemic options. 3. Asian Perspectives & Practical Management: We will present data confirming that Asian populations, who are highly sensitive to metabolic risks, achieve weight loss efficacy comparable to Western populations with Semaglutide and Tirzepatide (STEP-7, SURMOUNT-CN/J). Finally, we will address practical strategies for dose titration to mitigate GI adverse events and emphasize the necessity of chronic treatment to prevent weight regain. This presentation aims to equip clinicians with a precision medicine approach, ensuring the right AOM is prescribed to maximize both weight reduction and holistic health outcomes.
• Obesity Care in Special Populations
  Chun-Heng KuoTaiwan Speaker Obesity Care in Special Populations

• Psychological Burden in Diabetes: Understanding Distress and Its Clinical Impact
  Ye-Fong DuTaiwan Speaker Psychological Burden in Diabetes: Understanding Distress and Its Clinical ImpactDiabetes distress represents the emotional burden arising from the daily demands of diabetes self-management and is conceptually distinct from major depressive disorder. Large-scale epidemiological studies indicate that 20–40% of people with diabetes experience clinically significant distress, making it one of the most prevalent psychological complications of diabetes. A growing body of longitudinal evidence demonstrates that diabetes distress is strongly associated with poor glycemic control, reduced treatment adherence, unhealthy dietary and physical activity patterns, and lower engagement with healthcare services. Importantly, diabetes distress predicts future deterioration in HbA1c independent of depressive symptoms, suggesting that it is a direct and modifiable determinant of metabolic outcomes rather than a mere emotional comorbidity. Interventional studies show that structured diabetes education, psychosocial counseling, and digital health–based self-management support can significantly reduce diabetes distress and are accompanied by improvements in glycemic control and self-efficacy. These findings highlight the bidirectional relationship between psychological burden and metabolic regulation. In the era of precision medicine and digital diabetes care, systematic screening and targeted management of diabetes distress should be integrated into routine clinical practice to optimize both psychological well-being and long-term cardiometabolic outcomes.
• Enhancing Patient Experience in Diabetes Care: Communication and Empowerment Strategies
  Samuel ChenTaiwan Speaker Enhancing Patient Experience in Diabetes Care: Communication and Empowerment Strategies
• What Does Person-Centred Diabetes Care Really Mean in 2026?
  Amandeep SinghIndia Speaker What Does Person-Centred Diabetes Care Really Mean in 2026?
• Creating Happiness in the Diabetes Clinic: A Psychosocial Approach to Better Outcomes
  Sanjay KalraIndia Speaker Creating Happiness in the Diabetes Clinic: A Psychosocial Approach to Better Outcomes

• New Concept in Osteoporosis Management
  Daisuke InoueJapan Speaker New Concept in Osteoporosis Management- Japnaese Perspectives Operational definition of osteoporosis by WHO is currently "a BMD value -2.5SD or more below the young adult mean", which has been used worldwide for twenty years. WHO has recently initiated a process to revisit this definition as it is not sensitive enough to identify individuals at high risk of fracture, leading to unsatisfactory treatment of patients. Importantly, a history of fracture, particularly within the past two years (termed imminent fracture risk) has been shown to significantly contribute to the risk of subsequent fractures. Regarding a surrogate for evaluating the clinical efficacy of anti-osteoporotic drugs, a proposal from the FNIH-ASBMR-SABRE project has been submitted to the Food and Drug Administration (FDA). This proposal suggests that treatment-related increases in total hip BMD (TH-BMD) at two years could serve as a surrogate endpoint for fracture risk reduction in clinical trials. This is primarily based on the negative correlation observed between increases in total hip BMD and decreases in the incidence of hip fracture in various clinical trials of anti-osteoporotic drugs demonstrated by a meta-regression analysis. The significant role of BMD as a surrogate, along with availability of bone anabolic agents that can greatly increase BMD for a short period of time, has led to the concept of "Goal-directed treatment" of osteoporosis. Accordingly, "anabolic first" sequential therapy is recommended for individuals at high risk of fractures. In Japan, new Guidelines for Prevention and Treatment of Osteoporosis were issued on August 1, 2025. Recent trends in osteoporosis management, as described above, will be discussed in the context of these Japanese guidelines.
• Bone Fragility in Diabetes
  David LuiHong Kong, China Speaker Bone Fragility in DiabetesDiabetes and osteoporosis are emerging as major public health challenges across Asia, constituting a dual epidemic with significant individual and societal impacts. The Asia-Pacific region accounts for over one-third of the global diabetes population, while osteoporosis-related fractures pose a substantial burden, with one in three women and one in five men over 50 experiencing osteoporotic fractures in their lifetime. Evidence indicates a high fracture burden in Asia, compounded by the increased fragility and poorer outcomes observed in individuals with diabetes. This session will address the urgent need to optimize bone health in the context of the Asian diabetes epidemic. Despite recognition of the increased fracture risk among people with diabetes, the persistent gap representing diabetes-related excess fracture risk appears to remain. A multifaceted approach is needed to address this issue. Key strategies include achieving and maintaining optimal glycaemic control – targeting hyperglycemia, minimizing hypoglycemia, and reducing glycaemic variability – and early intervention for diabetes to reduce occurrence of diabetic complications which in turn are associated with fracture risks. Notably, individuals with type 2 diabetes often fracture at higher bone density T-scores than their non-diabetic counterparts, suggesting that the intervention threshold may need to be modified in this population. Proactive osteoporosis management is essential. Moreover, the high prevalence of coexisting cardiovascular and metabolic comorbidities in individuals with diabetes influences fracture risk, with medication choices potentially impacting skeletal health. Overall, it is hoped that a comprehensive approach integrating glycaemic optimization, proactive osteoporosis management and managing cardiometabolic comorbidities can address this Asian epidemic of diabetes and osteoporosis.
• Metabolic Bone Disorder in Thalassemia
  Wen-Pin YangTaiwan Speaker Metabolic Bone Disorder in ThalassemiaIntroduction: Thalassemia-associated osteoporosis (TAO) is a prevalent and debilitating complication in adult patients with β-thalassemia major (β-TM), despite advancements in transfusion and chelation therapies. Given the complexity of its pathogenesis, TAO presents a unique challenge to endocrinologists, requiring a nuanced understanding of the interplay between ineffective erythropoiesis, iron overload, and the endocrine axis. Pathogenesis & Endocrine Involvement: The aetiology of TAO is multifactorial. Chronic ineffective erythropoiesis leads to bone marrow expansion, causing mechanical disruption of the trabecular microarchitecture. Simultaneously, systemic iron overload (hemosiderosis) exerts direct toxicity on osteoblasts and induces secondary endocrine failures. Clinical evidence demonstrates that BMD in β-TM patients is significantly correlated with multiple endocrine parameters: it is negatively associated with TSH, HbA1c, iPTH, and FGF23 levels, while positively correlating with testosterone and IGF-1. Pituitary and thyroid hemosiderosis are major drivers of impaired peak bone mass accrual and accelerated bone loss. Diagnostic Considerations: While Dual-energy X-ray absorptiometry (DXA) remains the standard for monitoring, its accuracy is often limited by scoliosis, vertebral deformities, and marrow expansion. Complementary tools, such as bone turnover markers (CTX and P1NP) and opportunistic QCT, are essential for a comprehensive skeletal assessment and for identifying patients at high risk for fragility fractures. Therapeutic Strategies: Management requires a multidisciplinary approach beyond optimizing iron chelation and Vitamin D status. Antiresorptive agents, particularly Zoledronate and Denosumab, are effective in increasing BMD and reducing bone pain. However, in severe cases with prevalent fractures, anabolic therapy with Teriparatide has demonstrated superior efficacy, with significant BMD gains in both the lumbar spine and femoral neck. This presentation will emphasize the "sequential therapy" model—initiating with anabolic agents followed by antiresorptives—to maximize and maintain skeletal recovery. Conclusion: TAO requires lifelong vigilance and a tailored treatment plan. Early intervention targeting endocrine deficiencies and the strategic application of sequential pharmacological therapies are vital to preventing fractures and improving the quality of life for this aging population.

• Long-Term Changes of Urinary Exosomal Peptide Levels after Thyroidectomy in Patients with Thyroid Cancer: A Prospective Observational Study
  Chih-Yuan WangTaiwan Speaker Obesity 2026 updateObesity remains one of the most critical and rapidly evolving global health challenges entering 2026, characterized by persistently rising prevalence, expanding clinical consequences, and profound societal and economic impacts. Over the past three decades, the prevalence of overweight and obesity has more than doubled among adults and increased nearly threefold among children and adolescents worldwide, driven by complex interactions between genetic susceptibility, obesogenic environments, sedentary lifestyles, dietary transitions toward energy-dense ultra-processed foods, and broader socio-economic determinants. Projections indicate that, if current trends continue, more than half of the global adult population and a substantial proportion of children will be living with obesity within the next two decades, with particularly rapid increases occurring in low- and middle-income countries undergoing nutritional and urban transitions. This epidemiologic shift has translated into a marked escalation in obesity-related non-communicable diseases, including type 2 diabetes, cardiovascular disease, chronic kidney disease, non-alcoholic fatty liver disease, osteoarthritis, and several obesity-associated malignancies, positioning excess adiposity as a leading contributor to global morbidity, mortality, and disability-adjusted life years. Alongside the growing disease burden, the conceptual framework of obesity has undergone important refinement. While body mass index remains a pragmatic population-level screening tool, its limitations in capturing adiposity distribution and metabolic risk have prompted international efforts to redefine obesity as a chronic, relapsing disease characterized by excess or dysfunctional adipose tissue with heterogeneous clinical expression. Emerging diagnostic paradigms increasingly emphasize waist-based measures, ectopic fat accumulation, and the presence of obesity-related complications, distinguishing pre-clinical obesity from clinically manifest disease and enabling more precise risk stratification and individualized management. Therapeutically, the obesity landscape has been transformed by advances in incretin-based pharmacotherapy, particularly glucagon-like peptide-1 receptor agonists and dual or multi-agonist agents, which have demonstrated unprecedented and sustained weight reduction alongside meaningful improvements in cardiometabolic outcomes. The recent development of effective oral formulations further expands treatment accessibility and has the potential to improve long-term adherence, although challenges related to cost, equity, and health-system implementation remain substantial. Importantly, pharmacotherapy alone is insufficient to address the obesity epidemic, and contemporary management strategies emphasize multimodal, life-course approaches integrating nutritional therapy, physical activity promotion, behavioral and psychological interventions, digital health technologies, and, when appropriate, metabolic and bariatric surgery, tailored to individual risk profiles and comorbidity burdens. At the population level, global policy initiatives increasingly recognize that obesity is not solely an individual responsibility but a systems-driven condition requiring coordinated action across healthcare, education, food systems, urban planning, and regulatory environments to create supportive contexts for healthy living. Concurrently, ongoing research continues to elucidate the complex pathophysiology of obesity, including the roles of genetics, epigenetics, gut microbiota, neuroendocrine regulation, and adipose tissue inflammation, while implementation science seeks to bridge gaps between evidence and real-world practice. Collectively, the 2026 obesity update portrays a paradoxical landscape of escalating global burden alongside unprecedented scientific and therapeutic progress, underscoring that meaningful and sustainable impact will depend on integrating biomedical innovation with structural policy reform, equitable access to care, and sustained public health commitment to reverse current trajectories and improve outcomes across the lifespan.Long-Term Changes of Urinary Exosomal Peptide Levels after Thyroidectomy in Patients with Thyroid Cancer: A Prospective Observational StudyIn this prospective observational study, we investigated whether longitudinal changes in urinary exosomal peptide profiles after thyroidectomy could predict recurrence risk in patients with papillary thyroid cancer, a disease with reported recurrence rates of up to 30%. Adults older than 20 years with newly diagnosed papillary thyroid cancer who had undergone thyroidectomy were enrolled, and urine samples were collected at 12 months after study entry and again one year later for exosomal peptide identification and comparison. Seventy patients were included and stratified according to the interval between surgery and enrollment (<5 years, 5–10 years, and >10 years). During the two-year follow-up after enrollment, no recurrences were observed. Across groups and time intervals, there were no significant differences in serum protein levels or urinary exosomal peptide concentrations, and established high-risk clinical factors showed only weak correlations with these biomarkers. Collectively, these findings delineate the long-term basal fluctuation ranges of serum proteins and urinary exosomal peptides in post-thyroidectomy thyroid cancer survivors, suggesting that biomarker levels remaining within these ranges may be indicative of a lower long-term risk of recurrence in high-risk patients following thyroidectomy.
• Salvage Radiofrequency Ablation Followed by External Beam Radiotherapy for Inoperable Recurrent Differentiated Thyroid Cancer
  Chen-Kai ChouTaiwan Speaker Salvage Radiofrequency Ablation Followed by External Beam Radiotherapy for Inoperable Recurrent Differentiated Thyroid Cancer
• Re-Differentiation Therapy in RAI-Refractory Thyroid Cancer
  Samantha Peiling YangSingapore Speaker Harnessing Molecular Diagnostics in Cytologically-Indeterminate Thyroid NodulesCytologically indeterminate thyroid nodules (Bethesda III–IV) remain a common diagnostic challenge, as cytology alone cannot reliably distinguish benign from malignant disease. Molecular diagnostic tests have emerged as important adjuncts to refine malignancy risk and guide clinical management. This presentation reviews the molecular landscape of thyroid cancer relevant to indeterminate nodules, including key somatic alterations such as BRAF, RAS, and gene fusions (e.g., RET, NTRK, ALK), and discusses the performance of contemporary molecular diagnostic tests. Data from North America and emerging real-world experience in Singapore will be highlighted. The clinical utility of molecular diagnostics in reducing unnecessary diagnostic surgery and informing the extent of surgical management will be discussed, together with current guidance from the ATA 2025 guidelines on integrating molecular results with clinical, radiologic, and cytopathologic findings. Re-Differentiation Therapy in RAI-Refractory Thyroid CancerRadioactive iodine (RAI) therapy remains a cornerstone in the management of differentiated thyroid cancer. However, a subset of patients develop RAI-refractory disease due to loss of iodine-handling gene expression, including the sodium–iodide symporter (NIS). This loss is frequently associated with activation of the MAPK signalling pathway driven by oncogenic alterations such as BRAF and RAS mutations. While systemic therapy with multi-targeted or mutation-specific tyrosine kinase inhibitors (TKIs) can control disease progression, these treatments are generally not curative and do not consistently restore RAI sensitivity. Re-differentiation therapy has emerged as a promising strategy to restore iodine uptake by targeting MAPK signalling and re-inducing thyroid-specific gene expression. This presentation will review the biological rationale for re-differentiation therapy and summarize key clinical studies evaluating BRAF and MEK inhibition in patients with RAI-refractory thyroid cancer. Emerging approaches, optimal treatment duration, and potential predictors of response will also be discussed, highlighting the potential of re-differentiation therapy to restore the therapeutic benefit of RAI in selected patients.

• Sex-Specific Approaches in Precision Medicine: Advancing Endocrinology Care
  Shih-Li SuTaiwan Speaker Sex-Specific Approaches in Precision Medicine: Advancing Endocrinology CareSex differences are fundamental determinants of endocrine physiology and disease. Conventional approaches that treat men and women as biologically equivalent overlook variations in hormonal regulation, immune response, organ function, and pharmacologic metabolism. Precision medicine in endocrinology integrates these sex-specific biological and environmental factors to achieve individualized care. Emerging evidence shows that women are more prone to autoimmune thyroid disease, prolactinoma, and osteoporosis, largely due to estrogen-enhanced immune activity and X-chromosome dosage effects. Men, by contrast, experience higher rates of hypogonadism, visceral obesity, and aggressive endocrine tumors, reflecting androgen decline and single X-chromosome vulnerability. Hormonal effects, such as menopause-related bone loss, are often reversible, whereas chromosomal influences—such as those seen in Turner and Klinefelter syndromes—are irreversible and genetically determined. Pharmacokinetic and pharmacodynamic disparities further highlight the need for sex-informed dosing. Women generally have higher CYP3A4 activity and altered drug binding via increased sex hormone–binding globulin. In Asian populations, genetic polymorphisms, including the high prevalence of BRAF^V600E^ mutations in papillary thyroid cancer and variable androgen receptor CAG repeats, demand region-specific precision strategies. Sex-specific precision endocrinology moves beyond a uniform model of care by recognizing biological sex as a key variable in disease risk and treatment response. Incorporating sex-stratified analyses, adjusted diagnostic thresholds, and personalized pharmacotherapy can enhance diagnostic accuracy and therapeutic safety. For Asia, integrating genetic and environmental diversity is essential to advance equitable, individualized endocrine care.
• From the Bedside to the Digital World: Precision Medicine in Endocrinology with Al and ICT
  Miyuki KataiJapan Speaker From the Bedside to the Digital World: Precision Medicine in Endocrinology with Al and ICTPrecision medicine in endocrinology must account for biological variability, life-course hormonal transitions, and sociocultural determinants of health. However, in routine clinical practice, endocrine disorders are often detected only after prolonged symptomatic periods, particularly when symptoms are nonspecific or overlap with normal physiological transitions. Our work originates from bedside clinical challenges. In developing and operating a comprehensive women’s specialty clinic grounded in sex-specific medicine—representing an innovative clinical model in Japan—we evaluated more than 5,000 women. Among patients who presented to our clinic with a prior diagnosis of menopausal disorders, organic diseases were identified in 27%. Thyroid dysfunction accounted for approximately 15% of cases initially attributed to menopausal disorders. These findings suggest that menopausal diagnoses may contribute to delayed recognition of underlying diseases. Among conditions masked by such symptoms, endocrine disorders were frequently identified, likely because many endocrine diseases require additional targeted laboratory testing for definitive diagnosis. Within endocrine disorders, thyroid dysfunction was particularly prevalent in women. To address this unmet need, we developed the Women’s AI Symptom Evaluator (WaiSE), a digital platform designed to visualize multidimensional symptom patterns using AI-assisted structured questionnaires. WaiSE was developed to support detection of a broad spectrum of underrecognized conditions in women, including endocrine disorders such as thyroid disease. Importantly, these digital tools help women recognize and articulate complex autonomic symptom patterns commonly experienced during menopausal transitions, thereby enabling clinicians to better interpret symptom presentations and facilitating earlier detection of endocrine disorders. The platform is supported by a gender-specific clinical database derived from over 5,000 patients and more than 60,000 consultations, enabling symptom–diagnosis correlation modeling and development of sex-informed diagnostic algorithms. Building upon this clinical and digital foundation, we have recently initiated an integrated endocrine screening strategy through collaboration with the AI-based Thyroid Screening (AITS) platform. We collaborated with Cosmic Corporation, the developer of the AI-based Thyroid Screening (AITS) system. AITS is an AI-based screening system that analyzes routine blood test results obtained in general screening programs, including health checkups, to estimate the likelihood of thyroid dysfunction. The integrated WaiSE–AITS system combines patient-reported symptom assessment through WaiSE with objective clinical indicators derived from AITS to assist in identifying individuals who may require additional thyroid function testing. The integrated system is being developed with the aim of future regulatory approval as Software as a Medical Device (SaMD). This integrated platform can be utilized in clinical practice settings as well as in health screening programs and occupational health settings, demonstrating feasibility in capturing real-world symptom data beyond hospital-centered care. The combined system is designed as a physician-supervised clinical decision-support tool intended to assist healthcare professionals in identifying patients who may benefit from further thyroid evaluation, while maintaining physician responsibility for final diagnostic decisions. This presentation highlights the clinical background, digital innovation process, and emerging collaborative screening strategies, demonstrating how bedside endocrinology can evolve into digitally supported precision care incorporating a life-course approach for women. Acknowledgements:This research was supported by AMED (Grant Number: JP21gk0210024h9903) and by grants from METI, Japan.
• Precision Medicine in Diabetes: Perspectives from Asia
  Ronald MaHong Kong, China Speaker Precision Medicine in Diabetes: Perspectives from AsiaPrecision Medicine in Diabetes: Perspectives from Asia Abstract Diabetes is traditionally classified into type 1 diabetes, type 2 diabetes and gestational diabetes as the main forms of diabetes. However, there is increasing recognition that there is significant hidden heterogeneity within diabetes. Resolving this heterogeneity of diabetes can help facilitate personalized treatment and precision medicine in diabetes. For example, identification of specific monogenic forms of diabetes may facilitate tailored choices of diabetes medications. Precision diagnosis also includes the use of biomarkers to correctly identify adults presenting with autoimmune diabetes for appropriate treatment. Recent advances have included the use of clinical characteristics to empower subtyping of adult-onset diabetes through different clustering strategies. Regardless of the approach of subclassification, the essence of diabetes subtyping is to differentiate between individuals with diabetes due to different underlying pathophysiological defects, and hence have different prognosis towards complications or response to treatment. Recent advances in precision prognostics have also highlighted strategies that can identify high-risk individuals for more intensive treatment. An international consortium initiated by the American Diabetes Association and European Association for the Study of Diabetes (EASD) has reviewed the landscape for precision medicine in diabetes to map our current understanding, as well as outline future directions. The ability to resolve the heterogeneity in diabetes, and thereby provide treatment that is best tailored to the underlying pathophysiology, provides exciting opportunities to realize precision medicine in diabetes towards better patient outcomes. References 1. Leslie RD, Ma RCW, Franks PW, Nadeau KJ, Pearson ER, Redondo MJ. Understanding diabetes heterogeneity: key steps towards precision medicine in diabetes. Lancet Diabetes Endocrinol. 2023 Nov;11(11):848-860. 2. Tobias D, Merino J et al, Second International Consensus report on gaps and opportunities for the clinical translation of precision diabetes medicine. Nature Medicine 2023; 29: 2438-2457. Challenging Cases in EndocrinologyIn this meet the professor session, we will use 4-5 case scenarios to illustrate diagnostic challenges around clinical endocrinology and diabetes and discuss management strategies.

• Chronic Kidney Disease: Illuminating Disease Pathways Through Data Science
  Tai-Shuan LaiTaiwan Speaker Chronic Kidney Disease: Illuminating Disease Pathways Through Data Science Chronic kidney disease (CKD) represents an escalating global health burden, affecting more than 800 million individuals worldwide and contributing substantially to end-stage kidney disease, cardiovascular morbidity, and premature mortality. Although numerous epidemiological studies have identified potential CKD risk factors, progress in prevention and disease-modifying therapies has been hindered by the difficulty of distinguishing causal determinants from non-causal associations. The rapid expansion of large-scale biobanks, together with advances in genetic epidemiology—particularly genome-wide association studies (GWAS) and Mendelian randomization (MR)—offers an important opportunity to address these challenges and advance translational CKD research. In this session, we present an integrated, data-driven framework for investigating CKD pathogenesis by combining GWAS and MR, with a particular emphasis on insights derived from East Asian populations. Using the Taiwan Biobank, which comprises more than 180,000 extensively phenotyped participants with genome-wide data, we illustrate how genetic approaches can complement conventional observational analyses and support the development of precision nephrology. We first highlight Mendelian randomization as a quasi-experimental approach that exploits the random allocation of genetic variants at conception to strengthen causal inference. Using hyperuricemia as a representative example, we demonstrate how robust observational associations with incident CKD may not necessarily reflect causality. While elevated serum urate levels were consistently associated with increased CKD risk in traditional analyses, multiple MR methods using both individual-level and summary-level data did not support a causal effect on kidney disease progression. These findings are consistent with recent randomized clinical trials and underscore the value of MR in prioritizing therapeutic targets. We next extend the MR framework to complex and correlated biological systems through multivariable Mendelian randomization. Focusing on thyroid-related traits, including thyroid-stimulating hormone and free thyroxine, we show how multivariable MR can disentangle intertwined endocrine influences on kidney function. Across East Asian and European populations, genetically predicted thyroid-stimulating hormone exhibited a consistent causal inverse association with estimated glomerular filtration rate, whereas free thyroxine showed no independent causal effect. This example highlights the ability of MR to clarify mechanistic pathways that are difficult to resolve using observational data alone. Beyond causal inference, we demonstrate the value of GWAS in uncovering novel genetic determinants of CKD-related traits. A multi-trait GWAS approach using MTAG was applied to jointly analyze urinary albumin-to-creatinine ratio and kidney function, substantially enhancing discovery power. This strategy identified multiple novel loci associated with albuminuria in an East Asian population and implicated biologically relevant pathways, including proximal tubular albumin endocytosis and primary cilia function. Integrative gene prioritization incorporating kidney-specific expression quantitative trait loci, deleteriousness metrics, and Mendelian kidney disease gene databases further strengthened biological interpretation. Finally, we introduce trajectory GWAS as an innovative approach that leverages repeated measurements of kidney function to identify genetic determinants of longitudinal eGFR decline. By modeling kidney function trajectories rather than cross-sectional measures, this method revealed loci associated with progressive kidney function loss that were not detected by conventional GWAS designs. Conclusion. Taken together, the integration of GWAS, Mendelian randomization, and longitudinal biobank analyses provides a robust framework for improving causal understanding of CKD. Continued accumulation of high-quality population-specific data and international collaboration will be essential for translating these insights into clinical research and future strategies for CKD prevention and management.

  Chun-Liang LinTaiwan Moderator
• Investigating the Pathophysiological Role of Sweet Taste Receptor in the Development of Diabetes-
  Hung-Tsung WuTaiwan Speaker Investigating the Pathophysiological Role of Sweet Taste Receptor in the Development of Diabetes

  Horng-Yih OuTaiwan Moderator Investigating the Pathophysiological Role of Sweet Taste Receptor in the Development of Diabetes-

• Understanding Biology of Type 2 Diabetes and Related Metabolic Disorders - In Memory of the Late Professor Tai Tong-Yuan
  Lee-Ming ChuangTaiwan Speaker Understanding Biology of Type 2 Diabetes and Related Metabolic Disorders - In Memory of the Late Professor Tai Tong-YuanType 2 diabetes mellitus is one of the major non-communicable diseases and has a huge medical and societal impact in recent years and the years to come. Earlier understanding of diabetes is mainly from descriptive observations and epidemiological studies, albeit that the criteria of dysglycemia was only finally revised in year 2010 (ADA) & 2011 (WHO). With advent of new technologies, research of diabetes has bloomed from molecular epidemiology to multi-omic studies. These advances have provided us an opportunity and challenge for better understanding and management of type 2 diabetes and related metabolic disorders. Based on several different unbiased approaches, such as family-based genome-wide linkage analyses, genome-wide association studies, and mRNA differential display, we had been able to tease out certain candidate genes which are responsible disease processes, including insulin resistance, adipogenesis, obesity, and type 2 diabetes. I will illustrate translational medical studies of the genes from each of those approaches, such as Ribosome Binding Protein 1 (RRBP1), adiponectin (ADIPOQ), Vascular Adhesion Protein (VAP1), nocturnin (NOCT), and Prostaglandin Reductase 2 (PTGR2), respectively. With the Stanford Asia–Pacific Program for Hypertension and Insulin Resistance (SAPPHIRe) cohort study, which was established in 1995, our ongoing studies not only provide us a better understanding of the genes/factors on metabolic disorders but also pave a path for developing potential treatment of insulin resistance and the related clinical disorders. References. 1. Diabetes (2005) 54: 1200–1206 2. Journal of Biomedical Science (2023) 30:13 3. J Clin Endocrinol Metab (2001) 86: 3815–3819 4. EMBO Molecular Medicine (2025) 17:938-966
• Research on Albuminuria in Taiwanese Patients with Type 2 Diabetes Mellitus
  Chin-Hsiao TsengTaiwan Speaker Research on Albuminuria in Taiwanese Patients with Type 2 Diabetes Mellitus
• Overview of Prof. Tai’s Research Career
  Wei-Shiung YangTaiwan Speaker

• SGLT2 Inhibitors as a Novel Approach in Nephrolithiasis: Modulating Autophagy and Lysosomal Function
  Chan-Jung LiuTaiwan Speaker SGLT2 Inhibitors as a Novel Approach in Nephrolithiasis: Modulating Autophagy and Lysosomal Function

  Chieh-Hsiang LuTaiwan Moderator
• Panel Discussion
  Chih-Yuan WangTaiwan Moderator Obesity 2026 updateObesity remains one of the most critical and rapidly evolving global health challenges entering 2026, characterized by persistently rising prevalence, expanding clinical consequences, and profound societal and economic impacts. Over the past three decades, the prevalence of overweight and obesity has more than doubled among adults and increased nearly threefold among children and adolescents worldwide, driven by complex interactions between genetic susceptibility, obesogenic environments, sedentary lifestyles, dietary transitions toward energy-dense ultra-processed foods, and broader socio-economic determinants. Projections indicate that, if current trends continue, more than half of the global adult population and a substantial proportion of children will be living with obesity within the next two decades, with particularly rapid increases occurring in low- and middle-income countries undergoing nutritional and urban transitions. This epidemiologic shift has translated into a marked escalation in obesity-related non-communicable diseases, including type 2 diabetes, cardiovascular disease, chronic kidney disease, non-alcoholic fatty liver disease, osteoarthritis, and several obesity-associated malignancies, positioning excess adiposity as a leading contributor to global morbidity, mortality, and disability-adjusted life years. Alongside the growing disease burden, the conceptual framework of obesity has undergone important refinement. While body mass index remains a pragmatic population-level screening tool, its limitations in capturing adiposity distribution and metabolic risk have prompted international efforts to redefine obesity as a chronic, relapsing disease characterized by excess or dysfunctional adipose tissue with heterogeneous clinical expression. Emerging diagnostic paradigms increasingly emphasize waist-based measures, ectopic fat accumulation, and the presence of obesity-related complications, distinguishing pre-clinical obesity from clinically manifest disease and enabling more precise risk stratification and individualized management. Therapeutically, the obesity landscape has been transformed by advances in incretin-based pharmacotherapy, particularly glucagon-like peptide-1 receptor agonists and dual or multi-agonist agents, which have demonstrated unprecedented and sustained weight reduction alongside meaningful improvements in cardiometabolic outcomes. The recent development of effective oral formulations further expands treatment accessibility and has the potential to improve long-term adherence, although challenges related to cost, equity, and health-system implementation remain substantial. Importantly, pharmacotherapy alone is insufficient to address the obesity epidemic, and contemporary management strategies emphasize multimodal, life-course approaches integrating nutritional therapy, physical activity promotion, behavioral and psychological interventions, digital health technologies, and, when appropriate, metabolic and bariatric surgery, tailored to individual risk profiles and comorbidity burdens. At the population level, global policy initiatives increasingly recognize that obesity is not solely an individual responsibility but a systems-driven condition requiring coordinated action across healthcare, education, food systems, urban planning, and regulatory environments to create supportive contexts for healthy living. Concurrently, ongoing research continues to elucidate the complex pathophysiology of obesity, including the roles of genetics, epigenetics, gut microbiota, neuroendocrine regulation, and adipose tissue inflammation, while implementation science seeks to bridge gaps between evidence and real-world practice. Collectively, the 2026 obesity update portrays a paradoxical landscape of escalating global burden alongside unprecedented scientific and therapeutic progress, underscoring that meaningful and sustainable impact will depend on integrating biomedical innovation with structural policy reform, equitable access to care, and sustained public health commitment to reverse current trajectories and improve outcomes across the lifespan.Long-Term Changes of Urinary Exosomal Peptide Levels after Thyroidectomy in Patients with Thyroid Cancer: A Prospective Observational StudyIn this prospective observational study, we investigated whether longitudinal changes in urinary exosomal peptide profiles after thyroidectomy could predict recurrence risk in patients with papillary thyroid cancer, a disease with reported recurrence rates of up to 30%. Adults older than 20 years with newly diagnosed papillary thyroid cancer who had undergone thyroidectomy were enrolled, and urine samples were collected at 12 months after study entry and again one year later for exosomal peptide identification and comparison. Seventy patients were included and stratified according to the interval between surgery and enrollment (<5 years, 5–10 years, and >10 years). During the two-year follow-up after enrollment, no recurrences were observed. Across groups and time intervals, there were no significant differences in serum protein levels or urinary exosomal peptide concentrations, and established high-risk clinical factors showed only weak correlations with these biomarkers. Collectively, these findings delineate the long-term basal fluctuation ranges of serum proteins and urinary exosomal peptides in post-thyroidectomy thyroid cancer survivors, suggesting that biomarker levels remaining within these ranges may be indicative of a lower long-term risk of recurrence in high-risk patients following thyroidectomy.

• Update in Osteoporosis
  Dolores ShobackUnited States Speaker Update in OsteoporosisMany issues in osteoporosis management are challenging in clinical practice. Factors in fracture risk assessment include those in the FRAX algorithm as well as imminent fracture risk in the next 1-5 years. Highest risk individuals benefit most from aggressive therapies targeted to increase bone mineral density (BMD) and reduce fracture rates as rapidly as possible to enhance bone strength. Sequential therapeutic strategies with repeated courses of both anabolic and antiresorptive treatments are becoming the norm for highest risk patients. Yet clinicians are often without trial data to predict clinical outcomes. Bisphosphonate treatment holidays are often employed to allow for a return of bone remodeling with the goal of microdamage repair and avoiding oversuppression of turnover. Yet the duration and monitoring of such treatment interruptions have not been rigorously established. The safety and efficacy of repeated courses of anabolic agents in the lifespan of a patient have not been well studied. The biologic basis for achieving effective BMD responses in sequential therapy is not known. Despite the long use of denosumab and bisphosphonates in clinical care, how to interrupt safely, and how to sequence these therapies most effectively are not known. Rebound increases in bone remodeling after stopping treatment with the RANK-ligand inhibitor denosumab and the challenges of treating patients with advanced chronic kidney disease with denosumab remain unsolved. The bifunctional monoclonal antibody to sclerostin romosozumab, while potent at increasing BMD due to its anabolic and antiresorptive actions, may have off-target cardiovascular adverse effects. Patients who are obese or with diabetes using GLP1 receptor agonists and SGLT2 inhibitors have risks to bone health with rapid weight loss and or direct effects on bone. Ultimately, clinicians must make decisions on patient management based on individual risk assessment and anticipated pathophysiology of the low BMD and risk in that patient.Challenging Parathyroid CasesThis session will review cases of primary, secondary and tertiary hyperparathyoidism and their management. The recommendations for screening patients with possible MEN1 and its manifestations will be reviewed. The role for parathyroid autotransplantation in the management of MEN1 hyperparathyroidism and in postsurgical hypoparathyroidism will be reviewed. A newly released form of parathyroid hormone (PTH) replacement will be discussed in the setting of chronic hypoparathyroidism in adults. Palopegteriparatide has been released for the treatment of chronic hypoparathyroidism and has shown strong efficacy on the control of the biochemical parameters (serum and urine calcium levels, serum phosphate, the Ca x phosphate product) as well as on the quality of life. Updated guidance on considering the use of PTH replacement is being developed and will be discussed. Additionally, the role combined functional and structural localization of parathyroid tissue(s) in the setting of recurrent primary hyperparathyroidism will be reviewed.

• Exploring the World of Autoimmune Disease: from Genetic Manipulation to Disease Reversal
  Huey-Kang SytwuTaiwan Speaker Exploring the World of Autoimmune Disease: from Genetic Manipulation to Disease ReversalAbstract for Asia Oceania Congress of Endocrinology 2026 Huey-Kang Sytwu1 2 1 National Institute of Infectious Diseases and Vaccinology, National Health Research Institutes, Taiwan 2 Department of Microbiology and Immunology, National Defense Medical University, Taiwan TITLE: Exploring the world of autoimmune disease: From genetic manipulation to disease reversal Abstract: Insulin-dependent diabetes mellitus (IDDM) is a T cell-mediated autoimmune disease. To delineate the protective roles of some immune modulatory molecules, such as soluble decoy receptor 3 (DcR3), cytotoxic T lymphocyte antigen 4 (CTLA4), program death ligand 1 and 2 (PD-L1 and 2), heme oxygenase 1 (HO-1), and chemokine receptor D6 in the autoimmune process and to search for potential preventive and/or therapeutic targets in this disease, we have generated (a) insulin promoter (pIns)-sDcR3 transgenic non-obese diabetic (NOD) mice, (b) pIns-single chain anti-CTLA4 transgenic NOD mice, (c) pIns-single chain anti-4-1BB transgenic NOD mice, (d) pIns-PD-L1 transgenic NOD mice, (e) pIns-HO-1 transgenic NOD mice, and (f) pIns-D6 transgenic NOD mice and demonstrated their immunomodulatory potential and underlying mechanisms. Meanwhile, to explore the modulatory potential of interleukin-12, 23 and 27 on autoimmune diabetes, we have generated following transgenic, knockout and knockdown NOD mice: (1) Th1 and Th2 doubly transgenic (2) IL-12 knockout (3) IL-23 knockdown (4) IL-27 knockdown NOD mice. Our results revealed that 20% IL-12-deficient NOD mice still developed autoimmune diabetes, the diabetic incidence of IL-23 knockdown NOD mice is lower than that of control littermates, and the number and percentage of Th1 cells are dramatically decreased and Th17 cells are increased in IL-27 knockdown mice, indicating a differential role of IL-12 cytokine family in modulating Th1 and Th17 cell development during autoimmune diabetogenic process. Previously, we demonstrated that overexpression of B lymphocyte-induced maturation protein-1 (Blimp-1) in T cells decreases IL-21 expression and suppresses autoimmune diabetes, whereas, lacking Blimp-1 in T cells upregulates IL-21 and results in severe colitis and autoimmune encephalomyelitis in NOD mice. Here, we further illustrated that Blimp-1 represses IL-21 by reducing chromatin accessibility and evicting an IL-21 activator, c-Maf on its promoter. Moreover, an IL-21-accelerating autoimmune diabetogenesis in SUMO-defective c-Maf transgenic mice can be overridden by Blimp-1 overexpression-mediated reduction of permissive chromatin structures at Il21 locus. We also explored the fundamental mechanisms by which a high-salt diet (HSD) affects susceptibility to or modifies autoimmune diseases. we generated T-cell–specific STE20/SPS1-related proline/alanine–rich kinase (SPAK) knockout NOD mice and demonstrated that SPAK deficiency in T cells significantly attenuated diabetes development in NOD mice by downregulating IL-21 expression in CD4+ T cells. Furthermore, HSD-triggered diabetes acceleration was abolished in HSD-fed SPAK knockout mice when compared with HSD-fed NOD mice, suggesting an essential role of SPAK in salt-exacerbated T-cell pathogenicity. Finally, by using gain- and loss-of-function approaches, we demonstrated that T cell-specific Mgat5 overexpression-induced higher tetra-antennary N-glycans exacerbate autoimmune diabetes, whereas mutant Mgat5L188R-associated tetra-antenna deficiency completely prevents disease in a CD8+ T cell-dependent manner. Making full use of these unique mouse strains, we are quantitatively and qualitatively investigating the immunopathogenic mechanisms of autoimmune diabetes and providing valuable information for the development of novel immunotherapies.

• Do We Still Need Confirmatory Testing?
  Mitsuhide NaruseJapan Speaker Update in Primary AldosteronismPrimary aldosteronism (PA) is linked to significantly greater cardiovascular morbidity and mortality than essential hypertension, yet it offers a more favorable prognosis when appropriately treated. Early detection and targeted therapy are therefore essential for achieving optimal long-term outcomes and preserving quality of life. Since the release of the Endocrine Society’s guidelines in 2010, several countries—including Japan—have developed national recommendations (e.g., Endocrine Journal, 2021). This reflects growing awareness and research momentum, with over 3,500 publications in the past decade. In Japan, we have established a national PA registry and conducted multicenter studies under the Japan Primary Aldosteronism Study (JPAS), supported by AMED, resulting in more than 40 publications as Japan-originated evidence. Diagnostic protocols have become increasingly standardized, encompassing initial screening, confirmatory testing, subtype classification via adrenal venous sampling (AVS), and tailored treatment—mineralocorticoid receptor (MR) antagonists for bilateral PA and adrenalectomy for unilateral PA. The integration of PA screening into routine hypertension care, alongside the standardization of diagnostic methods, has led to substantial improvements in clinical practice. However, key challenges remain. These include variability in assay methods (e.g., PRA vs. ARC for renin; CLEIA vs. RIA for aldosterone), which affects diagnostic thresholds; uncertainty regarding optimal cutoffs for screening and confirmatory tests; lack of consensus on AVS protocols (with or without cosyntropin); and ongoing debates over the role of non-invasive imaging and advanced surgical approaches (laparoscopic vs. robot-assisted adrenalectomy). These unresolved issues warrant evaluation through a cost-effectiveness lens. As PA diagnostics become increasingly integrated into hypertension management, a fundamental question emerges: How far should we go in diagnosing PA? This presentation will provide an updated overview of clinical practice and address these critical challenges in PA management.Do We Still Need Confirmatory Testing?
• Skipping Confirmatory Tests: Modern Simplified Pathways
  Ada E. D. TeoSingapore Speaker Modern Simplified Pathways for PA: From Screening to LocalizationBy introducing emerging strategies to enable more accurate non-invasive localization, this session aims to help clinicians reduce reliance on adrenal vein sampling and streamline precision diagnosis in primary aldosteronism.
• From ARR to Subtyping: Practical Strategies for Streamlining Testing, Imaging, and AVS in Daily Practice
  Wasita Warachit ParksookThailand Speaker From ARR to Subtyping: Practical Strategies for Streamlining Testing, Imaging, and AVS in Daily PracticeBy integrating guideline recommendations with current evidence and practical clinical reasoning, this session aims to help clinicians navigate the diagnostic pathway from ARR screening to subtype classification more efficiently, reduce unnecessary testing, and optimize individualized treatment strategies for patients with primary aldosteronism.
• Medical vs Surgical Treatment in 2026: Optimizing MRA Therapy, ENaC Strategies, and Surgical Decision-Making
  Cheng Hsuan TsaiTaiwan Speaker Medical vs Surgical Treatment in 2026: Optimizing MRA Therapy, ENaC Strategies, and Surgical Decision-Making
• Discussion

• Key Highlights of the American Thyroid Association Thyroid and Pregnancy Guidelines
  Angela M. LeungUnited States Speaker Key Highlights of the American Thyroid Association Thyroid and Pregnancy GuidelinesThis session will present the key highlights of the American Thyroid Association 2026 guidelines for thyroid disease in preconception, pregnancy, and postpartum that have been published by a multidisciplinary group of experts with global perspective. The discussion will provide an overview of the methodology used to prepare these updated guidelines in partnership with and endorsed by several other collaborating societies. The presentation will cover the most notable changes and new recommendations surrounding thyroid function testing, iodine nutrition, infertility and assisted reproductive techniques, hypothyroidism, hyperthyroidism (including Graves’ disease), thyroid nodules, and thyroid cancers for women planning pregnancy, are pregnant, or seen for postpartum care.Thyroid Risks of Iodine ExcessIodine is a micronutrient that is required for the production of thyroid hormone. Iodine is commonly obtained from consuming an iodine-rich diet or iodine-fortified foods, amiodarone use, iodine-containing supplements, and iodinated contrast media. This session will review the potential forms of thyroid dysfunction arising from an acute iodine load, due to the failure to escape from the Wolff-Chaikoff effect and to the Jod-Basedow phenomenon. The risks of iodine excess in vulnerable populations, and current guidelines regarding the screening and monitoring of iodinated contrast-induced thyroid dysfunction, will be summarized.
• Precision Medicine in Gestational Thyroid Disease: Taking Care of Mother and Baby
  Marjorie A. RamosPhilippines Speaker Precision Medicine in Gestational Thyroid Disease: Taking Care of Mother and BabyPrecision medicine is revolutionizing the management of thyroid disorders in pregnancy by emphasizing individualized diagnosis, trimester-specific reference ranges, and tailored treatment strategies. Thyroid dysfunction is the second most common endocrine abnormality during gestation which poses significant risks to both maternal and fetal health, including miscarriage, preterm delivery, and impaired neurodevelopment. Guidelines now emphasize routine screening in high-risk populations, with tailored management protocols based on trimester-specific TSH and free T4 targets. For hypothyroidism, levothyroxine therapy is initiated early and titrated to maintain TSH in the lower half of the trimester-specific reference range, while hyperthyroidism is managed with antithyroid drugs at the lowest effective dose to minimize fetal risks. Recent updates to clinical guidelines highlight recommendations, including the importance of shared decision-making for women with Graves’ disease, and a shift from antibody-based to timing-based criteria for the treatment of subclinical hypothyroidism. These updates reflect evolving evidence from large randomized trials and systematic reviews, underscoring the need for flexibility and individualization in clinical practice. Future directions in precision medicine include the integration of genetic and molecular profiling to predict disease risk, response to therapy, and long-term outcomes. Machine learning and artificial intelligence are also being explored to enhance diagnostic accuracy and personalize prevention strategies for high-risk subgroups. By combining cutting-edge diagnostics with tailored therapeutic interventions, precision medicine aims to maximize maternal and fetal well-being, reduce adverse outcomes, and improve the overall quality of care for pregnant women with thyroid disorders. This presentation will review the latest evidence, guideline updates, and future innovations in precision medicine for gestational thyroid disease, providing clinicians with practical tools and insights for optimizing patient management in clinical practice and research settings
• Iodine Status in Pregnant Women in Taiwan
  Fan-Fen WangTaiwan Speaker Iodine Status in Pregnant Women in TaiwanIn the 1940’s, endemic goiter was the fifth most common disease in Taiwan. Then, in 1967, an island-wide salt-iodization campaign using 33 ppm potassium iodate was started. Four years after implementation of the campaign, goiter rates among schoolchildren had decreased from 21.6% to 4.3%, suggesting successful elimination of iodine deficiency. However, the mandatory salt iodization policy was discontinued in 2002. In recent surveys, the iodine nutrition status of the overall Taiwanese population has been found to be sufficient, but is at borderline level in pregnant women. Socioeconomic, environmental factors contribute to the incident iodine deficiency in subgroups. While about 92% of pregnant women in Taiwan take nutritional supplements, only about 49% take iodine-containing multi-vitamins. The iodine content of daily meals in Taiwan is currently under investigation, to support targeted dietary education and food fortification programs, which are indicated to improve the iodine status of pregnant women in Taiwan.

• Assessing and Managing Osteoporosis in Patients with Diabetes
  Jawl-Shan HwangTaiwan Speaker Assessing and Managing Osteoporosis in Patients with Diabetes
• Diabetes and Osteoarthritis: Metabolic Links and Clinical Implications
  Jia-Feng ChenTaiwan Speaker Diabetes and Osteoarthritis: Metabolic Links and Clinical Implications
• Sarcopenia in Diabetes: Pathophysiology, Diagnosis, and Management
  Tung-Wei KaoTaiwan Speaker Sarcopenia in Diabetes: Pathophysiology, Diagnosis, and Management Sarcopenia is emerging as a critical yet under-recognized dimension of diabetes, linking metabolic disease to progressive loss of muscle health and physical function. Beyond its traditional association with ageing, growing evidence shows that diabetes is linked to accelerated declines in muscle mass, strength, and physical performance. These changes have important clinical consequences, contributing to frailty, disability, and loss of independence. As the global burden of diabetes continues to rise, maintaining skeletal muscle health is becoming an increasingly important component of diabetes care. Recent advances in metabolic and musculoskeletal research have begun to illuminate the biological links between diabetes and accelerated muscle deterioration. Alterations in insulin signaling, ectopic fat accumulation within skeletal muscle, chronic low-grade inflammation, and mitochondrial dysfunction are increasingly recognized as converging pathways that compromise muscle quality and function. At the same time, new consensus frameworks—including the Asian Working Group for Sarcopenia 2025 update—have expanded the concept from sarcopenia alone toward a broader focus on muscle health across the lifespan. Importantly, emerging clinical evidence suggests that sarcopenia in diabetes is not merely a consequence of ageing but a potentially modifiable condition. Interventions such as resistance exercise, structured physical activity, and targeted nutritional strategies have shown promising benefits in improving muscle strength and functional capacity in individuals with diabetes. As the global burden of diabetes continues to rise, understanding the bidirectional relationship between metabolic disease and skeletal muscle health is becoming increasingly relevant for clinical practice. This lecture will review current perspectives on sarcopenia in diabetes, highlighting key mechanistic insights, evolving diagnostic approaches, and the growing body of evidence supporting preventive and therapeutic strategies aimed at preserving muscle health in this high-risk population.

• PitNET in Multiple Endocrine Neoplasm
  Sang Ouk ChinCanada Speaker PitNET in Multiple Endocrine NeoplasmMultiple endocrine neoplasia type 1 (MEN1) is a hereditary autosomal-dominant syndrome involving neoplasms of the parathyroid glands, pituitary gland, and endocrine components of the gastrointestinal system. Pituitary neuroendocrine tumors (PitNETs) develop in roughly 40% of individuals with MEN1 and constitute the initial clinical presentation in approximately 10% of cases. Recent epidemiological data indicate a modest female predominance, with tumors smaller than 1 cm occurring more frequently than larger lesions. Hormone-secreting PitNETs are observed more often than non-functioning tumors, representing nearly 36–48% of cases, and prolactin-secreting adenomas remain the most prevalent subtype. In comparison with sporadic PitNETs, those associated with MEN1 are more likely to exhibit plurihormonal secretion, greater tumor size, and locally aggressive behavior, while age at diagnosis and the relative frequency of functional tumors appear comparable. Patients lacking detectable MEN1 gene mutations often present with larger and more clinically apparent PitNETs at diagnosis. Although rare, pituitary carcinoma has been documented in six patients with MEN1, including one individual without an identifiable MEN1 mutation. Current evidence suggests that management strategies for MEN1-related PitNETs largely parallel those used for sporadic tumors. PitNETs have also been described in multiple endocrine neoplasia type 4 (MEN4), though comprehensive epidemiologic characterization remains limited, and MEN4 should be considered in patients with MEN1-like clinical features and negative MEN1 genetic testing.
• Oncologist Perspective of NET Management
  Stephen ChanHong Kong, China Speaker Oncologist Perspective of NET Management
• The impact of mutational status on the heterogeneity of MEN1
  Shyang-Rong ShihTaiwan Speaker The impact of mutational status on the heterogeneity of MEN1

• Mechanistic Insights into the Gut–Liver–Brain Axis in MASLD: Metabolic Crosstalk and Neuroinflammation
  Lee-Ling LimMalaysia Speaker Mechanistic Insights into the Gut–Liver–Brain Axis in MASLD: Metabolic Crosstalk and NeuroinflammationThe gut–liver–brain axis plays an important role in the pathogenesis and progression of metabolic dysfunction-associated steatotic liver disease (MASLD). Disruptions in gut microbiota, increased intestinal permeability, and microbial metabolites drive hepatic lipotoxicity and systemic inflammation. These hepatic signals, together with other metabolic dysfunctions, worsen neuroinflammatory responses and metabolic dysregulation. This lecture will discuss mechanistic links across the axis, and understanding these interconnected mechanisms offers opportunities to refine risk stratification and develop targeted interventions that address MASLD as a multisystem disease.Early-Onset Diabetes: Expanding the Spectrum of ComplicationsEarly-onset diabetes is increasing globally and is characterized by an accelerated trajectory of metabolic dysfunction. People diagnosed at a younger age experience a longer lifetime exposure to hyperglycaemia, adiposopathy, and inflammation, leading to an expanded spectrum of complications. Emerging evidence highlights earlier onset of kidney disease, heart failure, fatty liver disease, cognitive decline, and mental health disorders in this high-risk population. This lecture will synthesize current epidemiology, mechanistic insights, and evolving phenotypes, underscoring the urgent need for precision prevention, aggressive risk-factor modification, and integrated care models to reduce premature morbidity and mortality.
• MASLD and Cognitive Impairment Correlate with Diabetic Management
  Noriko Satoh-AsaharaJapan Speaker MASLD and Cognitive Impairment Correlate with Diabetic ManagementIn recent years, the coexistence of metabolic dysfunction–associated steatotic liver disease (MASLD) and cognitive decline in patients with diabetes has attracted growing attention. These conditions are not merely concurrent comorbidities but share common pathophysiological mechanisms involving insulin resistance, chronic inflammation, and gut dysbiosis. Using a large health checkup database, we reported that a body weight gain of more than 10 kg since the age of 20 is a significant risk factor for the development of MASLD (Nutrients, 2025). Moreover, we found that subsequent weight reduction markedly attenuated this risk, emphasizing the importance of appropriate weight management. In our multicenter diabetic cohort studies of the National Hospital Organization (JOMS/J-DOS2), we reported that circulating soluble TREM2 (sTREM2) —a receptor specifically expressed in monocytes and microglia—was significantly associated with cognitive decline in patients with diabetes, suggesting its potential as a predictive biomarker for dementia (Diabetes Metab, 2019; Front Endocrinol, 2022). Furthermore, our network meta-analysis in patients with type 2 diabetes revealed that SGLT2 inhibitors, GLP-1 receptor agonists, and thiazolidinediones may reduce the risk of cognitive impairment (Diabetes Obes Metab, 2025). Novel antidiabetic agents, particularly GLP-1 receptor agonists, have been shown to improve hepatic function and preserve cognitive performance. Collectively, these findings suggest that optimized diabetic management may hold the key to preventing both MASLD and dementia. In this presentation, I would like to summarize recent evidence and discuss optimal therapeutic strategies for MASLD and cognitive impairment in patients with diabetes.
• Diabetes Mellitus-Dementia Correlate with Diabetic Management
  Chaur-Jong HuTaiwan Speaker Diabetes Mellitus-Dementia Correlate with Diabetic ManagementDiabetes mellitus (DM) is a major metabolic disorder that substantially increases the risk of cognitive decline and dementia, including Alzheimer’s disease (AD) and vascular dementia. Growing evidence indicates that chronic hyperglycemia, insulin resistance, vascular injury, oxidative stress, and neuroinflammation are key mechanisms linking DM to neurodegeneration. Insulin resistance in the brain disrupts neuronal glucose utilization, enhances tau phosphorylation, and accelerates amyloid-β accumulation, while advanced glycation end-products (AGEs) and diabetes-related microvascular dysfunction further exacerbate neuronal injury. Effective diabetic management plays a critical role in mitigating dementia risk. Antidiabetic agents such as metformin, thiazolidinediones, and particularly glucagon-like peptide-1 receptor agonists (GLP-1RAs) have demonstrated neuroprotective effects beyond glycemic control. GLP-1RAs improve insulin signaling, reduce neuroinflammation, enhance mitochondrial function, promote autophagy, and inhibit apoptosis, leading to preserved cognitive functions in preclinical models. Clinical studies show that GLP-1RAs may improve specific cognitive domains in patients with type 2 DM and reduce the incidence of cognitive impairment. However, the recent phase 3 trials, Eoke and Evoke+ failed to show the beneficial effects on AD. Overall, the strong interplay between DM and dementia highlights the necessity of optimal glycemic control and strategic use of antidiabetic therapies with neuroprotective potential. Integrating metabolic management into dementia prevention frameworks may offer an effective approach to reducing the global burden of cognitive disorders.

• Consensus in Pituitary Pathology: Impact after New Classification for Japan
  Naoko InoshitaJapan Speaker Consensus in Pituitary Pathology: Impact after New Classification for JapanIn Japan, the brain tumor handling rules are essentially based on the WHO classification. However, the introduction of the term pituitary neuroendocrine tumour (PitNET) has occasionally led to misunderstanding in clinical practice, particularly regarding the implication of malignancy. In this lecture, I will present a consensus-oriented approach in pituitary pathology, focusing on practical strategies developed through multidisciplinary collaboration for the benefit of clinicians and patients. First, I will show how the addition of touch smear cytology to frozen section diagnosis during surgery can improve the accuracy of margin assessment and increase the likelihood of achieving the intended surgical goal, including adequate removal of hormone-producing tumours. Second, I will emphasize that truly malignant PitNETs are extremely rare, and that the term “NET” should not be equated with malignancy. Third, I will discuss the well-known discrepancy between hormone immunohistochemistry and clinical functionality, highlighting the importance of careful pathological interpretation. These perspectives reflect our pathology team’s commitment to accurate communication and clinically relevant pathological diagnosis.
• The Impact of the 2022 WHO PitNET Classification to the Clinical Practitioners. Does Silence Equal Acceptance?
  Szu-Tah ChenTaiwan Speaker The Impact of the 2022 WHO PitNET Classification to the Clinical Practitioners. Does Silence Equal Acceptance?The 2022 World Health Organization (WHO) Classification of Endocrine and Neuroendocrine Tumors redefined pituitary adenomas as pituitary neuroendocrine tumors (PitNETs) within the International Classification of Diseases for Oncology, 3rd Edition (ICD-O/3). This change reflects updated insights into tumor biology, recognizing a spectrum of clinical behaviors beyond the traditionally benign designation. A narrative review of the WHO 2022 classification updates was conducted, focusing on their clinical, diagnostic, and epidemiologic implications for practitioners in endocrinology, neurosurgery, and oncology. The reclassification emphasizes the potential for variability in tumor aggressiveness, recurrence, and invasiveness. Clinically, this shift necessitates more careful risk stratification, closer follow-up in selected cases, and a reassessment of treatment algorithms. From a reporting perspective, ICD-O/3 alignment may affect cancer registry data and epidemiologic tracking, altering disease burden estimates. Importantly, the new terminology presents challenges in patient communication, as the label “neuroendocrine tumor” may cause undue anxiety despite the indolent nature of most PitNETs. The WHO 2022 reclassification of pituitary adenomas as PitNETs represents a significant change for clinical practice. While it enhances awareness of potential aggressive behavior, it also requires balanced application in patient care to avoid overtreatment and misperceptions. Practitioners must adapt by refining diagnostic vigilance, tailoring follow-up strategies, and delivering clear patient-centered communication.
• Consensus in Pituitary Pathology: Impact after New Classification for Korea
  Jae Sung ParkSouth Korea Speaker Consensus in Pituitary Pathology: Impact after New Classification for KoreaThe management of pituitary neuroendocrine tumors (PitNETs) in South Korea is undergoing a significant transition following the 2022 WHO classification. While the shift from "adenoma" to "PitNET" implies a malignant potential, from a neurosurgical perspective, these tumors remain generally far more indolent than primary brain cancers such as high-grade gliomas. Identifying the specific subset of patients who require aggressive intervention is therefore paramount. Our recent institutional study indicates that high-risk non-functioning pituitary adenomas (NFPAs) are more prevalent in younger female patients and exhibit a higher incidence of cavernous sinus invasion. Consequently, a more proactive surgical approach is often warranted for these high-risk phenotypes. Beyond clinical considerations, the Korean healthcare system—characterized by government-led cost controls and supplemental private insurance—faces unique challenges. There is a growing trend of patients requesting malignancy-level ICD coding to secure broader insurance coverage, a phenomenon increasingly driven by external socio-economic factors. Although the Korean Brain Tumor Society (KBTS) previously debated this classification, a definitive consensus remains elusive. Rather than proposing a singular solution, this session aims to raise these multi-faceted issues from a neurosurgical viewpoint, inviting diverse expert perspectives to foster a collective dialogue on the nature of PitNETs within our evolving medical and socio-economic landscape.

• Brain Remodeling of Appetite Centers in Obesity - Results from Murine Omics Studies and Human Brain Imaging
  Tomohiro TanakaJapan Speaker Brain Remodeling of Appetite Centers in Obesity - Results from Murine Omics Studies and Human Brain ImagingBody weight is regulated by functional interplay between multiple organs, among which the hypothalamus plays a critical role through its modulatory functions on energy intake and expenditure. In early 1900s, professors Joseph Babinski and Alfred Frolich reported a case of acquired hypothalamic obesity, whose obesity was secondary to hypothalamic damage by brain tumor. The case provides the first evidence that the hypothalamus plays a key role in the maintenance of body weight in humans. In the 1970s and 1980s, experimental injury or electrical stimulation of the hypothalamic nuclei in rodents further led to an elucidation of its vital role in body weight regulation. Mechanistic insight has been addressed when the discovery of leptin followed by an elucidation of anorexigenic effect of GLP-1 has cast limelight on the endocrinologic aspect of body weight regulation. In fact, more than a dozen genetic forms of obesity has been reported, each of which is caused by mutations of a single gene with indispensable functions within leptin-hypothalamus axis. However, in routine clinical practice, tumors or genetic abnormalities in the hypothalamus are rarely observed in patients with obesity disease. The question, then, is whether the hypothalamus is functioning normally in such patients with primary obesity disease? In 2012, professor Joshua Thaler and colleagues reported that mice fed a high-fat diet exhibit early activation and proliferation of microglia and astrocytes within the hypothalamus - histologic changes suggestive of "hypothalamic inflammation". Subsequent pharmacologic and knockout mouse studies have demonstrated that this hypothalamic inflammation is not merely a result but a critical cause of obesity. We have studied the molecular landscape and its alterations during the development or the improvement of the obesity disease. Methodologically, our research involves transcriptomic and lipidomic analyses of hypothalamic nuclei in mice, with the aim of elucidating the molecular basis of hypothalamic remodeling observed in obese animal models. We have identified obesity-induced biochemical changes in the hypothalamus, such as inflammation-related transcriptome and region-specific accumulation of arachidonic acid esters. More clinically, we are investigating a potential reverse remodeling of the hypothalamus during weight loss in mouse models. Of note, in human subjects with obesity disease, reversible hypothalamic inflammation has been demonstrated using T2 relaxation time measurements in MRI studies. As such, hypothalamic inflammation, a common feature of hypothalamic pathology in rodents and humans, is attracting more attention as a focus of obesity research. In this session, I would like to discuss more of the status quo and future perspectives of the neuropathologic basis of the obesity disease.
• Obesity Management: What's New?
  Alice KongHong Kong, China Speaker Obesity: What Clinicians Should KnowRapid changes in technology, human behavior and lifestyle over the past few decades have resulted in a dramatic increase in the prevalence of obesity worldwide. Besides social stigmata and psychological consequences, obesity is associated with escalated risks of type 2 diabetes, coined the term "Diabesity", hypertension, dyslipidemia, sleep apnoea, metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as non-alcoholic fatty liver disease (NAFLD), polycystic ovarian syndrome, cancers, cardiovascular diseases and increased mortality. Body mass index (BMI) is a commonly adopted tool to identify people with obesity. Clinicians should note that the cutoff points of BMI for clinical actions are different between people with obesity from the East and the West, as well as the limitations of BMI in diagnosing obesity. Recently, the Lancet Diabetes and Endocrinology Commission proposed a new definition of obesity which differentiates excess adiposity with obesity-related illness (clinical obesity) from those without obesity-related diseases (pre-clinical obesity). Also, people with clinical obesity have many unmet needs requiring personalized treatment regimens, intensive counselling and emotional support. The 5 A's framework including Ask, Assess, Advise, Agree and Assist, provide a patient-centred approach to promote lasting behavioral change in obesity management. In addition to lifestyle modifications and behavioral changes, pharmacological agents for weight reduction, bariatric and metabolic surgeries are therapeutic options requiring careful selections for the appropriate patients with adequate counselling of the risks and benefits. Through case sharing approach, the use of weight reducing drugs and surgical strategies for people with preclinical and clinical obesity will be discussed in this session. Acknowledgement: The work described in this lecture was partially supported by funding from Health and Medical Research Fund (HMRF), Food and Health Bureau, Hong Kong SAR, China (Reference number:21223391), Matching Grant from Research Grants Council (reference number: 8601556), and Area of Excellence Scheme, Research Grants Council, Hong Kong SAR, China (Reference number: AoE/M-401/24-R). Obesity Management: What's New?Obesity is a global health hazard with rising prevalence in most parts of the world. Weight reduction by lifestyle modification remains the cornerstone in the prevention and treatment of obesity. However, weight management by lifestyle therapy alone is difficult to sustain in many obese individuals with rebound of body weight being observed as a common phenomenon. Given the invasiveness of bariatric and metabolic surgeries which are not accepted by many people with obesity, the use of pharmacological agents in weight management is increasingly popular. In 2025, the Lancet Diabetes and Endocrinology Commission proposed a new definition of obesity which differentiates excess adiposity with obesity-related illness (clinical obesity) from those without obesity-related diseases (pre-clinical obesity). Among the various obesity complications, diabetes is well recognized to be closely related to obesity, with the term 'Diabesity' coined to show the strong link between these two important modifiable risk factors of cardiovascular disease and premature death. In recent decades, many new generation anti-diabetic drugs are developed and found to have weight reducing properties. Looking ahead, more new drugs are in the pipeline of clinical trials, and the results may eventually change the landscape of obesity management. Acknowledgement: The work described in this lecture was partially supported by funding from Health and Medical Research Fund (HMRF), Food and Health Bureau, Hong Kong SAR, China (Reference number:21223391), Matching Grant from Research Grants Council (reference number: 8601556), and Area of Excellence Scheme, Research Grants Council, Hong Kong SAR, China (Reference number: AoE/M-401/24-R).
• The Hidden Barrier: Understanding and Overcoming Weight Bias
  Hai-Hua ChuangTaiwan Speaker The Hidden Barrier: Understanding and Overcoming Weight Bias

• Obesity 2026 Update
  Chih-Yuan WangTaiwan Speaker Obesity 2026 updateObesity remains one of the most critical and rapidly evolving global health challenges entering 2026, characterized by persistently rising prevalence, expanding clinical consequences, and profound societal and economic impacts. Over the past three decades, the prevalence of overweight and obesity has more than doubled among adults and increased nearly threefold among children and adolescents worldwide, driven by complex interactions between genetic susceptibility, obesogenic environments, sedentary lifestyles, dietary transitions toward energy-dense ultra-processed foods, and broader socio-economic determinants. Projections indicate that, if current trends continue, more than half of the global adult population and a substantial proportion of children will be living with obesity within the next two decades, with particularly rapid increases occurring in low- and middle-income countries undergoing nutritional and urban transitions. This epidemiologic shift has translated into a marked escalation in obesity-related non-communicable diseases, including type 2 diabetes, cardiovascular disease, chronic kidney disease, non-alcoholic fatty liver disease, osteoarthritis, and several obesity-associated malignancies, positioning excess adiposity as a leading contributor to global morbidity, mortality, and disability-adjusted life years. Alongside the growing disease burden, the conceptual framework of obesity has undergone important refinement. While body mass index remains a pragmatic population-level screening tool, its limitations in capturing adiposity distribution and metabolic risk have prompted international efforts to redefine obesity as a chronic, relapsing disease characterized by excess or dysfunctional adipose tissue with heterogeneous clinical expression. Emerging diagnostic paradigms increasingly emphasize waist-based measures, ectopic fat accumulation, and the presence of obesity-related complications, distinguishing pre-clinical obesity from clinically manifest disease and enabling more precise risk stratification and individualized management. Therapeutically, the obesity landscape has been transformed by advances in incretin-based pharmacotherapy, particularly glucagon-like peptide-1 receptor agonists and dual or multi-agonist agents, which have demonstrated unprecedented and sustained weight reduction alongside meaningful improvements in cardiometabolic outcomes. The recent development of effective oral formulations further expands treatment accessibility and has the potential to improve long-term adherence, although challenges related to cost, equity, and health-system implementation remain substantial. Importantly, pharmacotherapy alone is insufficient to address the obesity epidemic, and contemporary management strategies emphasize multimodal, life-course approaches integrating nutritional therapy, physical activity promotion, behavioral and psychological interventions, digital health technologies, and, when appropriate, metabolic and bariatric surgery, tailored to individual risk profiles and comorbidity burdens. At the population level, global policy initiatives increasingly recognize that obesity is not solely an individual responsibility but a systems-driven condition requiring coordinated action across healthcare, education, food systems, urban planning, and regulatory environments to create supportive contexts for healthy living. Concurrently, ongoing research continues to elucidate the complex pathophysiology of obesity, including the roles of genetics, epigenetics, gut microbiota, neuroendocrine regulation, and adipose tissue inflammation, while implementation science seeks to bridge gaps between evidence and real-world practice. Collectively, the 2026 obesity update portrays a paradoxical landscape of escalating global burden alongside unprecedented scientific and therapeutic progress, underscoring that meaningful and sustainable impact will depend on integrating biomedical innovation with structural policy reform, equitable access to care, and sustained public health commitment to reverse current trajectories and improve outcomes across the lifespan.Long-Term Changes of Urinary Exosomal Peptide Levels after Thyroidectomy in Patients with Thyroid Cancer: A Prospective Observational StudyIn this prospective observational study, we investigated whether longitudinal changes in urinary exosomal peptide profiles after thyroidectomy could predict recurrence risk in patients with papillary thyroid cancer, a disease with reported recurrence rates of up to 30%. Adults older than 20 years with newly diagnosed papillary thyroid cancer who had undergone thyroidectomy were enrolled, and urine samples were collected at 12 months after study entry and again one year later for exosomal peptide identification and comparison. Seventy patients were included and stratified according to the interval between surgery and enrollment (<5 years, 5–10 years, and >10 years). During the two-year follow-up after enrollment, no recurrences were observed. Across groups and time intervals, there were no significant differences in serum protein levels or urinary exosomal peptide concentrations, and established high-risk clinical factors showed only weak correlations with these biomarkers. Collectively, these findings delineate the long-term basal fluctuation ranges of serum proteins and urinary exosomal peptides in post-thyroidectomy thyroid cancer survivors, suggesting that biomarker levels remaining within these ranges may be indicative of a lower long-term risk of recurrence in high-risk patients following thyroidectomy.

• Incretin-Based Therapeutics: Bridging Theory and Practice, and Exploring New Horizons
  Daisuke YabeJapan Speaker Advancing toward a Cure for Diabetes: Insights from iPSC-Derived Islet Cell Transplantation TrialType 1 diabetes is characterized by absolute insulin deficiency and marked glycemic variability, creating a constant challenge for individuals who must maintain strict glycemic control to prevent complications and severe hypoglycemia. To address these persistent unmet medical needs, transplantation of pancreatic islet–like cells derived from embryonic stem (ES) or induced pluripotent stem (iPSC) cells has emerged as a promising therapeutic strategy. Encouraging advances have recently been reported from the United States and China. Notably, a world-first autologous transplantation of patient-specific iPSC-derived islet-like cells in China achieved insulin independence with near-normal glycemic control. Despite its promise, concerns remain regarding long-term safety, durability, and broad applicability, underscoring the need for further rigorous clinical evaluation. This lecture will provide an overview of current progress and ongoing challenges in β-cell replacement therapy aimed at curing type 1 diabetes. In addition, I will introduce the study design of our clinical trial at Kyoto University Hospital evaluating allogeneic transplantation of iPSC-derived islet cell sheets (OZTx-410). Through these insights, we aim to highlight both the steady steps already taken and the horizon of possibilities ahead in the pursuit of a functional cure for diabetes.Incretin-Based Therapeutics: Bridging Theory and Practice, and Exploring New HorizonsThe landscape of type 2 diabetes management has been transformed by the advent of incretin-based therapies, including dipeptidyl peptidase-4 (DPP-4) inhibitors and glucagon-like peptide-1 (GLP-1) receptor agonists. In Japan—where more than 70% of individuals with diabetes are aged 65 years or older and commonly present with a non-obese phenotype and reduced insulin secretory capacity—DPP-4 inhibitors continue to serve as a fundamental treatment option, offering effective glycemic control with minimal risk of hypoglycemia. In contrast, among younger adults with obesity, GLP-1 receptor agonists have emerged as essential agents that not only improve glycemic control but also promote weight reduction and confer cardiovascular and renal benefits. A major advance in 2023 was the approval of tirzepatide, a dual glucose-dependent insulinotropic polypeptide (GIP)/GLP-1 receptor agonist that engages both receptors. Tirzepatide has demonstrated robust glucose-lowering and weight-reducing effects in both clinical trials and real-world practice in Japan, further expanding therapeutic opportunities across the region. However, incretin-based therapies are not without challenges: gastrointestinal adverse events remain common, and potential associations with pancreatic and biliary diseases continue to require caution. In older adults, concerns regarding their impact on frailty and sarcopenia demand careful clinical judgment. Furthermore, inappropriate discontinuation of insulin therapy after initiating incretin treatment has occasionally resulted in severe clinical consequences, highlighting the critical need for decision-making that extends beyond the evidence from controlled trials. In response to these issues, the Japan Diabetes Society (JDS) Committee for the Safe Use of Medications released the Recommendations for the Safe Use of Incretin-Related Agents, Second Edition in 2024. Disseminating these recommendations across East Asia and the broader Asia–Oceania region will be essential to ensure the safe and effective application of incretin-based therapies in diverse clinical settings. In this plenary lecture, I will explore strategies to optimize type 2 diabetes management in Asia by harnessing the therapeutic potential of incretin-based agents while proactively mitigating associated risks. Together, we aim to build a future in which innovation, safety, and patient-centered care advance hand in hand.

• Genomic Alterations in Thyroid Cancer: Biological and Clinical Insights
  Maria E. CabanillasUnited States Speaker Genomic Alterations in Thyroid Cancer: Biological and Clinical InsightsGenomic alterations play a central role in the initiation, progression, and clinical behavior of thyroid cancers, offering critical insights into their underlying biology and therapeutic vulnerabilities. Follicular cell derived thyroid tumors commonly harbor driver mutations that constitutively activate the MAPK signaling pathway, most notably BRAFV600E and RAS mutations. These early events define major molecular subtypes and strongly influence differentiation status, tumor phenotype, and response to therapy. Progression toward aggressive or dedifferentiated forms, such as poorly differentiated and anaplastic thyroid carcinomas, is driven by additional alterations in key genes regulating chromatin remodeling, cell cycle control, and genomic stability, including TERT promoter mutations, TP53, PIK3CA, and EIF1AX. Actionable genomic alterations are increasingly leveraged to personalize treatment strategies in thyroid cancer and underscore the importance of genomic characterization in improving outcomes in thyroid cancer. Anaplastic Thyroid CancerAnaplastic thyroid cancer (ATC) is one of the most aggressive human malignancies, characterized by rapid local invasion, early metastasis, and near‑universal disease‑specific mortality and is considered a medical emergency. Current treatment strategies prioritize rapid assessment of resectability, with surgery pursued only when complete or near‑complete tumor removal is feasible, as partial debulking offers limited benefit. For unresectable disease, localized disease, combined modality therapy—typically external‑beam radiation with concurrent systemic therapy—remains the cornerstone of local control. Recent advances in molecular profiling have transformed systemic management, enabling targeted therapies for tumors harboring BRAFV600E mutations. These agents have demonstrated meaningful responses and, in select cases, have converted unresectable tumors to operable ones, expanding the role of surgery in modern care. However, due to the high risk of relapses, immunotherapy has been added to the treatment strategy. Patients with distant metastatic disease without a BRAFV600E mutation have a more complicated treatment regimen which is still under investigation but require systemic therapy combination strategies involving immunotherapy. These evolving strategies reflect a shift toward precision‑based, time‑critical management aimed at improving outcomes in this highly lethal cancer.

• Diagnosis and Evaluation of Obesity
  Hung-Yuan LiTaiwan Speaker Diagnosis and Evaluation of ObesityObesity is now widely recognized as a chronic, heterogeneous disease rather than a simple consequence of excess body weight. Contemporary perspectives emphasize that obesity-related health risk arises not only from the quantity of adipose tissue, but also from its distribution and functional status. In recent years, major international organizations—including the The Lancet Commission on Obesity, the American Association of Clinical Endocrinology (AACE), the European Association for the Study of Obesity (EASO), the Japan Society for the Study of Obesity (JASSO), and the American Diabetes Association (ADA)—have proposed evolving frameworks for obesity diagnosis that move beyond reliance on body mass index (BMI) alone. This session will review current concepts in the diagnosis and evaluation of obesity, integrating anthropometric measures, adiposity distribution, obesity-related complications, and functional consequences of excess fat. While BMI remains a practical and widely used screening tool, its limitations at the individual level are increasingly recognized. Complementary measures such as waist circumference and waist-to-height ratio provide important additional information, particularly for assessing central adiposity and cardiometabolic risk in Asian populations. A central theme of this lecture is the concept of obesity-related complications and diseases (ORCD), which can be broadly categorized into two interrelated entities. Fat mass disease refers to conditions driven predominantly by excessive fat mass and its mechanical or quantitative burden, whereas sick fat disease reflects adipose tissue dysfunction characterized by abnormal endocrine, inflammatory, and metabolic signaling. Both entities contribute to ORCD, either independently or in combination, and together account for the heterogeneous clinical manifestations of obesity. According to the definitions proposed by the Lancet Commission on Obesity, obesity can be conceptualized along a continuum from preclinical obesity to clinical obesity. Preclinical obesity is characterized by excess adiposity without established ORCD and corresponds conceptually to AACE stage 1, representing a key opportunity for primary prevention. In contrast, clinical obesity is defined by the presence of ORCD and aligns with AACE stage 2 and stage 3, in which clinical management focuses on secondary prevention, risk reduction, and complication management. This integration of Lancet Commission concepts with AACE staging provides a disease-oriented framework for risk stratification and therapeutic decision-making. Comprehensive obesity evaluation must also address psychological, behavioral, and socio-cultural factors. Mental health conditions such as binge-eating disorder, depression, and anxiety may both contribute to and result from obesity, forming bidirectional relationships that influence disease trajectory. In addition, weight stigma, health literacy, and environmental and cultural contexts significantly affect treatment acceptance, adherence, and long-term outcomes, and should be incorporated into routine clinical assessment. In conclusion, this session will propose a pragmatic, stepwise approach to obesity diagnosis and evaluation that integrates ORCD phenotyping with AACE stage 1–3 classification and the conceptual framework of the Lancet Commission. This approach is intended not only to inform clinical decision-making, but also to serve as the foundation for the forthcoming obesity-related clinical practice guidelines of the Diabetes Association of the Republic of China, bridging global concepts with local implementation.

• Thyroid Risks of Iodine Excess
  Angela M. LeungUnited States Speaker Key Highlights of the American Thyroid Association Thyroid and Pregnancy GuidelinesThis session will present the key highlights of the American Thyroid Association 2026 guidelines for thyroid disease in preconception, pregnancy, and postpartum that have been published by a multidisciplinary group of experts with global perspective. The discussion will provide an overview of the methodology used to prepare these updated guidelines in partnership with and endorsed by several other collaborating societies. The presentation will cover the most notable changes and new recommendations surrounding thyroid function testing, iodine nutrition, infertility and assisted reproductive techniques, hypothyroidism, hyperthyroidism (including Graves’ disease), thyroid nodules, and thyroid cancers for women planning pregnancy, are pregnant, or seen for postpartum care.Thyroid Risks of Iodine ExcessIodine is a micronutrient that is required for the production of thyroid hormone. Iodine is commonly obtained from consuming an iodine-rich diet or iodine-fortified foods, amiodarone use, iodine-containing supplements, and iodinated contrast media. This session will review the potential forms of thyroid dysfunction arising from an acute iodine load, due to the failure to escape from the Wolff-Chaikoff effect and to the Jod-Basedow phenomenon. The risks of iodine excess in vulnerable populations, and current guidelines regarding the screening and monitoring of iodinated contrast-induced thyroid dysfunction, will be summarized.

• Challenging Parathyroid Cases
  Dolores ShobackUnited States Speaker Update in OsteoporosisMany issues in osteoporosis management are challenging in clinical practice. Factors in fracture risk assessment include those in the FRAX algorithm as well as imminent fracture risk in the next 1-5 years. Highest risk individuals benefit most from aggressive therapies targeted to increase bone mineral density (BMD) and reduce fracture rates as rapidly as possible to enhance bone strength. Sequential therapeutic strategies with repeated courses of both anabolic and antiresorptive treatments are becoming the norm for highest risk patients. Yet clinicians are often without trial data to predict clinical outcomes. Bisphosphonate treatment holidays are often employed to allow for a return of bone remodeling with the goal of microdamage repair and avoiding oversuppression of turnover. Yet the duration and monitoring of such treatment interruptions have not been rigorously established. The safety and efficacy of repeated courses of anabolic agents in the lifespan of a patient have not been well studied. The biologic basis for achieving effective BMD responses in sequential therapy is not known. Despite the long use of denosumab and bisphosphonates in clinical care, how to interrupt safely, and how to sequence these therapies most effectively are not known. Rebound increases in bone remodeling after stopping treatment with the RANK-ligand inhibitor denosumab and the challenges of treating patients with advanced chronic kidney disease with denosumab remain unsolved. The bifunctional monoclonal antibody to sclerostin romosozumab, while potent at increasing BMD due to its anabolic and antiresorptive actions, may have off-target cardiovascular adverse effects. Patients who are obese or with diabetes using GLP1 receptor agonists and SGLT2 inhibitors have risks to bone health with rapid weight loss and or direct effects on bone. Ultimately, clinicians must make decisions on patient management based on individual risk assessment and anticipated pathophysiology of the low BMD and risk in that patient.Challenging Parathyroid CasesThis session will review cases of primary, secondary and tertiary hyperparathyoidism and their management. The recommendations for screening patients with possible MEN1 and its manifestations will be reviewed. The role for parathyroid autotransplantation in the management of MEN1 hyperparathyroidism and in postsurgical hypoparathyroidism will be reviewed. A newly released form of parathyroid hormone (PTH) replacement will be discussed in the setting of chronic hypoparathyroidism in adults. Palopegteriparatide has been released for the treatment of chronic hypoparathyroidism and has shown strong efficacy on the control of the biochemical parameters (serum and urine calcium levels, serum phosphate, the Ca x phosphate product) as well as on the quality of life. Updated guidance on considering the use of PTH replacement is being developed and will be discussed. Additionally, the role combined functional and structural localization of parathyroid tissue(s) in the setting of recurrent primary hyperparathyroidism will be reviewed.

• Anaplastic Thyroid Cancer
  Maria E. CabanillasUnited States Speaker Genomic Alterations in Thyroid Cancer: Biological and Clinical InsightsGenomic alterations play a central role in the initiation, progression, and clinical behavior of thyroid cancers, offering critical insights into their underlying biology and therapeutic vulnerabilities. Follicular cell derived thyroid tumors commonly harbor driver mutations that constitutively activate the MAPK signaling pathway, most notably BRAFV600E and RAS mutations. These early events define major molecular subtypes and strongly influence differentiation status, tumor phenotype, and response to therapy. Progression toward aggressive or dedifferentiated forms, such as poorly differentiated and anaplastic thyroid carcinomas, is driven by additional alterations in key genes regulating chromatin remodeling, cell cycle control, and genomic stability, including TERT promoter mutations, TP53, PIK3CA, and EIF1AX. Actionable genomic alterations are increasingly leveraged to personalize treatment strategies in thyroid cancer and underscore the importance of genomic characterization in improving outcomes in thyroid cancer. Anaplastic Thyroid CancerAnaplastic thyroid cancer (ATC) is one of the most aggressive human malignancies, characterized by rapid local invasion, early metastasis, and near‑universal disease‑specific mortality and is considered a medical emergency. Current treatment strategies prioritize rapid assessment of resectability, with surgery pursued only when complete or near‑complete tumor removal is feasible, as partial debulking offers limited benefit. For unresectable disease, localized disease, combined modality therapy—typically external‑beam radiation with concurrent systemic therapy—remains the cornerstone of local control. Recent advances in molecular profiling have transformed systemic management, enabling targeted therapies for tumors harboring BRAFV600E mutations. These agents have demonstrated meaningful responses and, in select cases, have converted unresectable tumors to operable ones, expanding the role of surgery in modern care. However, due to the high risk of relapses, immunotherapy has been added to the treatment strategy. Patients with distant metastatic disease without a BRAFV600E mutation have a more complicated treatment regimen which is still under investigation but require systemic therapy combination strategies involving immunotherapy. These evolving strategies reflect a shift toward precision‑based, time‑critical management aimed at improving outcomes in this highly lethal cancer.