Jenny GuntonProf. Australia

Jenny GuntonProf.
Professor Jenny Gunton completed her medical degree at University of Queensland followed by Endocrinology and Diabetes Specialist training and then a PhD in Molecular Biology with University of Sydney. Her post-doctoral studies were in the laboratory of Prof C Ron Kahn at Joslin Diabetes Centre and Harvard Medical School. Professor Gunton is currently the President-Elect for the Endocrine Society of Australia. She is the Director of the Centre for Diabetes and Obesity Research at the Westmead Institute for Medical Research and Chair of Medicine at Westmead Hospital, The University of Sydney. Prof Gunton’s clinical interests include diabetes, obesity, and brittle bone disease. Her research focusses on beta-cell function, islet transplantation and the intersection of transcription factors and their regulation by nutrients including iron and Vitamin D.

20 MARCH

Time Session
10:30
12:00
[Symposium] Diabetes Mellitus (1)
Future Management in Diabetes Mellitus
Vivien LimSingapore Moderator The Danger of Obesity in South East Asia and Practical Tips in the Clinic Obesity is steadily increasing in South East Asia (SEA) and with it comes complications naturally follow from it - metabolic, physical and mental. The talk will touch on the following: - the prevalence of this and the changes over time - the rising burden of it - practical tips that can aid in the clinic including busting myths and misconceptions that hamper its management
  • Advancing Toward a Cure for Diabetes: Insights from iPSC-Derived Islet Cell Transplantation Trial
    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.
  • AI-Driven Precision Drug Therapy: Tailoring Personalized Treatment for Type 2 Diabetes
    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 omics profiles, 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 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, to build robust, population-specific prediction models. 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.
  • Closing the Type 2 Diabetes Gap in Cardiovascular and Renal Disease
    Jenny GuntonAustralia Speaker Closing the Type 2 Diabetes Gap in Cardiovascular and Renal DiseasePeople with type 2 diabetes die, on average, 6-7 years earlier. This is mostly due to excess cardiovascular events. This presentation will discuss options for lowering cardiovascular and renal risk in people with type 2 diabetes.Managing Hyperglycaemia in Patients Receiving Immune Checkpoint InhibitorsIt is estimated that >20% of people treated with Immune Checkpoint Inhibitors (ICI) for their cancer will experience new or worsening hyperglycaemia. This presentation will discuss the differential diagnoses for the cause of hyperglycaemia in people treated with ICI and treatment strategies
101
13:10
13:40
Meet the Professor 1
Diabetes Mellitus
Sheng-Chiang SuTaiwan Moderator
  • Managing Hyperglycaemia in Patients Receiving Immune Checkpoint Inhibitors
    Jenny GuntonAustralia Speaker Closing the Type 2 Diabetes Gap in Cardiovascular and Renal DiseasePeople with type 2 diabetes die, on average, 6-7 years earlier. This is mostly due to excess cardiovascular events. This presentation will discuss options for lowering cardiovascular and renal risk in people with type 2 diabetes.Managing Hyperglycaemia in Patients Receiving Immune Checkpoint InhibitorsIt is estimated that >20% of people treated with Immune Checkpoint Inhibitors (ICI) for their cancer will experience new or worsening hyperglycaemia. This presentation will discuss the differential diagnoses for the cause of hyperglycaemia in people treated with ICI and treatment strategies
102

21 MARCH

Time Session
13:30
15:00
[Symposium] Diabetes Mellitus (3)
MASLD and Dementia Correlate with Diabetic Management
Chung-Ze WuTaiwan Moderator
Jenny GuntonAustralia Moderator Closing the Type 2 Diabetes Gap in Cardiovascular and Renal DiseasePeople with type 2 diabetes die, on average, 6-7 years earlier. This is mostly due to excess cardiovascular events. This presentation will discuss options for lowering cardiovascular and renal risk in people with type 2 diabetes.Managing Hyperglycaemia in Patients Receiving Immune Checkpoint InhibitorsIt is estimated that >20% of people treated with Immune Checkpoint Inhibitors (ICI) for their cancer will experience new or worsening hyperglycaemia. This presentation will discuss the differential diagnoses for the cause of hyperglycaemia in people treated with ICI and treatment strategies
  • 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.
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