[Symposium] Diabetes Mellitus (3)

21 Mar 2026 13:30 15:00
201DE
MASLD and Dementia Correlate with Diabetic Management
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Time Session
13:30
14:00
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.
201DE
14:00
14:30
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.
201DE
14:30
15:00
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.
201DE