Type 2 Diabetes Mellitus: A Metabolic Model of Accelerated Aging - Multi-Organ Mechanisms and Intervention Approaches

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Type 2 diabetes mellitus (T2DM) is a metabolic disease characterized by chronic high blood sugar levels and insulin resistance (IR). Modern medicine has shown that diabetes plays a role in speeding up the aging process of the body independently of age, making it an age-related aging disease. The oxidative stress caused by chronic high blood sugar and IR can lead to dysfunctional mitochondria, which in turn promotes changes in epigenetic regulation, shortening of telomeres, and cellular senescence. There is currently a lot of interest in understanding how T2DM contributes to senescence. This review synthesizes epidemiological and clinical research findings on aging across various organs, focusing on insulin resistance and oxidative stress as primary mechanisms. It introduces four diabetes-specific aging axes: glucose toxicity, toxicity of advanced glycation end-products (AGEs), immunoinflammatory aging, and protein amyloidosis, which are integrated into the "metabolism-inflammation-aging" network. Additionally, we provide new insights into interventions targeting aging in diabetes.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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