Accelerated biological ageing in type 2 diabetes mellitus: mechanistic, cellular, and systemic perspectives

Abstract

Type 2 diabetes mellitus (T2DM), a common chronic metabolic disease that affects multiple organ systems, is still a major global public health concern. Long-term diabetes is linked to cardiovascular disease, renal impairment, neurotoxicity, musculoskeletal weakness, and progressive pancreatic β-cell loss in addition to disruptions in glucose metabolism. These issues frequently start earlier and worsen faster than one may anticipate given one's age. According to recent research, type 2 diabetes may be considered a disorder of accelerated biological aging. Diabetes patients exhibit early activation of aging-related processes, including cellular senescence, oxidative stress, chronic low-grade inflammation, genomic instability, mitochondrial dysfunction, and epigenetic changes. Persistent hyperglycemia, insulin resistance, and metabolic stress intensify these pathways, which are similar to those seen during physiological aging. The main molecular and cellular processes such as dysregulated nutrient-sensing pathways, poor mitochondrial energy metabolism, inflammation, telomere shortening, and loss of tissue regeneration capacity that connect diabetes and aging are outlined in this study. The cardiovascular, renal, neurological, musculoskeletal, and endocrine systems are among the organ-specific signs of accelerated aging in type 2 diabetes that are highlighted. Knowing that type 2 diabetes is a condition of accelerated aging offers crucial information for managing and preventing the illness. In addition to good glycaemic management and lifestyle change, targeting ageing-related pathways may help prevent complications, maintain organ function, and enhance long-term health outcomes in people with type 2 diabetes.

Keywords: Insulin resistance, mitochondrial dysfunction, inflammation, type 2 diabetes mellitus, accelerated aging