Muscle health and type 2 diabetes mellitus: A comprehensive review of sarcopenia, inflammation, and nutritional interventions

Emerging evidence suggests that skeletal muscle health plays a critical role in glucose metabolism and the development of type 2 diabetes mellitus (T2DM). While low muscle mass and low muscle strength have individually been linked to diabetes, findings regarding their independent and combined effects remain inconsistent. Recent studies have also highlighted the roles of muscle quality, sarcopenia, sarcopenic obesity, and chronic inflammation in diabetes risk. This review aims to examine the associations of muscle mass, muscle strength, muscle quality, sarcopenia, and sarcopenic obesity with diabetes and to explore inflammation as a potential biological mechanism underlying these relationships. A narrative review of published literature from 2014 to 2025 was conducted using peer-reviewed articles, systematic reviews, meta-analyses, and population-based studies examining the relationship between skeletal muscle parameters and diabetes. Evidence consistently demonstrates that low muscle mass and low muscle strength are independently associated with an increased risk of diabetes. Individuals exhibiting both conditions have a substantially greater risk compared to those with either condition alone. Reduced muscle quality is also associated with impaired glucose metabolism and elevated diabetes prevalence. Sarcopenia, characterized by concurrent declines in muscle mass and strength, shows a stronger association with diabetes than isolated muscle deficits. Furthermore, sarcopenic obesity appears to exert synergistic effects on insulin resistance and metabolic dysfunction, resulting in a significantly higher risk of diabetes. Chronic low-grade inflammation, mediated through inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and C-reactive protein (CRP), may partially explain the association between impaired muscle health and diabetes. Inflammation appears to be a key mediator linking poor muscle health and metabolic dysfunction. Future longitudinal studies are required to establish causality and evaluate interventions targeting muscle preservation and inflammatory pathways for diabetes prevention.