Age is a known to be a contributing factor for diabetes. There is no definition to explain the age of the elderly or old age. Most developed countries adhere to the age of 60 and over as describing the definition of an elderly, mainly due to the traditional age of retirement. Aging is associated with a decline in muscle mass, quality, and strength with weakness and declining mobility that can culminate in the syndromes of sarcopenia or frailty. Risk factors for sarcopenia include obesity and insulin resistance, and insulin sensitizing agents significantly reduce loss of fat free mass in obese insulin resistant subjects.
A direct causal relationship between insulin resistance and sarcopenia however is uncertain. In some obese individuals, muscle mass is much lower than expected, a condition termed sarcopenic obesity. This syndrome is accompanied by changes in muscle fiber type ,fatty infiltration, and reduced muscle strength. These changes are at least partly attributable to inflammatory mediators and resultant lipotoxicity. On a cellular metabolic level, common obesity-associated derangements in mitochondrial function, endoplasmic reticulum stress, lipid deposition, and stress-related pathways appear to converge in both insulin resistance and sarcopenia, but the capacity for glucose utilization remains an undetermined component of the sarcopenia syndrome. Whether increased adiposity and loss of muscle mass (as evident in ‘sarcopenic obesity’) provide a complete explanation for any observed age-related increases in insulin resistance is unclear. However, even when study populations are matched for physical activity level and percent lean body mass, results have not been consistent.
Older individuals evaluated by the hyperinsulinemic-euglycemic clamp, the gold standard for assessment of insulin sensitivity, may or may not have reduced peripheral glucose uptake