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Skeletal muscle mass accounts for 40–50% of lean body mass in adults, and therefore the majority of whole‐body postprandial glucose disposal. Muscle mass is lost with age, leading to insulin resistance at the tissue level, with an adverse effect on glucose and energy homeostasis. The term “anabolic resistance” has been used to describe the reduced muscle protein synthesis in response to nutrients and the reduced insulin‐mediated suppression of proteolysis that occurs with sarcopenia [24]. It is known that people with type 2 diabetes mellitus (T2D) have a higher prevalence of sarcopenia, resulting in mobility limitations [25]. Increase in body fat in T2D may be one of the factors contributing to muscle dysfunction, by direct muscle fat infiltration or indirectly through upregulation of inflammatory cytokines. The coexistence of sarcopenia and obesity results in adverse cardiometabolic as well as functional outcomes [26, 27], although it is uncertain whether the process is sarcopenia leading to obesity or obesity leading to sarcopenia, and the term obese sarcopenia instead of sarcopenia obesity has been proposed to reflect the pathological sequence [28]. Current literature continues to use the term sarcopenic obesity, although there is no universal consensus definition to capture both conditions. Nevertheless, composite measures of both total body fat as well as sarcopenia measures predict mortality, incident mobility limitations, as well as cardiovascular diseases. However, the threshold values are different for different outcomes [29–31].