The primary mechanism of skeletal muscle insulin resistance, a major cause of type2 diabetes and metabolic syndrome, has been attributed to obesity-mediated lipid accumulation in skeletal muscle cells, caused by factors such as obesity-induced fat cell dysfunction, inflammation, and elevated free fatty acids in the blood. However, this hypothesis applies primarily to obese individuals in the West and cannot fully explain the fact that non-obese people in Japanese and East Asian populations often develop type2 diabetes. Furthermore, inactivity has been shown to be associated with mortality and the risk of type2 diabetes independent of obesity, highlighting the need to understand this mechanism in order to prevent and treat metabolic diseases in non- obese individuals.
Kakehi et al. (Thu,) studied this question.