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Skeletal muscle is the predominant site of insulin-dependent and non-insulin-dependent glucose disposal in humans. During hyperinsulinemia, insulin-mediated glucose uptake in skeletal muscle represents 75% and 95% of the body’s rate of glucose clearance at euglycemia and hyperglycemia, respectively. The first detectable cellular defect in patients with type 2 diabetes is frequently the inability of skeletal muscle to respond to normal levels of circulating insulin. Insulin resistance is rapidly increased after a few days of physical inactivity. Physical inactivity leads to prolonged periods of postprandial hyperglycemia and hyperinsulinemia.
These events are then analogous to the sequence of events leading to overt clinical type 2 diabetes.
Reduction in insulin action following short-term inactivity is the result of a decrease in insulin sensitivity (defined as a decrease in the concentration of insulin required to achieve a sub-maximal rate of glucose transport) and not a decrease in insulin responsiveness. Exercise increases insulin sensitivity because of increased number and activity of glucose transporters, both in muscle and adipose tissue. Long periods of inactivity are associated with a decreased insulin responsiveness, but not insulin sensitivity. The rate-limiting step in insulin- and exercise-induced glucose uptake is GLUT4 translocation to the cell membrane, where GLUT4 acts as a facilitated carrier of glucose into the cytoplasm from the extracellular space.
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