**6.2 IR in the muscle**

Glucose utilization by the skeletal muscle is mainly mediated by insulin and reaches about 5 g/hour in the postabsorptive state. In DM2 patients, this process is severely disrupted, glucose uptake is decreased, and the amount of stored glycogen is reduced.

Glycogenesis is approximately 60% lower due to a lower activity of the muscle glycogen synthase (GS) [33]. In the IR state, insulin is incapable of stimulating muscle GS; there is excess glucose in the postabsorptive state, but it is not deposited in the form of glycogen, such that this genetic defect directly contributes to postprandial hyperglycemia.
