Insulin resistance is present when the biological effects of insulin are subnormal for both glucose disposal in skeletal muscle and suppression of endogenous glucose production primarily in liver (5). In the fasting state, however, muscle accounts for only a small proportion of glucose disposal (less than 20%) while endogenous glucose production is responsible for all of the glucose appearing in plasma. In patients with type 2 diabetes and in patients with impaired fasting glucose (IFG) endogenous glucose production is accelerated (6,7). Since many of these subjects may (still) have basal hyperinsulinemia, at least early in the disease, hepatic
Insulin resistance with beta-cell compensation
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