Normal glucose tolerance depends primarily on 1) the ability of the body to secrete insulin, 2) the normal insulin action in target tissues, it means the ability of insulin to inhibit hepatic glucose production and to promote glucose uptake, 3) and the ability of glucose to enter the cells in the absence of insulin. Clinically overt non-insulin-dependent diabetes mellitus (NIDDM) is characterized by abnormality of insulin secretion combined with insulin resistance in glucose metabolism of all major target tissues. While the fasting hyperglycaemia depends primarily on decreased insulin ability to inhibit hepatic glucose production, in the postabsorptive state the main role is played by decreased insulin-stimulated glucose uptake in muscles and impaired glycogen synthesis. Because of hyperglycaemia, and increased insulin-independent glucose uptake, whole glucose utilisation is not altered in NIDDM. Combination of genetic and environmental factors leading to secondary changes in insulin action, contribute to the pathogenesis of insulin resistance and progression of NIDDM.

Keywords: Diabetes Mellitus, Type 2 /physiopathology/; Glucose /metabolism/; Humans; Insulin /physiology/; Insulin Resistance