Metabolic abnormalities in impaired glucose tolerance

Abstract

Impaired glucose tolerance (IGT) is a state in which there is postprandial hyperglycemia (> 7.8 mmol/L, or 140 mg/dL) with minimal elevations of fasting plasma glucose (>5.5 < 7.8 mmol/L, > 100 < 140 mg/dL). This condition generally precedes the development of diabetes mellitus (DM) by several years. However, in IGT many of the metabolic abnormalities of DM are already present and provide insight into the pathogenesis of DM. Impaired early insulin release is the most consistent defect almost universally observed. Insulin resistance, attributable mainly to obesity, decreased physical fitness, or glucose toxicity, is also often present. The main reason that postprandial hyperglycemia occurs in IGT is impaired suppression of endogenous (hepatic and renal) glucose release; this can be largely explained by impaired early insulin release and impaired suppression of glucagon release. Postprandial glucose disposal is normal or increased, the result of hyperglycemia and delayed hyperinsulinemia. Postabsorptive (fasting) rates of glucose release and disposal and circulating levels of free fatty acids, glycerol, ketone bodies, lactate, and alanine are generally normal.