Abstract

The total energy expenditure (EE) of human beings is represented by basal metabolic rate (which corresponds to 60-70% of EE), dietary-induced thermogenesis (10% of EE), and the energy expended in physical activity (20-30% of EE). Obese individuals have an increased total EE compared with lean subjects; this increase is essentially due to an increased lean body mass concomitant with obesity, and is completely reverted after weight loss. Glucose-induced thermogenesis (GIT), measured during an oral glucose tolerance test (OGTT) or hyperinsulinemic-euglycemic clamps, has been found to be decreased in obese individuals, although some discrepancy exists between studies. The observed decreases in GIT show a gradation, increasing progressively from obese patients with normal glucose tolerance to obese patients with impaired glucose tolerance (IGT) to obese patients with non-insulin-dependent diabetes mellitus (NIDDM) and an increased insulin response after OGTT to obese patients with NIDDM and a hypoinsulinemic response after OGTT. The defect in GIT appears to be related to impairment in nonoxidative glucose storage and with the degree of insulin resistance. Obese patients after weight loss show a further decrease in GIT after OGTT or during a euglycemic clamp, which remains unclear. Obese patients have an increased basal lipid oxidation and a decreased suppression of lipid oxidation after OGTT or during a euglycemic clamp. Glucose oxidation and storage are both markedly decreased during a euglycemic clamp. In contrast, the defect in glucose storage is less apparent after OGTT, due to the compensatory effect of hyperglycemia and hyperinsulinemia.(ABSTRACT TRUNCATED AT 250 WORDS)