A reduced thermic effect of glucose in non-insulindependent diabetes mellitus (NIDDM) has been previously reported. To investigate whether this defect is related to 1) a decreased rate of glucose storage, 2) a reduced energy cost of glucose storage, or 3) a defect in the sympathetically mediated component of thermogenesis, we studied the thermic effect of ingested and infused glucose in nine NIDDM obese Pima Indians [90.5 ± 3.9 kg, 39 ± 2% fat, fasting plasma glucose (FPG) 130 ± 10 mg/dl] and in nine nondiabetic obese Pima Indians (99.3 ± 7.2 kg, 38 ± 2% fat, FPG 103 ± 2 mg/dl). Energy expenditure and glucose storage were derived from indirect calorimetry measurements. The thermic effect of 100 g of glucose was found to be similar in both groups (4.0 ± 0.9 vs. 5.0 ± 1.3% of energy ingested in diabetic and nondiabetic subjects, respectively) but lower than that previously reported in nonobese subjects. The cost of glucose storage calculated after stimulating storage by constant glucose infusion (0.46 g/min) and variable insulin infusion (19.5 ± 3.8 vs. 2.9 ± 0.6 mU · kg−1 · min−1 in diabetic and nondiabetic subjects, respectively; P < .01) was similar in both groups (∼0.35 kcal/g glucose stored) and not different from that reported in lean subjects. As opposed to lean and obese Caucasian subjects, energy expenditure failed to markedly decrease during propranolol infusion in both nondiabetic and diabetic Pima Indians. We postulate that the decreased rate of tissue glucose uptake and storage associated with insulin resistance is the major cause of the lower thermic effect of ingested glucose in NIDDM. It is unlikely that a reduced thermic effect of glucose causes or perpetuates obesity in NIDDM, because a low thermic response is the consequence of the increased insulin resistance and is opposed by greater increases in resting metabolic rate.

This content is only available via PDF.