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Reduced Glucose-Induced Thermogenesis Is Present in Noninsulin-Dependent Diabetes Mellitus without Obesity^*

BARRY GUMBINER, ANNE W. THORBURN and ROBERT R. HENRY

Department of Medicine, University of California San Diego, California and Veterans Administration Medical Center San Diego, California 92161

Address all correspondence and requests for reprints to: Barry Gumbiner, M.D., Veterans Administration Medical Center, Medical Research Service (lllG), 3350 La Jolla Village Drive, San Diego, California 92161.

Recipient of an American Diabetes Association, California Affiliate, Fellowship Award.

Neil Hamilton Fairley Fellow funded by National Health and Medical Research Council of Australia.

Decreased glucose-induced thermogenesis has been observed in all forms of obesity. However, some studies implicate insulin resistance rather than obesity per se as the mechanism by which glucose-induced thermogenesis is reduced. To establish the role of insulin resistance in reduced thermogenesis independent of obesity, we compared energy expenditure in 9 nonobese individuals with noninsulin-dependent diabetes mellitus (NIDDM) to 16 nonobese control subjects using indirect calorimetry and the hyperinsulinemic clamp technique. To document the presence of insulin resistance and reduced glucoseinduced thermogenesis in nonobese NIDDM, 6 individuals from each group were studied under identical conditions of hyperinsulinemia (120 mU/m²·min) and euglycemia (5 mmol/1). Both glucose uptake (0.482 ± 0.042 vs. 0.737 ± 0.040 g/min) and energy expenditure above basal (0.04 ± 0.02 vs. 0.10 ± 0.02 kcal/min) were decreased in nonobese NIDDM compared to control subjects (both P < 0.05). To determine whether decreased glucose-induced thermogenesis could be overcome by correcting for reduced glucose uptake, the 9 nonobese NIDDM individuals were age- and weight-matched to 9 control subjects and clamps were performed at matched rates of glucose uptake. During a 40 mU/m²·min insulin infusion, the nonobese NIDDM individuals were studied at hyperglycemia (17.5 ± 1.9 mmol/L) and compared to the control subjects at euglycemia (5.1 ± 0.1 mmol/L; P < 0.05). Under these conditions, both groups achieved similar rates of glucose uptake (0.698 ± 0.040 vs. 0.688 ± 0.038 g/min, NIDDM and control subjects, respectively) and similar rates of energy expenditure above basal (0.08 ± 0.03 vs. 0.06 ± 0.02 kcal/min, P = NS). During 600 mU/m²·min clamps performed at hyperglycemia (19.0 ± 1.2 vs. 14.5 ± 1.1 mmol/L, NIDDM vs. control subjects, respectively; P < 0.05), rates of maximal glucose uptake (1.538 ± 0.093 vs. 1.518 ± 0.047 g/min) and energy expenditure above basal (0.34 ± 0.03 vs. 0.31 ± 0.03 kcal/min) were also similar (P = NS).

In conclusion nonobese NIDDM is associated with both decreased rates of glucose uptake and decreased glucose-induced thermogenesis. Decreased glucose substrate availability, due to impaired insulin action, appears to be the critical determinant of glucose-induced thermogenesis in nonobese NIDDM. These data indicate that decreased thermogenesis in NIDDM is a consequence of insulin resistance and can occur independent of obesity. (J Clin Endocrinol Metab 72: 801–807, 1991)

^* This study was supported in part by the Medical Research Service of the Veterans Administration, the American Diabetes Association, Grants DK-38949 from the National Institute of Diabetes and Digestive and Kidney Disease and Grant MO1-RR-00827 from the General Clinical Research Branch, Division of Research Resources, NIH.

Received September 2, 1990.

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