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American Journal of Clinical Nutrition, Vol 57, 851-856, Copyright © 1993 by The American Society for Clinical Nutrition, Inc
ORIGINAL RESEARCH COMMUNICATIONS |
M Laville, C Cornu, S Normand, G Mithieux, M Beylot and JP Riou
Institut National de la Sante et de la Recherche Medicale, Faculte de medecine Alexis Carrel, Lyon, France.
To investigate the possible existence of a defect of thermogenesis at the onset of obesity, we studied glucose-induced thermogenesis (GIT) during an oral glucose-tolerance test (OGTT) (1 g/kg body wt) in 12 women who were at the onset of obesity (group A) compared with 12 long- standing obese women (group B) and 8 lean control subjects. During OGTT hyperinsulinemia and glucose intolerance were measured in group B, suggesting an insulin-resistant state, but not in group A. A similar defect in GIT occurred in both obese groups (8.9 +/- 1.5% in control subjects vs 4.2 +/- 1.1% in group A and 4.3 +/- 1.0% in group B, P < 0.05) despite the absence of alteration in nonoxidative glucose metabolism. We conclude that a decrease in GIT already exists at the onset of obesity, which supports the hypothesis of a possible involvement of this defect in the genesis of obesity.
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