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Baylor College of Medicine (A.L.S., D.M.B., M.W.H.), Children’s Nutrition Research Center, Houston, Texas 77030; and Department of Electronics and Informatics (G.T., M.C.), University of Padua, 35131 Padua, Italy
Address all correspondence and requests for reprints to: Agneta L. Sunehag, M.D., Ph.D., Children’s Nutrition Research Center, 1100 Bates Street, Houston, Texas 77030. E-mail: asunehag{at}bcm.tmc.edu.
Context: Adolescent obesity is a serious public health concern.
Objective: The aim of the study was to determine whether obese adolescents can adapt metabolically to changes in dietary macronutrient intake.
Patients and Design: Using a random cross-over design, 13 healthy obese volunteers (six boys and seven girls; age, 14.7 ± 0.3 yr; body mass index, 34 ± 1 kg/m2; body fat, 42 ± 1%) were studied twice after 7 d of isocaloric, isonitrogenous diets with 60% carbohydrate (CHO) and 25% fat (high CHO), or 30% CHO and 55% fat (low CHO).
Main Outcome Measures and Methods: Glucose metabolism, insulin sensitivity, and first- and second-phase insulin secretory indices were measured by stable isotope techniques and the stable labeled iv glucose tolerance test. The results were compared with those of previously studied lean adolescents.
Results: Obese adolescents increased first- and second-phase insulin secretory indices by 18 (P = 0.05) and 36% (P = 0.05), respectively, to maintain normoglycemia during the high-CHO diet because they failed to increase insulin sensitivity as did the lean adolescents. Regardless of diet, in obese adolescents, insulin sensitivity was half (P < 0.05) and first- and second-phase insulin secretory indices twice (P < 0.01), compared with the the corresponding values in lean subjects. In obese adolescents, gluconeogenesis increased by 32% during the low-CHO (high-fat diet) (P < 0.01).
Conclusion: In obese adolescents, insulin secretory demands were increased regardless of diet. Failure to increase insulin sensitivity while receiving a high-CHO diet required a further increase in insulin secretion, which may lead to earlier ß-cell failure. A low-CHO/high-fat diet resulted in increased gluconeogenesis, which may be a prelude to the increased glucose production and hyperglycemia observed in type 2 diabetics.
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