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This version published online on May 31, 2005
Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2005-0626
A more recent version of this article appeared on August 1, 2005
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Submitted on March 22, 2005
Accepted on May 19, 2005

Effects of Dietary Macronutrient Intake on Insulin Sensitivity and Secretion, and Glucose and Lipid Metabolism in Healthy, Obese Adolescents

Agneta L. Sunehag*, Gianna Toffolo, Marco Campioni, Dennis M. Bier, and Morey W. Haymond

Baylor College of Medicine, Children's Nutrition Research Center, Houston, TX; Department of Electronics and Informatics, University of Padua, Italy

* To whom correspondence should be addressed. E-mail: asunehag{at}bcm.tmc.edu.

Context: Adolescent obesity is a serious public health concern.

Objective: 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 (6m/7fm; 14.7 ± 0.3y; 34 ± 1kg/m2; 42 ± 1% body fat) were studied twice following 7d of isocaloric, isonitrogenous diets with 60% CHO; 25% fat (high CHO) or 30% CHO; 55% fat (low CHO).

Main Outcome Measures and Methods: Glucose metabolism, insulin sensitivity and 1st and 2nd phase insulin secretory indices were measured by stable isotope techniques and the stable labeled IVGTT. The results were compared with those of previously studied lean adolescents.

Results: Obese adolescents increased 1st and 2nd 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 1st and 2nd 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 {beta}-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 type2 diabetics.
Key words: Glucose production • Gluconeogenesis • Insulin sensitivity • Insulin secretion • Stable Isotopes • Stable labeled IVGTT




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