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Effects of Nonglucose Nutrients on Insulin Secretion and Action in People With Pre-Diabetes

¹ Division of Endocrinology, Diabetes, Metabolism, and Nutrition, Mayo Clinic College of Medicine, Rochester, Minnesota
² Department of Electronics and Informatics, University of Padova, Padova, Italy

Address correspondence and reprint requests to Robert A. Rizza, MD, Mayo Clinic, 200 1st St. S.W., Rm. 5-194 Joseph, Rochester, MN 55905. E-mail: rizza.robert{at}mayo.edu

Abbreviations: DI, disposition index; IFG, impaired fasting glucose; IGT, impaired glucose tolerance; IGT-D, impaired glucose tolerance/diabetes; NFG, normal fasting glucose; NGT, normal glucose tolerance; OGTT, oral glucose tolerance test

To determine whether nonglucose nutrient–induced insulin secretion is impaired in pre-diabetes, subjects with impaired or normal fasting glucose were studied after ingesting either a mixed meal containing 75 g glucose or 75 g glucose alone. Despite comparable glucose areas above basal, glucose-induced insulin secretion was higher (P < 0.05) and insulin action lower (P < 0.05) during the meal than the oral glucose tolerance test (OGTT) in all subgroups regardless of whether they had abnormal or normal glucose tolerance (NGT). However, the nutrient-induced (meal minus OGTT) in insulin secretion and glucagon concentrations did not differ among groups. Furthermore, the decrease in insulin action after meal ingestion was compensated in all groups by an appropriate increase in insulin secretion resulting in disposition indexes during meals that were equal to or greater than those present during the OGTT. In contrast, disposition indexes were reduced (P < 0.01) during the OGTT in the impaired glucose tolerance groups, indicating that reduced glucose induced insulin secretion. We conclude that, whereas glucose-induced insulin secretion is impaired in people with abnormal glucose tolerance, nonglucose nutrient–induced secretion is intact, suggesting that a glucose-specific defect in the insulin secretory pathway is an early event in the evolution of type 2 diabetes.

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