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Diabetes 52:1280-1283, 2003
© 2003 by the American Diabetes Association, Inc.

Brief Genetics Reports

A Common Polymorphism in the Promoter of UCP2 Contributes to the Variation in Insulin Secretion in Glucose-Tolerant Subjects

Giorgio Sesti1, Marina Cardellini2, Maria Adelaide Marini2, Simona Frontoni3, Monica D’Adamo2, Silvia Del Guerra4, Davide Lauro2, Pierluigi De Nicolais1, Paolo Sbraccia2, Stefano Del Prato4, Sergio Gambardella3, Massimo Federici2, Piero Marchetti4, and Renato Lauro2

1 Dipartimento di Medicina Sperimentale e Clinica, Università di Catanzaro-Magna Græcia, Catanzaro, Italy
2 Laboratory of Molecular Medicine, University of Rome-Tor Vergata, Rome, Italy
3 Department of Internal Medicine, University of Rome-Tor Vergata, Rome, Italy
4 Department of Endocrinology and Metabolism, Metabolic Unit, University of Pisa, Pisa, Italy

It was reported that the common -866G/A polymorphism in the promoter of the human uncoupling protein-2 (UCP2) gene, which enhances its trascriptional activity, is associated with increased mRNA levels in human adipocytes and reduced risk of obesity. Studies in knockout mice and ß-cells indicate that UCP2 may play a role in ß-cell function. In this study, we addressed the question of whether the common -866G/A polymorphism in UCP2 gene contributes to the variation of insulin secretion in humans by genotyping 301 nondiabetic subjects who underwent an oral glucose tolerance test. Glucose-stimulated insulin secretion estimated by several indexes of ß-cell function was significantly lower in carriers of the -866A/A genotype compared with -866A/G or -866G/G according to the dosage of the A allele (P = 0.002–0.05). To investigate directly whether the UCP2 -866G/A polymorphism affects human islet function, pancreatic islets isolated from two -866G/G homozygous, seven -866G/A heterozygous, and one -866A/A homozygous nondiabetic donors were studied. Islets from -866A/A homozygous had lower insulin secretion in response to glucose stimulation as compared with -866G/G and -866G/A carriers. These results indicate that the common -866G/A polymorphism in the UCP2 gene may contribute to the biological variation of insulin secretion in humans.


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