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Diabetes 53:S215-S219, 2004
© 2004 by the American Diabetes Association, Inc.

Section V: The Incretin Pathway

The High-Fat Diet–Fed Mouse

A Model for Studying Mechanisms and Treatment of Impaired Glucose Tolerance and Type 2 Diabetes

Maria Sörhede Winzell, and Bo Ahrén

Department of Medicine, Biomedical Center, Lund University, Lund, Sweden

This study characterizes the high-fat diet–fed mouse as a model for impaired glucose tolerance (IGT) and type 2 diabetes. Female C57BL/6J mice were fed a high-fat diet (58% energy by fat) or a normal diet (11% fat). Body weight was higher in mice fed the high-fat diet already after the first week, due to higher dietary intake in combination with lower metabolic efficiency. Circulating glucose increased after 1 week on high-fat diet and remained elevated at a level of ~1 mmol/l throughout the 12-month study period. In contrast, circulating insulin increased progressively by time. Intravenous glucose challenge revealed a severely compromised insulin response in association with marked glucose intolerance already after 1 week. To illustrate the usefulness of this model for the development of new treatment, mice were fed an orally active inhibitor of dipeptidyl peptidase-IV (LAF237) in the drinking water (0.3 mg/ml) for 4 weeks. This normalized glucose tolerance, as judged by an oral glucose tolerance test, in association with augmented insulin secretion. We conclude that the high-fat diet–fed C57BL/6J mouse model is a robust model for IGT and early type 2 diabetes, which may be used for studies on pathophysiology and development of new treatment.

Address correspondence and reprint requests to Maria Sörhede Winzell, Dept. of Medicine, Biomedical Center (BMC), B11, S-221 84 Lund, Sweden. E-mail: maria.sorhede_winzell{at}medkem.lu.se


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