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Am J Physiol Endocrinol Metab 283: E738-E744, 2002. First published June 11, 2002; doi:10.1152/ajpendo.00199.2002
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Vol. 283, Issue 4, E738-E744, October 2002

Insufficient islet compensation to insulin resistance vs. reduced glucose effectiveness in glucose-intolerant mice

Bo Ahrén1 and Giovanni Pacini2

1 Department of Medicine, Lund University, SE-221 84 Lund, Sweden; and 2 Institute of Systems Science and Biomedical Engineering-Italian National Research Council, 35127 Padua, Italy

This study evaluated the relative contribution of insulin-dependent mechanisms vs. mechanisms independent on dynamic insulin for glucose intolerance induced by high-fat diet. C57BL/6J mice underwent a frequently sampled intravenous glucose tolerance test (1 g/kg glucose) at 1 wk and 1, 3, and 10 mo after initiation of a high-fat diet (58% fat; control diet 11% fat) to measure glucose effectiveness (SG) and disposition index (DI), i.e., insulin sensitivity (SI) times early or total insulin secretion. Glucose disappearance (KG) and SI were reduced in high-fat-fed mice at all time points. Total (50 min) insulin secretion was sufficiently increased at all time points to compensate for the reduced SI, as judged by normal DI50 min. In contrast, early (10 min) insulin secretion was not sufficiently increased; DI10 min was reduced after 1, 3, and 10 mo. SG was reduced after 1 wk; the reduction persisted throughout the study period. Thus glucose intolerance induced by high-fat diet is, in early phases, solely explained by reduced glucose effectiveness, whereas insufficient early insulin secretion is of importance after long-term feeding.

glucose tolerance; glucose intolerance; insulin secretion; high-fat diet


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