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Am J Physiol Endocrinol Metab 252: E420-E425, 1987;
0193-1849/87 $5.00
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AJP - Endocrinology and Metabolism, Vol 252, Issue 3 E420-E425, Copyright © 1987 by American Physiological Society

ARTICLES

Effect of diet on insulin binding and glucose transport in rat sarcolemmal vesicles

G. K. Grimditch, R. J. Barnard, E. Sternlicht, R. H. Whitson and S. A. Kaplan

The purpose of this study was to compare the effects of a high-fat, high-sucrose diet (HFS) and a low-fat, high-complex carbohydrate diet (LFC) on glucose tolerance, insulin binding, and glucose transport in rat skeletal muscle. During the intravenous glucose tolerance test, peak glucose values at 5 min were significantly higher in the HFS group; 0-, 20-, and 60-min values were similar. Insulin values were significantly higher in the HFS group at all time points (except 60 min), indicating whole-body insulin resistance. Skeletal muscle was responsible, in part, for this insulin resistance, because specific D-glucose transport in isolated sarcolemmal (SL) vesicles under basal conditions was similar between LFC and HFS rats (35 +/- 5 vs. 32 +/- 4 pmol/mg protein), despite the higher plasma insulin levels. Scatchard analyses of insulin binding curves to sarcolemmal vesicles revealed that the Ka of the high-affinity binding sites was significantly reduced by the HFS diet (0.63 +/- 0.09 vs. 0.35 +/- 0.05 X 10(9) M-1); no other binding changes were noted. Specific D-glucose transport in SL vesicles after maximum insulin stimulation (1 U/kg) was significantly depressed in the HFS group (87 +/- 7 vs. 58 +/- 7 pmol/mg protein), indicating that HFS feeding also caused a postbinding defect. These results indicate that the insulin resistance in skeletal muscle associated with a HFS diet is due to both a decrease in the Ka of the high-affinity insulin receptors and a postbinding defect.


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