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Am J Physiol Endocrinol Metab 282: E270-E276, 2002; doi:10.1152/ajpendo.00232.2001
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Vol. 282, Issue 2, E270-E276, February 2002

Calorie restriction increases muscle insulin action but not IRS-1-, IRS-2-, or phosphotyrosine-PI 3-kinase

Robert T. Davidson, Edward B. Arias, and Gregory D. Cartee

Biodynamics Laboratory, Department of Kinesiology, University of Wisconsin, Madison, Wisconsin 53706

Skeletal muscle insulin sensitivity improves with a moderate reduction in caloric intake. We studied possible mechanisms in calorie-restricted [CR: 60% ad libitum (AL) intake] compared with AL rats, utilizing a time-matched feeding protocol (3, 5, 10, or 20 days). Visceral fat mass was lower for CR vs. AL at 10 and 20 days, but insulin-stimulated muscle 3-O-methylglucose transport was higher in CR vs. AL rats only at 20 days. Fructose 6-phosphate (precursor for the hexosamine biosynthetic pathway, which has inverse relationship with insulin sensitivity) was reduced only at 3 days of CR. Insulin stimulation of insulin receptor substrate (IRS)-1-, IRS-2-, and antiphosphotyrosine-associated phosphatidylinositol 3-kinase (PI3K) was similar for CR and AL. A PI3K inhibitor, wortmannin, reduced insulin-stimulated 3-O-methylglucose transport to basal levels, regardless of diet. With brief time-matched CR, reduced visceral fat mass precedes increased insulin sensitivity; transient reduction in fructose 6-phosphate may trigger more persistent changes but does not coincide with enhanced insulin action; and PI3K is essential for insulin-stimulated 3-O-methylglucose transport in CR as well as AL rats, although insulin-stimulated PI3K is not significantly greater in CR compared with AL animals.

glucose transport; food restriction; dietary restriction; insulin signaling


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