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Insulin Resistant Glucose Transport Activity in Adipose Cells from the SHR/N-Corpulent Rat¹

Deborah L. Baly, Mary Jane Zarnowski, Nancy Carswell and Otho E. Michaelis

Department of Nutrition, Rutgers University, New Brunswick, NJ 08903 Molecular Cellular and Nutritional Endocrinology Branch, NIDDK, National Institutes of Health, Bethesda, MD 20205 Carbohydrate Nutrition Laboratories, Beltsville Human Nutrition Research Center, Agricultural Research Service, U.S. Department of Agriculture, Beltsville, MD 20705

Young male obese (cp/cp) and lean (cp/+ or +/+) littermates of the SHR/N-corpulent (cp) strain were fed purified diets containing 54% carbohydrate as either sucrose or cooked starch for 12 wk. A significant effect of phenotype (obese > lean) was observed on body weight, epididymal fat pad weight and fat cell size. A diet effect (sucrose > starch) was observed on body weight, fat pad weight, and fat cell size. No effect of phenotype or diet was observed on basal 3-O-methylglucose transport in isolated adipose cells. However, insulin-stimulated glucose uptake was decreased 70–80% in isolated adipose cells from obese SHR/N-cp rats. No effect of diet on insulin-stimulated glucose uptake was observed in obese SHR/N-cp rats. Scatchard analysis of insulin binding data demonstrated no differences in the dissociation constant (K_D) for the insulin receptoninsulin complex. However, obese rats exhibited a decreased number of insulin receptors compared to lean SHR/N-cp rats. These data demonstrate that the obese SHR/N-cp rat exhibits insulin-resistant glucose transport. This altered insulin sensitivity may be one factor contributing to the development of noninsulin-dependent diabetes mellitus in these animals.

KEY WORDS: • glucose transport • insulin binding • obesity

¹ This work was supported by state funds and a grant from the Juvenile Diabetes Foundation. This is publication D-14133-1-89 of the New Jersey Agricultural Experiment Station.

Manuscript received 10 August 1988. Revision accepted 17 November 1988.