INSULIN SENSITIVITY OF ADIPOCYTES FROM INBRED MOUSE STRAINS RESISTANTOR SENSITIVE TO DIET-INDUCED OBESITY

We evaluated insulin sensitivity in epididymal adipocytes from two mou se strains shown to be either sensitive (AKR/J, n = 14) or resistant ( SWR/J, n = 12) to the development of obesity when fed a high-fat diet. Half of each strain was fed a chow (CH) diet (12% fat), and half rece ived a sweetened condensed milk (CM) diet (33% fat). After 1 wk, epidi dymal adipose depots were removed and digested with collagenase, and g lucose transport was measured with labeled 2-deoxyglucose. Plasma gluc ose and insulin were slightly higher in AKR/J than SWR/J mice (glucose : 139.7 vs. 118.8 mg/dl, P < 0.06; insulin: 3.45 vs. 2.99 ng/ml, P < 0 .04). One week of high-fat feeding increased adipose depot mass and ca rcass lipid in both strains to approximately the same extent. Adipocyt es from AKR/J mice had greater insulin-stimulated glucose transport co mpared with SWR/J mice at both submaximal and maximal insulin levels ( P < 0.0001). Short-term feeding of the high-fat diet increased AKR/J a dipocyte insulin sensitivity but decreased the sensitivity of SWR/J ad ipocytes to insulin. The differences in adipocyte insulin sensitivity between strains were not explained by differences in adipocyte cell si ze. Access to the high-fat CM diet for 12 wk increased total dissected adipose depot size by 209% in the AKR/J mice and 82% in the SWR/J mic e. These data clearly demonstrate that the two strains differ in adipo cyte insulin sensitivity as well as sensitivity to dietary obesity. In creased adipocyte insulin sensitivity could contribute to a predisposi tion to increase adipose tissue lipid stores with diets high in fat co ntent.