Blood flow to five adipose tissue depots and five other organs was measured in unanesthetized free-moving obese and lean male Zucker rats using the radiolabeled microsphere technique. Cardiac output and blood pressure were also measured. Obese rats were significantly heavier and had larger fat depots characterized by more and larger adipocytes. Cardiac output and blood pressure were similar in lean and obese rats. Blood flow to adipose tissue was substantially reduced in all five depots of obese rats when expressed per square millimeter of cell surface. When blood flow was expressed per cell, it was reduced in obese rats in the dorsal subcutaneous and inguinal depots and significantly elevated in the obese mesenteric adipose depot. Significant interdepot differences in blood flow were observed in both lean and obese rats. Nonadipose organ blood flow was not different between obese and lean rats, but when expressed on a per gram basis, blood flow through triceps surae muscle, epididymis, and testis was elevated in obese rats. These findings suggest that there is a substantial alteration of hemodynamics in obesity that may contribute to or reflect the altered metabolism of adipose tissue in obese rats. Furthermore, interdepot differences of adipose tissue blood flow also parallel reported interdepot differences in metabolism.
We evaluated insulin sensitivity in epididymal adipocytes from two mouse 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 received a sweetened condensed milk (CM) diet (33% fat). After 1 wk, epididymal adipose depots were removed and digested with collagenase, and glucose transport was measured with labeled 2-deoxyglucose. Plasma glucose 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 carcass lipid in both strains to approximately the same extent. Adipocytes from AKR/J mice had greater insulin-stimulated glucose transport compared 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 adipocyte insulin sensitivity but decreased the sensitivity of SWR/J adipocytes to insulin. The differences in adipocyte insulin sensitivity between strains were not explained by differences in adipocyte cell size. 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 mice. These data clearly demonstrate that the two strains differ in adipocyte insulin sensitivity as well as sensitivity to dietary obesity. Increased adipocyte insulin sensitivity could contribute to a predisposition to increase adipose tissue lipid stores with diets high in fat content.
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