An effort was made to determine to what degree the hyperinsulinemia found in the genetically obese Zucker rat is the result of the carbohydrate content of the diet. When Zucker obese rats are fed precisely the same amount of carbohydrate as lean controls and allowed to become obese by drinking vegetable oil, their pancreatic islets still release 59% more insulin than do those from lean controls. When their diet contains even more carbohydrate, fed from weaning, and they become equivalently obese, their islet insulin release is increased by an additional 46%. An obese Zucker rat fed a high-carbohydrate diet possesses muscle sensitivity to insulin and enlarged adipocytes undergoing active lipogenesis. A rat becoming equivalently obese on a high-fat diet has an absence of insulin sensitivity in muscle and diminished lipogenesis in adipocytes. Clearly, the composition of the diet plays an important role in the metabolic consequences of obesity, but neither diet nor changes in peripheral glucose metabolism can completely explain the hyperinsulinemia.

Intraperitoneal GH administration of 15 days duration to the post weanling rat leads to: (1) a depletion of epididymal fat stores, exclusively the result of a reduction in rat cell size since rat eell number is unaltered; (2) no change in glucose conversion to C02 or triglyceride in the fat cell preparation when results are expressed on a per mg TG basis; but (3) d~ pressed basal and insulin stimulated glucose conversion into CO2 an~ TG when results are expressed on a cellular basis.

In lIitro basal and insulin stimulated glucose metabolism (14 C02 production and 14 C glucose incorporation into fatty acids) are enhanced in the epididymal fat pads of fed Sprague Dawley rats exposed to intraperitoneal growth hormone (GA) both acutely (90 minutes after a single 1 mg injection) and chronicaUy (24 hours after the last of a 15 day series of 1 mg GA injections). This enhancement of the glucose metabolism in the fat pad is accompanied by depletion of its lipid conten!. This alteration in glucose metabolism in adipose tissue exposed to GH ;n 11;110 may be related to the action of GH in accelerating intracellular free fally aeid turnover and/or may be subsequent to a decrease in the size of the fat cello