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Am J Physiol 228: 543-548, 1975;
0002-9513/75 $5.00
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American Journal of Physiology, Vol 228, Issue 2, 543-548
Copyright © 1975 by American Physiological Society


ARTICLES

Pancreatic insulin release and peripheral tissue resistance in Zucker obese rats fed high- and low-carbohydrate diets

JS Stern, PR Johnson, BR Batchelor, LM Zucker, and J Hirsch

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.


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D. X Gram, A. J Hansen, M. Wilken, T. Elm, O. Svendsen, R. D Carr, B. Ahren, and C. L Brand
Plasma calcitonin gene-related peptide is increased prior to obesity, and sensory nerve desensitization by capsaicin improves oral glucose tolerance in obese Zucker rats
Eur. J. Endocrinol., December 1, 2005; 153(6): 963 - 969.
[Abstract] [Full Text] [PDF]




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