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

Am J Physiol. 1975 Feb;228(2):543-8. doi: 10.1152/ajplegacy.1975.228.2.543.

Abstract

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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adipose Tissue / cytology
  • Adipose Tissue / drug effects
  • Adipose Tissue / metabolism
  • Animals
  • Blood Glucose
  • Body Composition
  • Body Weight
  • Carbon Dioxide / metabolism
  • Cell Count
  • Dietary Carbohydrates*
  • Dietary Fats
  • Glucose / metabolism
  • Glycogen / metabolism
  • Insulin / metabolism*
  • Insulin / pharmacology
  • Insulin Secretion
  • Islets of Langerhans / metabolism*
  • Obesity / blood*
  • Obesity / metabolism
  • Rats
  • Triglycerides / metabolism

Substances

  • Blood Glucose
  • Dietary Carbohydrates
  • Dietary Fats
  • Insulin
  • Triglycerides
  • Carbon Dioxide
  • Glycogen
  • Glucose