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Journal of Nutrition Vol. 113 No. 10 October 1983, pp. 1984-1994
Copyright © 1983 by American Society for Nutrition
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Lipoprotein Lipid and Protein Responses to Dietary Fat and Diabetes in Rats1,2,

Bernhard Hennig3 and Jacqueline Dupont4

Department of Food and Nutrition, Iowa State University, Ames, IA 50011

Dietary and insulin-deficiency types of hyperlipidemia were compared in adult normal and streptozotocin-induced diabetic male breeder rats. High beef tallow, high corn oil or low fat diets (BT, CO and LF, respectively) were fed ad libitum for 2 months. Glucose and insulin were measured in plasma and total cholesterol, free cholesterol, cholesteryl ester, triglycerides and apoproteins in very low density, low density and high density lipoproteins (VLDL, LDL and HDL, respectively). Diet did not affect plasma glucose or insulin levels. LDL-triglycerides were higher in BT and diabetic than in CO and LF rats. HDL-free cholesterol levels were higher in CO- and LF- than in BT-fed rats. Diabetes resulted in a decrease in HDL-cholesterol. Diabetic animals had higher HDL-apoA-I (apolipoprotein A-I) levels than did CO- and LF- but not BT-fed rats. VLDL-triglycerides were higher in diabetic than in normal rats, with no dietary differences in normal rats. In LDL, apoB levels were lower and apoE levels were higher in LF-fed rats than in animals fed high fat diets. Diabetes resulted in an increase in LDL-apoB but a decrease in LDL-apoE. HDL-apoE levels were higher, although HDL-apoA-I levels were lower in LF than in high fat-fed rats. The results related to lipoprotein composition supported the hypothesis that excess intake of a diet high in saturated fat may contributed to a metabolic pattern that resembles that of a diabetic state.


KEY WORDS: • dietary fat • diabetes • lipoprotein • apoprotein • glucose • insulin • rat

1 Journal Paper No. J-10841 of the Iowa Agriculture and Home Economics Experiment Station, Ames, IA; Project No. 2438.

2 Supported in part by U.S. Public Health Service, National Institutes of Health (project L23598) and the Iowa State University Research Foundation.

3 Present address: College of Medicine, Dept. of Biochemistry, The University of Iowa, Iowa City, IA 52242.

4 To whom correspondence should be addressed.

Manuscript received 21 March 1983.





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