Doctoral Dissertations

Date of Award

8-1984

Degree Type

Dissertation

Degree Name

Doctor of Philosophy

Major

Human Ecology

Major Professor

Dileep S. Sachan

Committee Members

Roy E. Beauchene, Hugh O. Jaynes, Sharon L. Melton

Abstract

The lipotropic and hypolipidemic effects of carnitine and its precursors, namely lysine (Lys) and methionine (Met), was examined in male Sprague-Dawley rats fed ethanol as 36% of the total calories for a duration of 56 days (Experiment I). Ethanol produced significant hepatic steatosis and hypertriglyceridemia as evidenced from elevated concentrations of total lipids, triglycerides, cholesterols, and phospholipids. Supplementation of the ethanol diet with 1.0% D,L-carnitine and 0.5% L-Lys plus 0.2% L-Met significantly reduced ethanol-induced elevation of the various lipid classes with the exception of free fatty acids. The triglyceride contents in liver and plasma were inversely related to the concentrations of carnitine, acylcarnitines, and total carnitine. The effects of a combination of carnitine and its precursors were not greater than those of carnitine alone. It is suggested, therefore, that a deficiency of functional carnitine may exist in a chronic alcoholic state which can be improved by dietary carnitine.

In two following experiments, animals were fed the ethanol liquid diets supplemented with various levels (Experiment II: 0.0, 0.2, 0.6, 1.0, and 2.0%; Experiment III: 0.0, 0.1, 0.5, 0.8, 1.2, and 1.6%) of D,L-carnitine for 28 and 45 days. In the 28 day experiment, the effects of supplemental carnitine were significant only in the plasma triglycerides and reduction in hepatic lipid classes were minimal. In the 45 day experiment, various lipid classes of the alcohol-compromised liver and plasma were significantly reduced with carnitine treatment, and the effect was dose-dependent. The optimum lipotropic and hypolipidemic effect were produced by 0.8% D,L-carnitine. thus it is concluded that in rats, supplemental D,L-carnitine ameliorated ethanol-induced hyperlipidemia and hepatic steatosis in a dose-dependent manner.

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