Effect of Chronic Ethanol Consumption on Vitamin a Metabolism (beta-Carotene, Rats)

A number of stresses place additional demands on an organism for vitamin A, and chronic ethanol consumption is suspected of causing a similar response. Therefore, this study was undertaken to determine the effect of chronic elevated ethanol consumption on vitamin A status and metabolism in rats. Ethanol-containing liquid diets were fed to male rats, which as demonstrated in a preliminary experiment, needed to be pair-fed. Despite equivalent dietary intakes, hepatic vitamin A levels were lower in ethanol-fed rats. This occurred when either retinyl acetate or (beta)-carotene were the dietary source of vitamin A. In comparison to rats fed a moderate fat diet, a greater decrease of liver vitamin A levels occurred in ethanol-fed rats on a high fat diet. Decreased hepatic vitamin A storage resulted despite only a slight elevation of total liver lipids, which suggests no marked liver damage. Therefore, decreased vitamin A storage is not likely a secondary effect of chronic ethanol consumption on hepatic tissue. The activities of several enzymes involved in both ethanol and vitamin A metabolism were not altered by ethanol consumption. Malabsorption of vitamin A in ethanol-fed rats was not indicated, since ethanol-fed rats excreted less of an intragastric dose of labelled vitamin A in feces than did control rats, and since no change in absorption of the labelled vitamin occurred from intestinal loops. Since no difference in the excreted amount of label from an intragastric dose of vitamin A resulted in ethanol-fed rats, increased catabolism of the vitamin does not appear to be a mechanism involved in decreased hepatic vitamin A storage. Increased nonhepatic tissue vitamin A accumulation, primarily in the adrenals and lungs, and increased recovery of label from vitamin A in nonhepatic tissues occurred in ethanol-fed rats. In contrast, kidney vitamin A levels were either lower or unchanged in ethanol-fed rats. Decreased hepatic vitamin A levels may be explained, in part, by increased nonhepatic tissue accumulation of vitamin A.

Name thesis:degree_name

Ph.D.

Level thesis:degree_level

Dissertation

Discipline thesis:degree_discipline

Food Science

Grantor

University of Illinois at Urbana-Champaign

Year dc:date

2015

Author dc:creator

• Grummer, Mary Ann

• Health Sciences, Nutrition

Language dc:language

eng

Identifier

(UMI)AAI8502158

OAI identifier oai:identifier

oai:www.ideals.illinois.edu:2142/77449