Effects of Ethanol and Liver Disease on the Vitamin-A Status of Rats and Humans
McCauley, Karen Marie
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https://hdl.handle.net/2142/77460
Description
Title
Effects of Ethanol and Liver Disease on the Vitamin-A Status of Rats and Humans
Author(s)
McCauley, Karen Marie
Issue Date
1987
Doctoral Committee Chair(s)
Erdman, John, Jr.,
Department of Study
Food Science
Discipline
Food Science
Degree Granting Institution
University of Illinois at Urbana-Champaign
Degree Name
Ph.D.
Degree Level
Dissertation
Keyword(s)
Health Sciences, Nutrition
Language
eng
Abstract
Pathological responses to ethanol vary, and are often not predictable based upon the amount or duration of ethanol intake. These studies focused on the vitamin A status response to ethanol intake, using animal models to mimic chronic and binge ethanol intake with and without liver disease development. Ethanol was used in models without liver disease development; carbon tetrachloride (CCl$\sb4$) inhalation and dietary phenobarbitol was used in models of liver disease. A mixed group of human alcoholics was also studied.
Depleted hepatic vitamin A reserves and increased extrahepatic tissue vitamin A were found in rats chronically exposed to ethanol or CCl$\sb4$. In the binge drinking models, lower hepatic vitamin A was found after one ethanol dose, but no differences in hepatic or extrahepatic vitamin A were found after repeated doses. Rats receiving three ethanol doses also received an intragastric dose of radiolabelled vitamin A. Label recovery was greater in the ethanol-dosed rats' livers and urines than controls'.
Increased total hepatic vitamin A was found after two acute exposures to CCl$\sb4$. However, after four or six exposures, this difference wasn't found. Animals exposed to CCl$\sb4$ on six occasions also received an intragastric dose of labelled vitamin A; larger amounts being recovered from liver and urine than in controls.
Of twenty-eight human alcoholics, sixteen and seven had low serum retinol and retinol binding protein (RBP), respectively. Seventeen had low molar ratios of retinol to RBP: four had elevated ratios. All alcoholics with elevated serum bilirubin levels had low serum retinol levels. Serum triglycerides, zinc, and RBP were used to mathematically predict serum retinol levels. This equation may be useful in hospitals where retinol analyses are not routinely available.
It therefore appears that differences in vitamin A distribution are found depending upon whether the hepatotoxin is given acutely or chronically. CCl$\sb4$ exposure with dietary phenobarbitol is a more potent hepatotoxin than ethanol, and may prove to be a good model for mimicking human alcoholics who develop liver disease. Further investigations using ethanol and CCl$\sb4$ models may aid in understanding some of the variation seen in human alcoholics concerning their vitamin A status.
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