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Urinary ascorbic acid excretion and sugar consumption as indices of enzyme induction and hypoglycemia in recovering alcoholic rats

In an effort to assess whether the craving for sweets experienced by some abstaining alcoholics is physiologically based, 48 Wistar rats were divided into 4 groups. Groups 1 and 3 were fed a liquid diet containing 35.5 percent energy as alcohol; groups 2 and 4 were fed a control diet with dextrins substituted for alcohol, all for 24 days. Group 4 was pair-fed to group 3. For the next 10 days, all rats were provided with sucrose and water ad libitum and all groups were continued on their liquid diet except that alcoholic group 3 was placed on the control diet and pair-fed group 4 was no longer pair-fed. Urine was collected at the end of the baseline, alcohol-induction, and recovery periods and analyzed for L-ascorbic acid. The mean consumption of sucrose was highest for rats still receiving alcohol and declined in all groups during the 10 days. The mean consumption of sucrose (% kcal as sucrose) for the first 4 days was 33.2, 19.5, 19.0, and 13.8% for groups 1, 2, 3, and 4 declining to 24.6, 11.2, 9.0, and 8.5 percent, respectively by the last 4 days. The sugar intake of alcoholic group 3 animals was significantly higher than pair-fed control group 4 during the first 4 days. L-ascorbic acid excretion was significantly increased in the groups receiving alcohol and declined during the recovery period. This study has raised the possibility that increased urinary excretion of ascorbic acid may suppress glycogen synthesis, leading to hypoglycemia. / Master of Science

Identiferoai:union.ndltd.org:VTETD/oai:vtechworks.lib.vt.edu:10919/76249
Date January 1982
CreatorsSiegel, Janet R.
ContributorsHuman Nutrition and Foods
PublisherVirginia Polytechnic Institute and State University
Source SetsVirginia Tech Theses and Dissertation
Languageen_US
Detected LanguageEnglish
TypeThesis, Text
Formatvii, 89, [2] leaves, application/pdf, application/pdf
RightsIn Copyright, http://rightsstatements.org/vocab/InC/1.0/
RelationOCLC# 8890684

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