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Roles of Hormonal and Nutritional Factors in the Regulation of Rat Liver Alcohol Dehydrogenase Activity and Ethanol Elimination Rate in Vivo
Author(s) -
Lakshman M. R.,
Chambers Laura L.,
Chirtel Stuart J.,
Ekarohita Nisa
Publication year - 1988
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1988.tb00217.x
Subject(s) - medicine , endocrinology , glucagon , insulin , carbohydrate , hormone , meal , ethanol , alcohol dehydrogenase , in vivo , stimulation , carbohydrate metabolism , biology , chemistry , biochemistry , microbiology and biotechnology
Fasting reduced the liver alcohol dehydrogenase (ADH) activity by 51% ( p < 0.001). Insulin, within 2 hr, increased the ADH activity found in fasted animals by 28% ( p < 0.02). Insulin administration failed to stimulate the reduced ADH activity in diabetic rats. However, ADH activity in the diabetic‐fed rats decreased by 52‐54% ( p < 0.001) compared to normal‐fed rats regardless of whether they were meal‐fed or refed the normal chow. Glucagon blocked by 15% ( p < 0.02) the increase in ADH activity associated with refeeding. Furthermore, insulin caused a marginal stimulation of ethanol elimination rate (EER) when administered to fasted rats. All these results imply that insulin and glucagon may not be the only determining factors in the control of liver ADH activity associated with fasting and refeeding. Meal‐feeding or refeeding a high carbohydrate fat‐free diet compared to the normal chow‐diet caused 29% ( p < 0.001) and 36% ( p < 0.05) decreases in ADH activity, respectively. Concomitant decreases in EER caused by high carbohydrate fat‐free diet feeding were also observed under identical conditions. These results raise the possibility that the amount and the type of carbohydrate may be crucial in the regulation of ADH and EER. Alternatively, the presence of fat may be important in maintaining the normal level of ADH and EER.