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Role of Vitamin A Degradation in the Control of Hepatic Levels in the Rat^1,2,

Section of Liver Disease and Nutrition, Alcohol Research and Treatment Center, Bronx Veterans Administration Medical Center and Mt. Sinai School of Medicine, City University of New York, New York, NY 10468

The relationship between excess vitamin A intake and accumulation in various tissues, including the liver, was studied in rats fed for 45 d four levels of vitamin A: 1, 6, 30 and 100 IU/kcal. As vitamin A intake increased, progressively smaller fractions of the administered vitamin A were recovered in tissue. The decrease in fractional recovery in the tissues examined was calculated from the differences between intake, tissue level and excretion, and was found to increase after administration of high vitamin A diets. This could be explained, at least in part, on the basis of an enhanced rate of vitamin A degradation as a function of the increased concentration of retinol in the liver. At high tissue retinol concentrations, calculated rates of retinol metabolism via the hepatic cytosolic retinol dehydrogenase (EC 1.1.1.1) and the recently discovered microsomal retinol dehydrogenase and oxidase vastly exceeded the decrease in fractional recovery of vitamin A accumulation in the tissues. This calculated rise in metabolic rate was verified by a corresponding increase in urinary polar metabolites derived from labeled retinol. Thus, accelerated catabolism as a function of increased hepatic vitamin A concentration may provide a homeostatic mechanism which offsets in part excessive vitamin A accumulation.

KEY WORDS: • vitamin A metabolism • liver • homeostatic control • rat

¹ Supported by Department of Human Health Services grants DK 32810, AA 03508 and AA 05934 and the Veterans Administration.

² Presented in part at the Meeting of the International Association for the Study of the Liver, Toronto, Canada, Nov. 4, 1988 [Hepatology 8: 1423 (abs.), 1988].

Manuscript received 29 November 1988. Revision accepted 29 March 1989.