Role of Hypophysis and Adrenals in Fatty Infiltration of Liver Resulting From Acute Ethanol Intoxication

Abstract

Acute ethanol intoxication was found to promote the fatty infiltration of liver in rats. The liver lipid concentrations gradually rose to peak values, then slowly returned to normal. The duration of the fatty infiltration, and the peak liver lipid values obtained, were functions of the dose of ethanol administered. Female rats showed a more severe fatty infiltration than did males, under the same conditions. The prior administration of large quantities of choline reduced the intensity of the fatty infiltration provoked by the ethanol. In contrast to intact animals, neither adrenalectomized nor hypophysectomized rats showed an accumulation of liver lipids as a result of acute ethanol intoxication. Adrenalectomized rats maintained on cortisone, and adrenal demedullated rats, however, showed the same liver lipid response to ethanol as did intact rats. Rats chronically intoxicated for a period of 30 days exhibited hypertrophy of the adrenals. Acute intoxication produced by isopropanol administration also resulted in the accumulation of liver lipid. It is suggested that ethanol intoxication may cause the mobilization of fat from the depots to the liver, and that pituitary and adrenal cortical hormones are involved in the mechanism of this mobilization.