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.

Hormonal regulation of hepatic soluble phosphatidate phosphohydrolase

“…A single intraperitoneal injection of a saline pituitary homogenate equivalent to a whole rat pituitary gland [3] increased the activity of the hepatic phosphatidate phosphohydrolase in preliminary experiments by more than 2-fold (data not shown). Since this injection is also capable of causing fat accumulation in the liver [3], the effects of those pituitary hormones, the secretion of which is influenced by the administration of ethanol were investigated in vivo (table 1).…”

“…Since this injection is also capable of causing fat accumulation in the liver [3], the effects of those pituitary hormones, the secretion of which is influenced by the administration of ethanol were investigated in vivo (table 1). Somatotropin and corticotropin increased the activity of hepatic phosphatidate phosphohydrolase by 66% and 43%, respectively, whereas vasopressin was without effect.…”

Effects of Prolonged Ethanol Intake: Production of Fatty Liver Despite Adequate Diets*

“…When given acutely without food in a large single dose by gastric tube, alcohol was found to produce fat accumulation in the liver (26)(27)(28)(29)(30), but the mechanisms involved in these acute experiments do not necessarily apply to more prolonged alcohol intake, such as is observed commonly in chronic alcoholic patients.…”

Heterogeneity of the sn-glycerol 3-phosphate pool in isolated hepatocytes, demonstrated by the use of deuterated glycerols and ethanol

“…From these studies it has been concluded that both hepatic ethanol oxidation and increased peripheral lipolysis may be involved (Blomstrand & Forsell, 1971;Mallov & Bloch, 1956). Ethanol oxidation in the liver results in an increased concentration of sn-glycerol 3-phosphate (Reitz, 1979;Nikkila & Ojala, 1963), and this might result in an increased formation of triacylglycerols and phosphoglycerides (Wirthensohn et al, 1980;Debeer et al, 1981).…”