Hepatic triglyceride accumulation and the ethanol physical withdrawal syndrome in mice.
Physical dependence on ethanol was induced in TO strain mice by chronic administration of ethanol by inhalation. The severity of the behavioral syndrome of withdrawal from ethanol was quantified by a subjective scoring method. During the chronic administration of ethanol, triglycerides accumulated in livers of male or female mice with a time course similar to that of the induction of physical dependence. When ethanol was withdrawn from adult or weaning dependent mice, a relationship was observed between the decline of triglyceride concentrations in liver and the duration of the ethanol withdrawal syndrome. The addition of DL-carnitine (7% w/w) to diet during the administration of ethanol markedly inhibited the accumulation of triglycerides, and significantly reduced the intensity of the ethanol withdrawal syndrome. Administration of carbon tetrachloride ((1.3 ml/kg i.p.), however, although augmenting hepatic triglyceride accumulation, had no significant effect on the withdrawal syndrome. The results are interpreted as suggesting either that ethanol-induced liver dysfunction plays a part in dependence, or, more likely, that triglyceride accumulation reflects an ethanol-induced metabolic disorder which is itself related to the induction of dependence.
D000437:Alcoholism / Q000378:metabolism*; D000818:Animals; D002251:Carbon Tetrachloride / Q000494:pharmacology; D002331:Carnitine / Q000494:pharmacology; D000431:Ethanol; D005260:Female; D006801:Humans; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D051379:Mice; D013375:Substance Withdrawal Syndrome / Q000378:metabolism*; D013997:Time Factors; D014280:Triglycerides / Q000378:metabolism*
D014280:Triglycerides; D000431:Ethanol; D002251:Carbon Tetrachloride; D002331:Carnitine