Ethanol‐Induced Hepatic Triglyceride Accumulation in Mice and Genetic Differences in the Ethanol Physical Withdrawal Syndrome

Three strains of mice (DBA, TO and C5T) were exposed to ethanol vapour in separate inhalation chambers for 10 days. The concentration of ethanol in inspired air was carefully controlled so that similar concentrations of ethanol in blood (c. 2 mg ml^‐1) were produced in each strain. No significant differences between strains mere observed, in ethanol or acetaldehyde concentrations in blood or in liver after administration of ethanol for 10 days. On withdrawal of ethanol some mice of each strain were assessed for the ethanol withdrawal syndrome (convulsions, tremor, piloerection, and tail erection) using a subjective scoring system. The remainder were killed for measurement of hepatic triglyceride concentration. The DBA strain of mice showed a very severe ethanol withdrawal syndrome. Hepatic triglyceride concentration in this strain showed an increase of 892 per cent compared to controls. The C57 strain in contrast showed little evidence of a physical withdrawal syndrome, and triglyceride concentrations in liver were increased only 235 per cent above control concentrations. TO mice were intermediate both in withdrawal syndrome severity and in accumulation of triglycerides in liver (365 per cent above control). The results suggest an association between genetic differences in ethanol‐induced changes in hepatic lipid metabolism and the seventy of the ethanol physical withdrawal syndrome.