Studies on the Hepatic Accumulation of Triglyceride Induced by Chronic Ethanol Administration in Rats Fed with Various Diets

ABSTRACT

Investigation in our laboratory has been undertaken to study the effect of ethanol on the triglyceride (TG) content in the liver, the free fatty acid (FFA) content in the serum and the glycogen in the liver of rats which were fed on various diets. Four hours after administration of a sing1e dose of glucose (5g/kg BW.) and ethanol (6g/kg BW.) by gavage tube to rats fed a norma1 diet for 20 days then fasted for 18 hours, TG content in the liver increased by 80%, 10% compared to the control. When a sing1e dose of equal amounts of both glucose and ethanol were administered to another group, TG content in the liver was 42% higher than the control. There was no great change in serum FFA content in the glucose treated group as compared with the control, however, there was an increment of serum FFA content in the ethanol treated group and in the group treated with both ethanol and glucose by 81% and 71% of the control, respectively. The results indicate that ethanol administration had an inhibitory effect on the TG accumulation in the liver of rats fed by glucose. There is a correlation between TG accumulation in the liver and FFA content in the serum, and it appears that the ethanol administration did not induce the TG accumulation in the liver but the increment of serum FFA content in rats is probably due to the increased fatty acid mobilization from adipose tissue. However, countercurrent results were observed in the glucose treated group as compared with the ethanol treated group suggesting that glucose administration does induce TG accumulation in the liver but does not increase the serum FFA content in rats. The increment of serum FFA content in rats. The increment of serum FFA content by ethanol treatment was not ameliorated by glucose administration. In the liver perfusion experiment with rats fed both ethanol and various other diets, the results of incorporation of ethanol-1-14C into the total lipid in the high carbohydrate, high fat, low carbohydrate and control diet group were 1925 +/- 257 (cpm/g liver), 1237 +/- 76, 1269 +/- 105, 2041 +/- 74, respective1y. The results indicate that amount of dietary carbohydrate and high fat had an effect on the total lipid accumulation derived from ethanol-1-14C molecule in the liver. Liver glycogen content in the control on rats, high fat, 1ow carbohydrate and high carbohydrate diets were 91.5 +/- 7.9(mg%), 93.0 +/- 1.8, 99.1 +/- 4.4, and 153.7 +/- 26.0, respectively. There were no great differences between each dietary group and the rest control group except in the case of the high carbohydrate group which was over 1.5 times greater than that of the control. The incorporation of labelled ethanol into liver glycogen in the control rats and those on high fatdiet, low carbohydrate diet and high carbohydrate diet were 525, 401, 351 and 806 cpm/g liver, respectively. The increased incorporation of ethanol-1-14C into liver glycogen in the high carbohydrate diet group is thought to be due to the increased gluconeogenesis from acetyl CoA derived from 14C from ethanol because rats were fasted for 18 hours before perfusion. It might be the result of increased gluconegenesis of acetyl CoA derived from ethanol-1-14C by spare action of high carbohydrate on acetyl CoA. During the liver perfusion, 14CO2 production from ethanol-1-14C was higher in the high fat diet and low carbohydrate diet groups than in the control group, however, no great difference was observed between the high carbohydrate and control groups. The higher production of 14CO2 from the single ethanol-1-14C dose in rats on the high fat diet and low carbohydrate diet groups than in the control group is probably due to the increased metabolism of ethanol through Kreb's cycle rather than the incorporation of it into the liver fat.