Role of dietary, adipose, and endogenously synthesized fatty acids in the pathogenesis of the alcoholic fatty liver.

Open Access
Publisher Website
Google Scholar
Abstract
In rats, one large dose of ethanol (7.5 g per kg) produced moderate hepatic accumulation of fatty acids resembling those of adipose tissue; in contrast, after prolonged ethanol intake, fatty liver was more pronounced and had a fatty acid composition different from depot fats. Rats given 24 days of ethanol with low-fat diets (2% of calories) had a linoleate concentration in hepatic triglycerides one-fifth that of adipose tissue with, however, 50% more palmitate, an endogenously synthesized fatty acid. In rats given alcohol with fat-containing diets (43% of calories), fatty acids accumulating in the liver triglycerides had a large component of dietary fatty acids (either laurate plus myristate or linolenate), whereas these fatty acids when administered to "prelabel" adipose tissue were found to be much less abundant in liver triglycerides than in depots. Despite the same ethanol intake, significantly less steatosis developed in rats given isocaloric diets containing carbohydrate instead of fat. After 24 days, the rise in total hepatic lipids was 1.5-fold on the 2% fat diet compared to 2.6-fold on the 43% fat diet; corresponding triglyceride changes were 2.6- and 6.3-fold respectively. Whereas ethanol had no apparent effect on intestinal palmitate-C14 absorption or uptake by the liver of chylomicron-C14 administered intravenously, hepatic lipid labeling was enhanced 2 to 6 hours after palmitate-C14 intubation or 3 hours after chylomicron-C14 injection. These studies indicate that the source and the magnitude of the fatty acids accumulating in hepatic triglycerides after alcohol administration depend on the dose and duration of alcohol intake as well as the fat content of the associated diet.