Severe fatty liver in rats fed a fat‐free ethanol diet, and its prevention by small amounts of dietary arachidonate

Abstract

Rats were fed ethanol and a fat-free diet for 30 days to determine whether dietary fat is needed for the development of fatty liver. The severity of fatty liver was similar to that of rats fed an isocaloric diet with 35% fat. Small amounts (29 mg/day) of dietary arachidonic acid prevented alcoholic fatty liver. Rats fed either the alcohol (AF) or control (CF) fat-free diets developed essential fatty acid deficiency (EFAD) as measured by the triene/tetraene ratio of liver and plasma lipids. Rats fed arachidonic acid (AA, alcohol and CA, control diets) did not develop EFAD. Although EFAD alone did not cause the development of fatty liver, the combination of dietary ethanol and EFAD did. The ratios of 16:1/16:0 and 18:1/18:0 in liver lipids indicated that desaturase enzymes were less active and lipogenesis was reduced in rats fed the AA diet compared to those fed the AF diet. In contrast, stimulated lipogenesis appears to have been the cause of fatty liver in rats fed the AF diet.

Severe and progressive steatosis and focal necrosis in rat liver induced by continuous intragastric infusion of ethanol and low fat diet

“…Indeed, a recent study with a fat-free ethanol diet showed that diebary fat was not needed for the development of fatty liver similar to that observed in rats fed an isocaloric diet with 35% fat (18). In this regard, data on the fatty acid composition in liver t.riglycerides have suggested that fatty liver produced in this study was due to the stimulated de novo synthesis of fatty acids rather than deposition of dietary fat.…”

Reversal of hepatic steatosis by omega‐3 fatty acids measured non‐invasively by 1H‐magnetic resonance spectroscopy in a rat model

“…An important discrepancy of the HCLF steatosis model with human NASH, however, is the induction of essential FA deficiency (EFAD, defined by a mead acid (20:3‐ω9):arachidonic acid (20:4‐ω6) ratio of > 0.2), and thus a lack of hepatic omega‐6 and omega‐3 FA. Steatosis prevention by omega‐3 FA intake in the HCLF model can thus in part be explained by correcting the EFAD status, as has been shown by Groheen et al ., 30 rather than by correcting the hepatic omega‐6:3 FA ratio. The MCD diet‐induced steatosis model therefore seems to be more suitable for the type of intervention studies as performed here.…”

The route of lipid administration affects parenteral nutrition–induced hepatic steatosis in a mouse model

“…However, one explanation for the severe steatosis found in the PN-O animals is essential fatty acid deficiency because this group received only PN without dietary lipid supplementation during the 19-day study protocol. Previous studies have shown that essential fatty acid deficiency alone can cause steatosis in the liver [27] and that reversing essential fatty acid deficiency can prevent steatosis [28]. To measure essential fatty acid status, we performed fatty acid analyses on serum from all study groups.…”