Polyenylphosphatidylcholine Attenuates Alcohol-Induced Fatty Liver and Hyperlipemia in Rats , ,

Abstract

Chronic administration of a soybean-derived polyenylphosphatidylcholine (PPC) extract prevents the development of cirrhosis in alcohol-fed baboons. To assess whether this phospholipid also affects earlier changes induced by alcohol consumption (such as fatty liver and hyperlipemia), 28 male rat littermates were pair-fed liquid diets containing 36% of energy either as ethanol or as additional carbohydrate for 21 d, and killed 90 min after intragastric administration of the corresponding diets. Half of the rats were given PPC (3 g/l), whereas the other half received the same amount of linoleate (as safflower oil) and choline (as bitartrate salt). PPC did not affect diet or alcohol consumption [15.4 +/- 0.5 G/(kg.d)], but the ethanol-induced hepatomegaly and the hepatic accumulation of lipids (principally triglycerides and cholesterol esters) and proteins were about half those in rats not given PPC. The ethanol-induced postprandial hyperlipemia was lower with PPC than without, despite an enhanced fat absorption and no difference in the level of plasma free fatty acids. The attenuation of fatty liver and hyperlipemia was associated with correction of the ethanol-induced inhibition of mitochondrial oxidation of palmitoyl-1-carnitine and the depression of cytochrome oxidase activity, as well as the increases in activity of serum glutamate dehydrogenase and aminotransferases. Thus, PPC attenuates early manifestations of alcohol toxicity, at least in part, by improving mitochondrial injury. These beneficial effects of PPC at the initial stages of alcoholic liver injury may prevent or delay the progression to more advanced forms of alcoholic liver disease.

Effects of β‐carotene on antioxidant status in rats with chronic alcohol consumption

“…19 The plasma AST and ALT activities in group E were significantly higher than those in group C, which is consistent with the long-term effects of ethanol administration on liver injury. 20 In contrast, the elevation of these two enzyme activities in group EþB was significantly less than that in group E, which indicate a reduction in ethanol-induced liver damage. Similarly, from the light micrograph of liver, fat accumulation was observed in group E, which might have been due to enhanced mobilization of free fatty acids from adipose tissue and increased hepatic biosynthesis of lipids, as previously suggested.…”

Ethanol feeding enhances age-related deterioration of the rat hepatic mitochondrion

“…Figure 3 and Table 1 show a clear interaction existing between ethanol feeding and the age of the animal with regard to hepatomegaly. Chronic ethanol consumption is associated with an increase in hepatocyte volume due to increased intracellular water retention (28), decreased protein secretion (5), impaired protein catabolism (18), and elevated fat deposition (45). Young animals fed ethanol for 21 days showed significantly increased liver weights (Fig.…”

Conversation with Charles S. Lieber

“…102 Finally, impaired hepatic oxygen utilization was de ned as an important mechanism for the hepatotoxicity of alcohol. 103 It was corrected with PPC, 79 which was also shown to attenuate alcohol-induced apoptosis. 104 Clinical trials with PPC are ongoing in patients with alcoholic liver disease and preliminary bene cial effects have been reported at the 2000 AASLD meeting.…”