Lipotropic

Abstract: Experimental dietary hepatic injury (diffuse or focal necrosis and cirrhosis in rats, with or without ascites and pleural and pericardial effusion) is determined by the dietary factors instrumental also in the production of fat infiltration of the liver and thus opposed to the lipotropic activity of casein. Accordingly, rats maintained on a diet low in casein with a moderately high or high content of fat and without choline regularly exhibited hepatic injury after between 100 and 150 days. Supplements of l-cystine had an aggravating effect on the production of cirrhosis of the liver, whereas a supplement of choline alone reduced the severity and the incidence of hepatic injury, although not decisively. The combined administration of l-cystine plus choline or of dl-methionine in adequate doses, however, proved to be highly effective in preventing injury to the liver. These conclusions have been corroborated by the use of different modifications of the basal diet. Rats with dietary hepatic injury exhibit, in sequence, changes that vary from diffuse necrosis resembling human acute or subacute yellow atrophy to advanced portal cirrhosis. Diffuse necrotizing nephrosis was a frequent accompaniment of the hepatic injury. Cystine again, proved to be a factor which aggravated this condition.

Abstract: Rats maintained for a period of 7 months on a fluid intake of 15 per cent alcohol and a diet marginal in lipotropic activity developed fatty infiltration and mild fibrosis of the liver. Similar changes were observed in pair-fed controls given an isocaloric equivalent of sucrose instead of alcohol, but not in pair-fed controls receiving neither alcohol nor sucrose supplements. To exclude the possibility that the alcohol effect was related to an augmentation of the caloric intake, a third group of controls was given the same amount of alcohol, but a limited number of calories. This was accomplished by subtracting from the basal diet an amount of sucrose equivalent in calories to the alcohol consumed. Under these conditions the hepatic changes following alcohol ingestion appeared to be enhanced. Choline or methionine, on the other hand, abolished the effects of both alcohol and sucrose supplements. There was no increase in fecal nitrogen excretion following alcohol ingestion, and no histological changes were observed in the pancreas. These results are consistent with the hypothesis that alcohol increases the choline requirement of the rat, but do not support the contention that this effect is the consequence of an augmented caloric intake. Further studies are needed to establish conclusively the relationship between alcohol ingestion and the choline requirement, and to elucidate the mechanisms involved.

Abstract: Background Betaine is a methyl donor and has been considered as a lipotropic effect substance. But its mechanism remains unclear. Hepatic steatosis is associated with abnormal expression of genes involved in hepatic lipid metabolism. DNA methylation contributes to the disregulation of gene expression. Here we hypothesized that betaine supplement and subsequent DNA methylation modifications alter the expression of genes that are involved in hepatic lipid metabolism and hence alleviate hepatic triglyceride accumulation.