Effects of Dietary Methionine and Folate Supplementation in Ethanol-Fed Rats

Chronic alcohol consumption is associated with perturbation of hepatic metabolism of sulphur-containing amino acid Thc goal of present study was to evaluate the influence of dietary supplementation of methionine or folate to chronically ethanol-fed rats on the metabolism of sulfur-containing amino acids and one-carbon metabolism Sprague-Dawley male rats were fed Lieber-Decarli liquid diet with 0% ethanol (control), 36% ethanol (E), 36% ethanol combined with methionine supplement (EM) or folate supplement (EF) for 8 weeks. Hepatic S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH), plasma folate and homocysteine (Hcy), urinal)' excretion of folate and formiminoglutamate were investigated after feeding experimental diets. Growth was retarded by 36% ethanol consupmtion (E, EM and EF) (p＜0.01). Liver total fat (p＜0.05) and plasma ALT (p＜0.01) were increased by methionine supplementation (EM), implicating fatty liver and liver injury. Liver folate was increased slightly by folate supplementation (EF) (p=0.077). Urinal)' folate loss was increased 2.3 fold by ethanol consumption (E) and 17.2 fold by folate supplementation (EF), while decreased by methionine supplementation (EM) (p＜0.0001). Plasma Hey was increased 1.9 fold by methionine supplementation (EM) in ethanol-fed rats (p＜0.05), which was related with decreased methionine synthase activity (p<0.05). Hepatic SAM/SAD ratio was depressed by methionine supplementation in ethanol-fed rats (EM) (p＜0.05). Urinary formininoglutamate (Figlu) excretion after histidine loading was increased by ethanol ingestion and reduced by methionine supplementation (p＜0.001). Based on these dam, methionine supplementation appears to accelerate histidine oxidation. In conclusion, dietary supplementation of methionine to ethanol-fed rats exacerbates alcoholic liver injury possibly by complicating sulphur-containing amino acid metabolism, as while it may have beneficial effects on folate and histidine metabolism.