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Free Methionine Supplementation Limits Alcohol‐Induced Liver Damage in Rats
Author(s) -
Parlesak Alexandr,
Bode Christiane,
Bode J. Christian
Publication year - 1998
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1998.tb03660.x
Subject(s) - methionine , alcohol , medicine , endocrinology , triglyceride , ethanol , liver injury , chemistry , ingestion , biochemistry , biology , cholesterol , amino acid
Alcohol feeding to rats that were submitted to a jejunoileal bypass operation has been shown to result in liver damage being comparable with alcohol‐induced liver disease in man. In the present study, a striking effect of free methionine consumption on histological liver injury, triglyceride accumulation, and energy‐rich nucleoside content in the liver of rats with a jejunoileal bypass is demonstrated. The animals obtained 0, 30, and 120 mg of methionine in the control group and 0,30,120, and 240 mg in the alcohol‐fed group per day and per kilogram of body weight for 12 weeks. Methionine was found to strongly improve the alcohol‐induced histological changes in the liver. Triglyceride content of the liver was found to decrease in a dose‐dependent manner with increasing methionine ingestion (from 255 ± 20.7 to 49.7 ± 6.1 μmol/g of protein in the control group and from 233 ± 17.3 to 42.1 ± 7.2 μmol/g of protein in the alcohol group). Hepatic adenosine triphosphate content increased significantly with higher methionine consumption (13.5 ± 0.8 vs. 26.9 ± 2.8 μmol/g of protein in the control group and 11.9 ± 1.4 vs. 20.5 ± 2.5 μmol/g of protein in the alcohol group), whereas no differences were found in the protein and DNA content of the liver. These results underscore the impairment of the transmethylation/transsulfuration pathway in the development of alcohol‐induced liver diseases.