Free methionine supplementation limits alcohol-induced liver damage in rats
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Free methionine supplementation limits alcohol-induced liver damage in rats. / Parlesak, Alexandr; Bode, Christiane; Bode, J Christian.
In: Alcoholism: Clinical and Experimental Research, Vol. 22, No. 2, 1998, p. 352-358.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Free methionine supplementation limits alcohol-induced liver damage in rats
AU - Parlesak, Alexandr
AU - Bode, Christiane
AU - Bode, J Christian
N1 - (Ekstern)
PY - 1998
Y1 - 1998
N2 - 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.
AB - 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.
KW - Adenosine nucleosides
KW - Alcohol
KW - Alcoholic liver disease
KW - Fatty liver
KW - Methionine
U2 - 10.1111/j.1530-0277.1998.tb03660.x
DO - 10.1111/j.1530-0277.1998.tb03660.x
M3 - Journal article
C2 - 9581640
AN - SCOPUS:0031979059
VL - 22
SP - 352
EP - 358
JO - Alcoholism: Clinical and Experimental Research
JF - Alcoholism: Clinical and Experimental Research
SN - 0145-6008
IS - 2
ER -
ID: 317458168