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 journalJournal articleResearchpeer-review

Harvard

Parlesak, A, Bode, C & Bode, JC 1998, 'Free methionine supplementation limits alcohol-induced liver damage in rats', Alcoholism: Clinical and Experimental Research, vol. 22, no. 2, pp. 352-358. https://doi.org/10.1111/j.1530-0277.1998.tb03660.x

APA

Parlesak, A., Bode, C., & Bode, J. C. (1998). Free methionine supplementation limits alcohol-induced liver damage in rats. Alcoholism: Clinical and Experimental Research, 22(2), 352-358. https://doi.org/10.1111/j.1530-0277.1998.tb03660.x

Vancouver

Parlesak A, Bode C, Bode JC. Free methionine supplementation limits alcohol-induced liver damage in rats. Alcoholism: Clinical and Experimental Research. 1998;22(2):352-358. https://doi.org/10.1111/j.1530-0277.1998.tb03660.x

Author

Parlesak, Alexandr ; Bode, Christiane ; Bode, J Christian. / Free methionine supplementation limits alcohol-induced liver damage in rats. In: Alcoholism: Clinical and Experimental Research. 1998 ; Vol. 22, No. 2. pp. 352-358.

Bibtex

@article{13995677c9a94f508a15614c52cd7633,
title = "Free methionine supplementation limits alcohol-induced liver damage in rats",
abstract = "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.",
keywords = "Adenosine nucleosides, Alcohol, Alcoholic liver disease, Fatty liver, Methionine",
author = "Alexandr Parlesak and Christiane Bode and Bode, {J Christian}",
note = "(Ekstern)",
year = "1998",
doi = "10.1111/j.1530-0277.1998.tb03660.x",
language = "English",
volume = "22",
pages = "352--358",
journal = "Alcoholism: Clinical and Experimental Research",
issn = "0145-6008",
publisher = "Wiley-Blackwell",
number = "2",

}

RIS

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