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Effect of Dietary Epigallocatechin-3-gallate on Cytochrome P450 2E1-Dependent Alcoholic Liver Damage: Enhancement of Fatty Acid Oxidation
Author(s) -
Jun-Won Yun,
Young Kyung Kim,
ByoungSeok Lee,
Chae-Wook Kim,
Jin-Sook Hyun,
Joo-Hyun Baik,
JungJu Kim,
Bae-Hwan Kim
Publication year - 2007
Publication title -
bioscience biotechnology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.509
H-Index - 116
eISSN - 1347-6947
pISSN - 0916-8451
DOI - 10.1271/bbb.70403
Subject(s) - cyp2e1 , chemistry , fatty liver , aspartate transaminase , catechin , ethanol , epigallocatechin gallate , alcoholic fatty liver , alanine transaminase , biochemistry , steatosis , transaminase , medicine , liver injury , pharmacology , cytochrome p450 , polyphenol , antioxidant , metabolism , enzyme , alkaline phosphatase , disease
This study was designed to determine whether dietary epigallocatechin-3-gallate (EGCG), the most abundant catechin polyphenol in green tea, can protect the liver from cytochrome P450 2E1 (CYP2E1)-dependent alcoholic liver damage. Compared with an ethanol group, when EGCG was present in the ethanol diet, the formation of a fatty liver was significantly reduced and the serum aspartate transaminase (AST) and alanine transaminase (ALT) levels were much lower. Ethanol treatment significantly elevated hepatic CYP2E1 expression while simultaneously reducing hepatic phospho-acetyl CoA carboxylase (p-ACC) and carnitine palmitoyl-transferase 1 (CPT-1) levels. While EGCG markedly reversed the effect of ethanol on hepatic p-ACC and CPT-1 levels, it had no effect on the ethanol-induced elevation in CYP2E1 expression. EGCG prevents ethanol-induced hepatotoxicity and inhibits the development of a fatty liver. These effects were associated with improvements in p-ACC and CPT-1 levels. The use of EGCG might be useful in treating patients with an alcoholic fatty liver.

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