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Normalization of dietary fructose‐induced liver injury in rats by green tea extract is accompanied by lower hepatic methylglyoxal accumulation
Author(s) -
Masterjohn Christopher,
Guo Yi,
Noh Sang K.,
Koo Sung I.,
Bruno Richard S.
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.95.3
Subject(s) - green tea extract , methylglyoxal , medicine , fructose , endocrinology , chemistry , liver injury , triglyceride , cholesterol , biochemistry , green tea , food science , enzyme
Fructose (F) consumption has increased dramatically in recent decades and may induce liver injury by promoting methylglyoxal (MGO) accumulation. In the present study we examined whether the hepatoprotective activities of green tea extract (GTE) would protect against dietary F‐induced liver injury. Male Sprague Dawley rats (n = 34; 7 wk old) were fed a low‐F diet (10% F, 50% starch) containing no GTE, or a high‐F diet (60% F) containing 0%, 0.5%, or 1.0% GTE for 9 wk. Rats were sacrificed in the fed state. Hepatic MGO and plasma MGO, triglyceride (TG), cholesterol, glucose, and alanine (ALT) and aspartate (AST) aminotransferases were measured. F increased liver mass by 13% ( P <0.05) without affecting body mass. F also increased hepatic MGO by 23%, plasma AST by 60%, ALT by 87%, TG by 35%, and glucose by 21%. GTE normalized plasma levels of ALT and AST to those of low‐F controls without affecting liver mass. GTE also normalized hepatic MGO and decreased plasma TG, but plasma glucose was unaffected. Plasma MGO and cholesterol were unaffected by F or GTE. These data suggest that GTE protects against the hepatotoxic effects of excessive fructose consumption, possibly by reducing hepatic MGO accumulation. Additional study is warranted to define the role of MGO in regulating F‐induced liver injury. Supported by a USDA‐NRI grant to RSB (2007‐02303).