Premium
Green tea extract (GTE) attenuates adipose inflammation by restoring glutathione redox status in high fat diet‐induced nonalcoholic fatty liver disease (NAFLD)
Author(s) -
Park Hea Jin,
Chung MinYu,
Koo Sung I,
Bruno Richard S
Publication year - 2010
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.24.1_supplement.722.15
Subject(s) - adipose tissue , medicine , glutathione , endocrinology , inflammation , nonalcoholic fatty liver disease , oxidative stress , fatty liver , liver injury , chemistry , biochemistry , enzyme , disease
Adipose and hepatic inflammation contributes to NAFLD. We hypothesized that the anti‐inflammatory activities of GTE would decrease inflammation, restore glutathione redox status and attenuate hepatic injury in NAFLD. Wistar rats (16‐wk old, n=63) were fed a low‐fat (LF) diet containing no GTE or a high‐fat (HF) diet containing 0, 1, or 2% GTE for 8 wks. HF controls had greater (p<0.05) adipose and hepatic monocyte chemoattractant protein‐1 (MCP‐1) and tumor necrosis factor‐α (TNF‐α) compared to LF controls. GTE decreased MCP‐1 by 25–64% and TNF‐α by 40–42% in adipose and liver. GTE increased adipose and hepatic glutathione (GSH) by 19–43% that was decreased by HF feeding. HF controls had decreased adipose glutathione disulfide (GSSG) that was normalized by GTE to levels of LF controls. GTE lowered serum alanine aminotransferase (ALT) by 39% relative to HF controls. Adipose TNF‐α and hepatic TNF‐α and MCP‐1 were correlated to ALT. Adipose TNF‐α and GSH/GSSG ratio were positively correlated whereas hepatic MCP‐1 and GSH were inversely correlated suggesting that tissue inflammation alters thiol redox status. ALT and adipose total GSH were inversely correlated suggesting that higher adipose thiol levels are associated with the amelioration of hepatic injury. Thus, GTE decreased HF‐induced inflammation and hepatic injury in NAFLD by altering tissue GSH redox status. Supported by the USDA‐NRI (2007‐02303) to RSB.