title: Green tea extract attenuates hepatic steatosis by decreasing adipose lipogenesis and enhancing hepatic antioxidant defenses in ob/ob mice.
abstract: Excess hepatic lipid accumulation and oxidative stress contribute to nonalcoholic fatty liver disease (NAFLD). Thus, we hypothesized that the hypolipidemic and antioxidant activities of green tea extract (GTE) would attenuate events leading to NAFLD. Obese mice (ob/ob; 5 weeks old, n=38) and their lean littermates (n=12) were fed 0%, 0.5% or 1% GTE for 6 weeks. Then, hepatic steatosis, oxidative stress and inflammatory markers were measured. Obese mice, compared to lean controls, had greater hepatic lipids and serum alanine aminotransferase (ALT). GTE at 1% lowered (P<.05) hepatic lipids and ALT in obese mice. The GTE-mediated attenuation in hepatic steatosis was accompanied by decreased mRNA expression of adipose sterol regulatory element-binding protein-1c, fatty acid synthase, stearoyl CoA desaturase-1, and hormone-sensitive lipase and decreased serum nonesterified fatty acid concentrations. Immunohistochemical data indicated that steatotic livers from obese mice had extensive accumulation of tumor necrosis factor-α (TNF-α), whereas GTE at 1% decreased hepatic TNF-α protein and inhibited adipose TNF-α mRNA expression. Hepatic total glutathione, malondialdehyde and Mn- and Cu/Zn-superoxide dismutase activities in obese mice fed GTE were normalized to the levels of lean littermates. Also, GTE increased hepatic catalase and glutathione peroxidase activities, and these activities were inversely correlated with ALT and liver lipids. Collectively, GTE mitigated NAFLD and hepatic injury in ob/ob mice by decreasing the release of fatty acids from adipose and inhibiting hepatic lipid peroxidation as well as restoring antioxidant defenses and decreasing inflammatory responses. These findings suggest that GTE may be used as an effective dietary strategy to mitigate obesity-triggered NAFLD.
authors.affiliation: Department of Nutritional Sciences, University of Connecticut, Storrs, CT 06269-4017, USA.
authors.forename: Hea Jin
authors.initials: HJ
authors.lastname: Park
authors.forename: Dana A
authors.initials: DA
authors.lastname: DiNatale
authors.forename: Min-Yu
authors.initials: MY
authors.lastname: Chung
authors.forename: Young-Ki
authors.initials: YK
authors.lastname: Park
authors.forename: Ji-Young
authors.initials: JY
authors.lastname: Lee
authors.forename: Sung I
authors.initials: SI
authors.lastname: Koo
authors.forename: Meeghan
authors.initials: M
authors.lastname: O'Connor
authors.forename: Jose E
authors.initials: JE
authors.lastname: Manautou
authors.forename: Richard S
authors.initials: RS
authors.lastname: Bruno
mesh_terms: D000273:Adipose Tissue / Q000187:drug effects / Q000378:metabolism; D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D000975:Antioxidants / Q000378:metabolism* / Q000494:pharmacology; D002374:Catalase / Q000378:metabolism; D005234:Fatty Liver / Q000517:prevention & control; D005978:Glutathione / Q000096:biosynthesis; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051379:Mice; D008820:Mice, Obese; D065626:Non-alcoholic Fatty Liver Disease; D010936:Plant Extracts / Q000494:pharmacology*; D002787:Sterol Esterase / Q000378:metabolism; D051780:Sterol Regulatory Element Binding Protein 1 / Q000096:biosynthesis; D013662:Tea / Q000737:chemistry*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000975:Antioxidants; D010936:Plant Extracts; D051780:Sterol Regulatory Element Binding Protein 1; D013662:Tea; D014409:Tumor Necrosis Factor-alpha; D002374:Catalase; D000410:Alanine Transaminase; D002787:Sterol Esterase; D005978:Glutathione