Abstract

Oxidative stress and excess hepatic lipid are implicated in nonalcoholic fatty liver disease. Based on our previous observation that GTE attenuated hepatic lipid accumulation and injury, we hypothesized that GTE would decrease hepatic oxidative stress. Obese mice (ob/ob, n = 38) were fed a diet containing 0, 0.5 or 1% GTE for 6 wk. Lean mice, as a control, were fed 0% GTE. Serum ALT was 7.3‐times higher (p < 0.05) in obese compared to lean mice and GTE at 0.5 or 1% attenuated it by 25%. Obese mice, compared to lean mice, had greater oxidative stress as suggested by 16% lower hepatic total glutathione (tGSH) and 40% higher malondialdehyde (MDA). tGSH in obese mice fed GTE at 1% was increased to that observed in lean mice. Hepatic MDA in obese mice fed GTE at 0.5 or 1% was 16‐22% lower (p < 0.05) than in obese controls. Obese mice had 2.3‐times greater (p < 0.05) hepatic total lipid (TL) compared to lean mice which was lowered by 13% in obese mice fed GTE at 1%. This effect was consistent with hepatic triglyceride (TG) and total cholesterol (TC). Alterations in lipogenic gene expression may be involved in the hepatic lipid lowering effect of GTE. ALT was correlated (p < 0.05) to tGSH (r = ‐0.339) and MDA (r = 0.358), as well as TL (r = 0.895), TG (r = 0.777) and TC (r = 0.634). The data suggest that GTE attenuates hepatic injury by inhibiting lipid accumulation and decreasing oxidative stress. Supported by USDA NRI (2007‐02303) to RSB.

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