Abstract

GTE contains catechins and may protect against oxidative stress implicated in NAFLD. We hypothesized that GTE would protect against NAFLD by regulating hepatic enzymatic antioxidant (AOX) defenses. We fed 5‐wk old obese mice (ob/ob; n = 38) a diet containing 0, 0.5, or 1% GTE and 0% GTE to lean mice (n = 12) for 6‐wk. Then, serum alanine aminotransferase (ALT) and hepatic AOX defenses were measured. Obese compared to lean controls had 7‐fold greater ALT (p < 0.05) and GTE at 0.5 or 1% decreased ALT by 19‐25%. Mn and CuZn superoxide dismutase (SOD) activities were 25‐29% lower in obese mice and GTE increased Mn‐ and CuZn‐SOD by 29‐42% and 26‐28%, respectively. Catalase (CAT) activity was 40% lower in obese mice and GTE at 0.5 or 1% increased it 26‐42%. Glutathione peroxidase (GPx) activity of obese mice was 30% lower than lean controls and GTE increased it 14‐15%. Glutathione S‐transferase activity was greater in obese mice and further increased by GTE at 1% only. Glutathione reductase activity was higher in obese mice and unaffected by GTE. ALT was inversely related (p < 0.05) to CAT (r = ‐0.395) and GPx (r = ‐0.562) suggesting that these enzymatic AOX activities protect against hepatic injury. Collectively, these data suggest that GTE, in part, restores those AOX defenses impaired by obesity and that GTE may protect against hepatic injury associated with NAFLD. Supported by a grant from the USDA‐NRI (2007‐02303) to RSB.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call