TAILIEUCHUNG - Báo cáo hóa học: " Exploring the molecular mechanisms underlying the potentiation of exogenous growth hormone on alcohol-induced fatty liver diseases in mice"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: Exploring the molecular mechanisms underlying the potentiation of exogenous growth hormone on alcohol-induced fatty liver diseases in mice | Qin and Tian Journal of Translational Medicine 2010 8 120 http content 8 1 120 JOURNAL OF TRANSLATIONAL MEDICINE RESEARCH Open Access Exploring the molecular mechanisms underlying the potentiation of exogenous growth hormone on alcohol-induced fatty liver diseases in mice Ying Qin Ya-ping Tian Abstract Background Growth hormone GH is an essential regulator of intrahepatic lipid metabolism by activating multiple complex hepatic signaling cascades. Here we examined whether chronic exogenous GH administration via gene therapy could ameliorate liver steatosis in animal models of alcoholic fatty liver disease AFLD and explored the underlying molecular mechanisms. Methods Male C57BL 6J mice were fed either an alcohol or a control liquid diet with or without GH therapy for 6 weeks. Biochemical parameters liver histology oxidative stress markers and serum high molecular weight HMW adiponectin were measured. Quantitative real-time PCR and western blotting were also conducted to determine the underlying molecular mechanism. Results Serum HMW adiponectin levels were significantly higher in the GH1-treated control group than in the control group gg mL vs. gg mL P . GH1 therapy reversed HMW adiponectin levels to the normal levels in the alcohol-fed group. Alcohol feeding significantly reduced hepatic adipoR2 mRNA expression compared with that in the control group vs. P which was reversed by GH therapy. GH1 therapy also significantly increased the relative mRNA vs. and protein levels of SIRT1 vs. in the alcohol-fed group compared with those in the control group both P . The alcohol diet decreased the phosphorylated and total protein levels of hepatic AMP-activated kinase-a AMPKa phosphorylated protein vs. total protein vs. both P and peroxisome proliferator activated receptor-a PPARa phosphorylated protein

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