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J.Health Sci., 52(4), 390-396, 2006

Effect of Cordyceps Sinensis on Uncoupling Protein 2 in Experimental Rats with Nonalcoholic Fatty Liver

Dong-Ling Dai,a Wei Shen,*, b Hai-Feng Yu,c Xiao-Qin Guan,d and Yong-Fen Yid

aInternal Medicine Department of ShenZhen Children's Hospital, YiTian Road 7019, FuTian District, ShenZhen City, GuangDong Province 518026, R.P. China, bThe Second Affiliated Hospital of Chongqing Medical University, LinJiang Road 76, YuZhong District, ChongQing City, R.P. China, cGeneral Hospital of ChongQing Steel Corporation, DaYanSanCun 1, DaDuKou District, ChongQing City, R.P. China, and dChongqing University of Medical Science, YiXue Yuan Road 1, YuZhong District, ChongQing City, R.P. China

[Objective] To investigate the effect of cordyceps sinensis (CS) on expression of uncoupling protein-2 (UCP2) and so to elucidate the role of UCP2 in development of nonalcoholic fatty liver diseases (NAFLD). [Methods] Rats were administrated with high-fat diet to produce NAFLD animal model and intervened by cordyceps sinensis. Triglyceride (TG), total cholesterol (TC) in liver were measured by biochemistry, adenosine triphosphate (ATP) by luciferin-luciferinase, and UCP2 expression by Northern blotting and immunohistochemistry. Liver histopathology was evaluated. [Results] High-fat diet fed rats developed obesity and showed a gradual increase in body weight, liver index, and a decrease in ATP level. More advanced liver disease was found histopathologically for longer high-fat diet. Up-regulation of liver UCP2 by high-fat diet stopped after week 12. However codyceps sinensis induced UCP2 up-regulation continuously, and kept liver ATP a relatively high level. [Conclusion] NAFLD rat models were produced successfully. Liver UCP2 up-regulation in NAFLD rats may be a definite beneficial adaptation to lipid exposure. Cordyceps sinensis may serve a protective role to prevent NAFLD from progression. One of the possible mechanisms involves in modulating UCP2 expression and thereby, regulating fat metabolism, energy homeostasis.