%0 Journal Article
%T Effects of ursolic acid in ameliorating insulin resistance in liver of KKAy mice via peroxisome proliferator-activated receptors ¦Á and ¦Ã
%A Lin Wang
%A De-zeng Zhu
%J Zhong Xi Yi Jie He Xue Bao
%D 2012
%I 
%X OBJECTIVE: To explore the effects and mechanism of ursolic acid in improving hepatic insulin resistance in KKAy mice with spontaneous type 2 diabetes.METHODS: Thirty-five KKAy mice were divided into five groups according to the randomized block design, namely, control, rosiglitazone, fenofibrate, and high- and low-dose ursolic acid groups with seven mice in each group. C57BL/6J mice were used as the normal control group. At the end of the 4th week, free fatty acid (FFA), tumor necrosis factor-¦Á (TNF-¦Á) and adiponectin contents in serum were detected by enzyme-linked immunosorbent assay; the protein expressions of phosphoenolpyruvate carboxykinase (PEPCK), insulin receptor substrate-2 (IRS-2) and glucose transport factor-2 (GLUT-2) were detected by Western blot method; the mRNA expressions of PEPCK, IRS-2 and GLUT-2 were detected by real-time polymerase chain reaction; the expressions of peroxisome proliferator-activated receptor ¦Á (PPAR¦Á) and peroxisome proliferator-activated receptor ¦Ã (PPAR¦Ã) in liver tissue were detected by immunohistochemical method.RESULTS: After four weeks of intervention, the contents of FFA, TNF-¦Á and adiponectin in serum of the high-dose ursolic acid group had changed, showing statistically significant difference compared to those of the control group (P<0.01); high dose of ursolic acid had depressant effect on the expressions of PEPCK protein and PEPCK mRNA (P<0.01); low dose of ursolic acid depressed the expression of PEPCK mRNA and induced phosphorylation of IRS-2 in the liver (P<0.05); both high and low dose of ursolic acid improved the expression of PPAR¦Á in the liver (P<0.01).CONCLUSION: The effects of ursolic acid in improving hepatic insulin resistance in KKAy mice with spontaneous type 2 diabetes may be closely related to affecting the contents of FFA, TNF-¦Á and adiponectin, improving the expression of PPAR¦Á protein, regulating transcription of PEPCK protein and inducing phosphorylation of IRS-2.
%K hypoglycemic agents (TCD)
%K ursolic acid
%K PPAR¦Á
%K PPAR¦Ã
%K insulin resistance
%K diabetes mellitus
%K experimental
%K procetofen
%K mice
%U http://www.jcimjournal.com/en/FullText2.aspx?articleID=jcim20120710