Objective To investigate the effect of 17β-estradiol on insulin resistance and the expression of insulin receptor-α in skeletal muscle of ovariectomized rats with insulin resistance induced by high fructose.Methods Forty-eight mature female Sprague-Dawley (SD) rats were randomly divided into four groups: the normal control group (NC, n= 12) rats were fed with the normal diet for 8 weeks; the model group (M, n= 12)rats were ovariectomized and fed with the high fructose diet for 8 weeks, meanwhile the physiological-dose of 17βestradiol (30 μg · kg-1 · d-1 ) was injected subcutaneously every day; the vehicle control group (VC, n= 12) rats were ovariectomized and fed with the high fructose diet for eight weeks, meanwhile equivalent alcohol was injected subcutaneously every day. Systolic blood pressure (SBP), fasting blood sugar (FBS), and fasting serum insulin (FSI) were measured and insulin sensitivity index (ISI) was calculated. The expressions of mRNA and protein of insulin receptor-α in quadriceps femoris were measured by RT-PCR and Western-blot. Results Compared with the normal control group, SBP (P<0.05), FBS (P<0.05) and FSI (P<0.01) were increased significantly while ISI was decreased significantly (P < 0. 05) in the model group. The expressions of mRNA and protein of insulin receptor-α and phosphorylated Akt were decreased significantly in quadriceps femoris in the model group (P<0.05), compared with the normal control group. However, these effects were reversed by 17β-estradiol in the 17βestradiol replacement group. Conclusions 17β-Estradiol inhibits insulin resistance, and up-regulates the expression of insulin receptor-α and the level of phosphorylated Akt in ovariectomized rats with insulin resistance induced by high fructose diet.

Objective To construct five shRNA-expression plasmids and to investigate the expression of Smad2 in TGF-?/ Smads signal transduction treated with shRNA-expression plasmid.Methods Five shRNA-Smad2 DNA sequences from mRNA sequence of mouse Smad2 gene were designed and synthesized.DNA oligonucleotides encoding an appropriate shRNA were inserted to shRNA expression vector respectively.Five shRNA-Smad2 expression plasmids were obtained and then transfected into NIH/3T3 cells.The suppressed expression of Smad2 was assessed by RT-PCR and Western-blotting.Results The shRNA-expression plasmid numbered 2.4 could markedly reduce the expression of Smad2.The suppression effect of the RNAi-pool composed of four different plasmids was more obvious than that of any single.Conclusion The shRNA-expression plasmids were successfully constructed,which could specifically and effectively suppress the expression of Smad2.The method of using a mixture of RNAi plasmids to improve the RNAi efficiency was established.

Aim To investigate the effects of arecoline on glucose and lipid metabolism in type 2 diabetic rats and its mechanisms in glucose metabolism.Methods A type 2 diabetic rat model was established by fed with high fructose-high fat diet.The animals were randomly divided into 7 groups: control group,high fructose-high fat diet group(HF)and high fructose-high fat diet+arecoline(1 mg?kg-1,5 mg?kg-1,10 mg?kg-1,20 mg?kg-1,50 mg?kg-1)groups.The blood glucose,lipid level,hepatic function and liver histology were measured.The mRNA expression of liver glucose-6-phosphatase(G6Pase),phosphoenolpyruvate carboxykinase(PEPCK),Forkhead Box O1(FoxO1)and peroxisome proliferator-activated receptor-? coactlvator-1? (PGC-1?)were observed through RT-PCR.Results In comparison with the high fructose-high fat diet group,the fasting blood glucose and TC of the rats were significantly decreased by arecoline in a dose-dependment manner in high fructose-high fat diet+arecoline group.But hepatic function was damaged by 10 mg?kg-1,20 mg?kg-1 and 50 mg?kg-1 arecoline.The mRNA expression of hepatic G6Pase,PEPCK,FoxO1 and PGC-1? was decreased by treatment with 1 mg?kg-1 and 5 mg?kg-1 arecoline compared with the high fructose-high fat diet group.Conclusions Low dose arecoline can decrease fasting blood glucose and TC in type 2 diabettic rats,and the mechanism in glucose metabolism may be related to its effect on the inhibition of hepatic gluconeogenesis.

Objective: To investigate the incidence and possible risk factors of small intestinal bacterial overgrowth(SIBO) in patients with chronic kidney disease(CKD). Methods : 92 patients with CKD were selected as subjects.SIBO was assessed by lactulose hydrogen methane breath test(LHMBT),fat tissue index(FTI) was determined using multifrequency bioelectrical impedance analysis, and gastrointestinal symptoms were evaluated by gastrointestinal symptom rating scale(GSRS).According to the results of LHMBT,the patients were divided into SIBO group and non-SIBO group.The demographic data, laboratory and clinical indicators, gastrointestinal symptoms and other differences between the two groups were compared.Binomial logistic stepwise regression was used to analyze the possible risk factors of SIBO in CKD patients. Results : The incidence of SIBO in these 92 patients was 47.8%.Compared with the non-SIBO group, the GSRS score of the SIBO group was higher, and the difference was statistically significant [(23.27±3.97)vs(21.13±4.39),t=2.451,P=0.016].Multivariate stepwise logistic regression analysis showed that low serum potassium(OR=0.396,95%CI0.176-0.893,P=0.025) and high FTI(OR=1.182,95%CI1.037-1.348,P=0.013) were independent risk factors for SIBO in patients with CKD. Conclusion The incidence of SIBO is high in CKD patients.Symptoms of dyspepsia are more prominent in SIBO positive patients.Low serum potassium and high FTI are independent risk factors for SIBO in patients with CKD.