Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 2 de 2
Filter
Add filters








Language
Year range
1.
Chinese Journal of Endocrinology and Metabolism ; (12): 695-698, 2010.
Article in Chinese | WPRIM | ID: wpr-387911

ABSTRACT

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.

2.
Chinese Pharmacological Bulletin ; (12)2003.
Article in Chinese | WPRIM | ID: wpr-566636

ABSTRACT

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.

SELECTION OF CITATIONS
SEARCH DETAIL