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Chinese Journal of Geriatrics ; (12): 1112-1116, 2012.
Artigo em Chinês | WPRIM | ID: wpr-430221

RESUMO

Objective To investigate the effect of 17-β-estradiol (17-β-E2) on the expression of glucose transporter 4 (GLUT4) in rat primary culture skeletal muscle cells with insulin resistance (IR) induced by palmitinic acid (PA).Methods Rat skeletal muscle was primarily cultivated.The cells were identified by the technology of immunofluorescence.Cells were inclubated with 0.6 mmol/L palmitinic acid for 24 h to induce IR.The concentration of glucose in the medium was measured.The mRNA and protein expressions of protein kinase B (PKB/Akt) and GLUT4 were measured by real time polymerase chain reaction (PCR) and Western blot respectively.Results Compared the control with PA treated rats,the concentration of glucose in the medium was increased [(3.86±0.64)mmol/L vs.(5.43±0.55) mmol/L,q=4.13,P<0.05],uptake of glucose stimulated by insulin was decreased (P<0.01),the expressions of GLUT4 and phosphorylation PKB/Akt were reduced in the PA group (all P<0.05).In the 17-β-E2 (100 nmol/L) versus control,the concentration of glucose in the medium was higher [(3.86±0.64) vs.(3.77±0.35)mmol/L,q= 4.76,P<0.05],uptake of glucose stimulated by insulin was increased (P<0.01) and the expressions of GLUT4 and p-Akt were also increased (all P<0.05).17-β-E2 (10 nmol/L and 100 nmol/L) reversed the decrease of basal and insulin-stimulated uptake of glucose induced by PA,reversed the decrease of GLUT4 and p-Akt expression induced by PA compared with the PA group (all P< 0.05).Conclusions 17-β-E2 inhibits insulin resistance induced by PA in rat primary culture skeletal muscle cells,the mechanism may be correlated with the up-regulation of expression of phospho-Akt and GLUT 4 induced by 17-β-E2.

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