中华临床医师杂志(电子版)
中華臨床醫師雜誌(電子版)
중화림상의사잡지(전자판)
CHINESE JOURNAL OF CLINICIANS(ELECTRONIC VERSION)
2013年
7期
3015-3018
,共4页
耿东华%张国峰%王勇%周勇%刘源%刘金钢
耿東華%張國峰%王勇%週勇%劉源%劉金鋼
경동화%장국봉%왕용%주용%류원%류금강
脂联素%受体,脂联素%葡萄糖摄取
脂聯素%受體,脂聯素%葡萄糖攝取
지련소%수체,지련소%포도당섭취
Adiponectin%Receptors,adiponectin%Glucose uptake
目的探讨脂联素在HepG2细胞中改善葡萄糖摄取的机制。方法检测不同浓度脂联素干预对HepG2细胞中脂联素受体2(AdipoR2)表达的影响,进而应用siRNA沉默HepG2细胞AdipoR2,观察脂联素通过上调AdipoR2表达对HepG2细胞糖摄取的影响。结果脂联素浓度为50μg/ml时,干预HepG2细胞后使AMPK和GLUT2 mRNA上调,而使PEPCK和G6Pase mRNA下调(P<0.05),siRNA沉默AdipoR2后, PEPCK和G6Pase mRNA显著上调,AMPK和GLUT2 mRNA显著下调(P<0.05)。结论脂联素可以通过增加HepG2细胞AdipoR2的表达,上调细胞内的AMPK表达,增加GLUT2数量,降低PEPCK和G6Pase表达水平,改善细胞葡萄糖摄取。
目的探討脂聯素在HepG2細胞中改善葡萄糖攝取的機製。方法檢測不同濃度脂聯素榦預對HepG2細胞中脂聯素受體2(AdipoR2)錶達的影響,進而應用siRNA沉默HepG2細胞AdipoR2,觀察脂聯素通過上調AdipoR2錶達對HepG2細胞糖攝取的影響。結果脂聯素濃度為50μg/ml時,榦預HepG2細胞後使AMPK和GLUT2 mRNA上調,而使PEPCK和G6Pase mRNA下調(P<0.05),siRNA沉默AdipoR2後, PEPCK和G6Pase mRNA顯著上調,AMPK和GLUT2 mRNA顯著下調(P<0.05)。結論脂聯素可以通過增加HepG2細胞AdipoR2的錶達,上調細胞內的AMPK錶達,增加GLUT2數量,降低PEPCK和G6Pase錶達水平,改善細胞葡萄糖攝取。
목적탐토지련소재HepG2세포중개선포도당섭취적궤제。방법검측불동농도지련소간예대HepG2세포중지련소수체2(AdipoR2)표체적영향,진이응용siRNA침묵HepG2세포AdipoR2,관찰지련소통과상조AdipoR2표체대HepG2세포당섭취적영향。결과지련소농도위50μg/ml시,간예HepG2세포후사AMPK화GLUT2 mRNA상조,이사PEPCK화G6Pase mRNA하조(P<0.05),siRNA침묵AdipoR2후, PEPCK화G6Pase mRNA현저상조,AMPK화GLUT2 mRNA현저하조(P<0.05)。결론지련소가이통과증가HepG2세포AdipoR2적표체,상조세포내적AMPK표체,증가GLUT2수량,강저PEPCK화G6Pase표체수평,개선세포포도당섭취。
Objective To explore the mechanisms of adiponectin stimulating glucose uptake in HepG 2 cells.Methods HepG2 cells were treated with different concentrations of adiponectin or with siRNA targeting adipnectin receptor ( AdipoR2) in HepG2 cells and the evaluation of glucose uptake via upregulation of AdipoR 2 was determined.Results AMPKα2 and GLUT2 were increased(P<0.05),while PEPCK and G6Pase were decreased in transcriptionallevel(P <0.05)after addition of adiponectin(50 μg/ml)in HepG2.After using siRNA targeting AdipoR2,mRNA expression of PEPCK and G6Pase were increased ( P <0.05 ), while AMPK and GLUT2 were decreased ( P<0.05 ) .Conclusions Adiponectin improves glucose uptake in HepG 2 cells via up regulation of AdipoR2 expression,which increases GLUT2 and AMPK expression and reduce PEPCK and G 6Pase.