体育科学
體育科學
체육과학
China Sport Science
2010年
5期
41~48
,共null页
龚豪杰 张楠 姚璐 谢谨 张缨
龔豪傑 張楠 姚璐 謝謹 張纓
공호걸 장남 요로 사근 장영
AMPKα2高表达转基因小鼠 AMPKα2基因敲除小鼠 GLUT4 肌糖原 低氧训练
AMPKα2高錶達轉基因小鼠 AMPKα2基因敲除小鼠 GLUT4 肌糖原 低氧訓練
AMPKα2고표체전기인소서 AMPKα2기인고제소서 GLUT4 기당원 저양훈련
AMPKα2 over-expression mouse; AMPKα2 knockout mouse; GLUT4; glycogen; hypoxia; hypoxia training
目的:研究2周低氧、低氧训练对AMPKα2三种不同基因状态鼠骨骼肌GLUT4表达及肌糖原含量的影响,以探讨低氧、低氧训练对小鼠骨骼肌GLUT4基因和蛋白表达的影响及可能机制。方法:野生小鼠和AMPKα2高表达转基因小鼠,AMPKα2基因敲除小鼠各30只,分别随即分为常氧对照组、低氧暴露组和低氧训练组。低氧暴露组小鼠于低氧房(模拟海拔4000m高度,氧浓度约为12.3%)低氧暴露2周,低氧训练组小鼠2周低氧暴露同时每天于同浓度低氧房中跑台运动1h,跑台速度12m/min。最后一次跑台训练后12h取材,测定小鼠骨骼肌GLUT4基因和蛋白表达、AMPKα2蛋白表达以及肌糖原水平。结果:1)野生鼠,2周低氧暴露以及2周低氧训练后GLUT4基因和蛋白含量,与常氧对照组相比均显著增加,且低氧训练组小鼠比低氧暴露组增加更为显著。2)AMPKα2的高表达小鼠与野生鼠相比,2周低氧暴露后GLUT4蛋白和基因含量并没有显著差异,而经过2周低氧训练后,AMPKα2的高表达鼠骨骼肌GLUT4蛋白和基因表达量比野生鼠增加更为显著。3)AMPKα2基因敲除小鼠骨骼肌GLUT4表达量2周低氧训练后与野生鼠相比无显著差异,而2周低氧暴露后显著低于野生鼠。结论:1)低氧及低氧训练均能引起骨骼肌GLUT4表达的增多,且低氧和训练引起的GLUT4表达的增多可能有叠加效应。2)在低氧+训练双重刺激下,AMPKα2的高表达参与了调节GLUT4基因和蛋白表达的增加。3)低氧暴露引起的GLUT4基因和蛋白表达的增加至少部分是依赖AMPKα2调节,而在低氧+训练双重刺激下,机体还可以募集其他的信号通路完全代偿AMPKα2对GLUT4表达的调节作用。
目的:研究2週低氧、低氧訓練對AMPKα2三種不同基因狀態鼠骨骼肌GLUT4錶達及肌糖原含量的影響,以探討低氧、低氧訓練對小鼠骨骼肌GLUT4基因和蛋白錶達的影響及可能機製。方法:野生小鼠和AMPKα2高錶達轉基因小鼠,AMPKα2基因敲除小鼠各30隻,分彆隨即分為常氧對照組、低氧暴露組和低氧訓練組。低氧暴露組小鼠于低氧房(模擬海拔4000m高度,氧濃度約為12.3%)低氧暴露2週,低氧訓練組小鼠2週低氧暴露同時每天于同濃度低氧房中跑檯運動1h,跑檯速度12m/min。最後一次跑檯訓練後12h取材,測定小鼠骨骼肌GLUT4基因和蛋白錶達、AMPKα2蛋白錶達以及肌糖原水平。結果:1)野生鼠,2週低氧暴露以及2週低氧訓練後GLUT4基因和蛋白含量,與常氧對照組相比均顯著增加,且低氧訓練組小鼠比低氧暴露組增加更為顯著。2)AMPKα2的高錶達小鼠與野生鼠相比,2週低氧暴露後GLUT4蛋白和基因含量併沒有顯著差異,而經過2週低氧訓練後,AMPKα2的高錶達鼠骨骼肌GLUT4蛋白和基因錶達量比野生鼠增加更為顯著。3)AMPKα2基因敲除小鼠骨骼肌GLUT4錶達量2週低氧訓練後與野生鼠相比無顯著差異,而2週低氧暴露後顯著低于野生鼠。結論:1)低氧及低氧訓練均能引起骨骼肌GLUT4錶達的增多,且低氧和訓練引起的GLUT4錶達的增多可能有疊加效應。2)在低氧+訓練雙重刺激下,AMPKα2的高錶達參與瞭調節GLUT4基因和蛋白錶達的增加。3)低氧暴露引起的GLUT4基因和蛋白錶達的增加至少部分是依賴AMPKα2調節,而在低氧+訓練雙重刺激下,機體還可以募集其他的信號通路完全代償AMPKα2對GLUT4錶達的調節作用。
목적:연구2주저양、저양훈련대AMPKα2삼충불동기인상태서골격기GLUT4표체급기당원함량적영향,이탐토저양、저양훈련대소서골격기GLUT4기인화단백표체적영향급가능궤제。방법:야생소서화AMPKα2고표체전기인소서,AMPKα2기인고제소서각30지,분별수즉분위상양대조조、저양폭로조화저양훈련조。저양폭로조소서우저양방(모의해발4000m고도,양농도약위12.3%)저양폭로2주,저양훈련조소서2주저양폭로동시매천우동농도저양방중포태운동1h,포태속도12m/min。최후일차포태훈련후12h취재,측정소서골격기GLUT4기인화단백표체、AMPKα2단백표체이급기당원수평。결과:1)야생서,2주저양폭로이급2주저양훈련후GLUT4기인화단백함량,여상양대조조상비균현저증가,차저양훈련조소서비저양폭로조증가경위현저。2)AMPKα2적고표체소서여야생서상비,2주저양폭로후GLUT4단백화기인함량병몰유현저차이,이경과2주저양훈련후,AMPKα2적고표체서골격기GLUT4단백화기인표체량비야생서증가경위현저。3)AMPKα2기인고제소서골격기GLUT4표체량2주저양훈련후여야생서상비무현저차이,이2주저양폭로후현저저우야생서。결론:1)저양급저양훈련균능인기골격기GLUT4표체적증다,차저양화훈련인기적GLUT4표체적증다가능유첩가효응。2)재저양+훈련쌍중자격하,AMPKα2적고표체삼여료조절GLUT4기인화단백표체적증가。3)저양폭로인기적GLUT4기인화단백표체적증가지소부분시의뢰AMPKα2조절,이재저양+훈련쌍중자격하,궤체환가이모집기타적신호통로완전대상AMPKα2대GLUT4표체적조절작용。
Purpose:To investigate the effects of two weeks hypoxia treatment and hypoxia training on GLUT4 expression in mouse skeletal muscle and explore whether AMPK was involved in regulation of muscle GLUT4 expression induced by hypoxia treatment and hypoxia training.Methods:Expressions of GLUT4 mRNA and protein as well as the content of glycogen in quadriceps femoris muscle from control, hypoxia treatment and hypoxia training groups of AMPKα2 over-expression (OE), AMPKα2 knockout (KO), and corresponding wild-type (WT) mice was measured.Mice of hypoxia treatment groups were living in rooms with enriched nitrogen, simulating an altitude of 4,000 meter, in normobaric hypoxia (O2 12.3%) for two weeks.Hypoxia training groups were also living in this room but had an additional 60 min treadmill running training in normobaric hypoxia at the speed of 12m/min every day.Results:1)The content of GLUT4 mRNA and protein both increased significantly after two weeks hypoxia treatment as well as two weeks hypoxia training.2)The expression of muscle GLUT4 protein in AMPKα2-OE mice was significant higher than that in WT mice after two weeks hypoxia training.3)The expression of GLUT4 and the content of muscle glycogen in α2-KO mice,which were same with those in WT mice after two weeks hypoxia training,were significantly lower than that in WT mice after two weeks hypoxia treatment.Conclusion:1)The effectiveness of the hypoxia treatment and hypoxia training on expression of GLUT4 was validated in the present study.2)The AMPKα2-OE was involved in up-regulation of muscle GLUT4 expression induced by hypoxia training.3)The present study demonstrated that the cellular mechanism underlying the up-regulation of GLUT4 expression by hypoxia treatment and hypoxia training must be at least partly different,while hypoxia treatment induced GLUT4 expression in mouse skeletal muscle through a mechanism that was partially mediated by AMPKα2,pathways other than AMPKα2 were important in mediating the hypoxia training-induced GLUT4 expression.