CAJ | 학술논문

目的研究蛋白激酶B(Akt/PKB)的持续激活与灭活对3T3-L1脂肪细胞内脂联素蛋白表达的影响. 方法通过腺病毒表达系统将持续激活的Akt(myrAkt)和无酶活性的Akt(Akt-AA)导入3T3-L1脂肪细胞内,应用免疫印迹法检测3T3-L1脂肪细胞脂联素蛋白的表达. 结果表达myrAkt的3T3-L1脂肪细胞中脂联素明显减少,表达Akt-AA的3T3-L1脂肪细胞中脂联素无明显变化. 结论 Akt的激活抑制了3T3-L1脂肪细胞中脂联素蛋白的表达,且Akt的激活是影响脂联素的充分条件,而不是必要条件.
목적연구단백격매B(Akt/PKB)적지속격활여멸활대3T3-L1지방세포내지련소단백표체적영향. 방법통과선병독표체계통장지속격활적Akt(myrAkt)화무매활성적Akt(Akt-AA)도입3T3-L1지방세포내,응용면역인적법검측3T3-L1지방세포지련소단백적표체. 결과표체myrAkt적3T3-L1지방세포중지련소명현감소,표체Akt-AA적3T3-L1지방세포중지련소무명현변화. 결론 Akt적격활억제료3T3-L1지방세포중지련소단백적표체,차Akt적격활시영향지련소적충분조건,이불시필요조건.
Objective To investigate the effects of the continuously activated Akt(myrAkt) and dominant-negative Akt(Akt-AA) on adiponectin secretion in 3T3-L1 adipocytes. Methods The myrAkt and Akt-AA were introduced into 3T3-L1 adipocytes with the use of adenovirus vectors. Adiponectin secretion in 3T3-L1 adipocytes was messured by Western blot. Results In 3T3-L1 adipocytes expressing myrAkt, adiponectin secretion decreased significantly compared with that of control. Little change of adiponectin secretion could be found in 3T3-L1 adipocytes expressing Akt-AA. Conclusions Activation of Akt kinase can inhibit adiponectin secretion. Akt activation is a sufficient , but not necessary, condition for regulating on adiponectin secretion.