持续激活的Akt减少了 3T3-L1脂肪细胞脂联素蛋白的表达

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。

Continuously activated Akt inhibits adiponectin secretion in 3T3-L1 adipocytes

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.