水通道蛋白7对蛋白激酶B的影响  

The Effect of Aquaglyceroporin 7 on Protein Kinase B Signaling Pathway

作　　者：潘伟[1] 沈飞霞[1] 谷雪梅[1] 叶菁[1] 顾雪疆[1] 倪连松[1] 李卫平[2] 

机构地区：[1]温州医学院附属第一医院内分泌科,温州325000 [2]汕头大学医学院第一附属医院内分泌科,汕头515000

出　　处：《中国细胞生物学学报》2013年第2期203-208,共6页Chinese Journal of Cell Biology

基　　金：浙江省自然科学基金(批准号:Y2080418);国家自然科学基金青年(批准号:81000356)资助的课题~~

摘　　要：该文旨在探讨水通道蛋白7(AQP7)在3T3-L1脂肪细胞不同分化阶段的表达以及其对胰岛素信号通路中蛋白激酶B(PKB)的影响。通过培养3T3-L1前体脂肪细胞,诱导分化为成熟的脂肪细胞,用荧光定量PCR、Western blot、酶学方法分析显示,随3T3-L1脂肪细胞分化过程,AQP7与PKB磷酸化水平同步上升,同时培养基中释放的甘油浓度伴随AQP7的表达平行增加。以TNF-α处理分化成熟的脂肪细胞构建胰岛素抵抗模型,AQP7与PKB磷酸化水平均下降,转染高表达AQP7基因的重组腺病毒载体(Ad-AQP7)之后,随着AQP7表达上调,胰岛素刺激下的PKB磷酸化水平提高,并且葡萄糖代谢能力增强。由此可见,AQP7水平随3T3-L1脂肪细胞分化过程逐渐上升,其高表达可能通过增加PKB磷酸化水平改善胰岛素敏感性,提示AQP7可能成为治疗肥胖的一个重要作用靶点。Aquaglyceroporin 7 （AQP7） is a water transporting protein which also regulates the glycerol effiux in adipocytes. The study of AQP7 might shed new light on the prevention and control of obesity. In this study, we aimed to analyze expression profiles of AQP7 in the different differentiation phase of adipocytes and the relationship between AQP7 and PKB in the insulin pathway. 3T3-L1 preadipocyte cells were induced fully differentiated. Insulin resistance in differentiated adipocytes was induced by TNF-a. Adenovirus overexpression AQP7 （Ad-AQP7） was constructed and transfected to adipocytes. The expression levels of AQP7 and phosphorylated PKB （p-PKB） were measured. The glycerol release from adipocytes and the change of glucose concentration in the culture medium were also tested.The AQP7 levels were gradually up-regulated along with the differentiation phase of 3T3-L1 preadipocytes, which was consistent with the expression levels of p-PKB. Overexpression of AQP7 by transfecting Ad-AQP7 to insulin resistant adipocytes could improve insulin sensitivity and glucose utilization, in accroding with the level of p-PKB expression. The expression of AQP7 correlated with phosphorylation of PKB. Overexpression of AQP7 contributed to improve insulin resistance in adipocytes.

关 键 词：水通道蛋白7 蛋白激酶B 胰岛素敏感性 

分 类 号：R587.1[医药卫生—内分泌] R589.2[医药卫生—内科学]