GLP-1通过下调ATGL表达参与3T3-L1脂肪细胞脂质代谢  

Glucagon-like peptide-1 regulates lipometabolism by down-regulating adipose triglyceride lipase in 3T3-L1 adipocytes

作　　者：朱慧丽[1,2] 翁泽平[1,2] 林琛莅[2] 马继伟[2] 钟雪云[2] 

机构地区：[1]暨南大学附属第一医院,广东广州510630 [2]暨南大学医学院病理系,广东广州510632

出　　处：《南方医科大学学报》2013年第10期1499-1503,共5页Journal of Southern Medical University

基　　金：广东省医学科研基金(B2011159)

摘　　要：目的探讨胰高血糖素样肽-1(GLP-1)对胰岛素抵抗模型3T3-L1脂肪细胞的影响及其可能的机制。方法分别使用GLP-1、胰岛素、胰岛素加GLP-1干预胰岛素抵抗模型3T3-L1脂肪细胞,Western blotting检测脂肪组织甘油三酯水解酶(ATGL)、葡萄糖转运蛋白4(GLUT4)、Akt1、Akt2及其磷酸化蛋白表达量;免疫荧光法检测GLP-1干预后脂肪细胞的成脂情况。结果胰岛素刺激下3T3-L1脂肪细胞Akt1、Akt2活化不明显。GLP-1刺激下3T3-L1脂肪细胞磷酸化Akt1、Akt2表达明显增加,同时促进GLUT4向细胞膜上转移,并抑制ATGL蛋白的表达。在胰岛素的协同作用下这一现象更加明显。结论 GLP-1通过降低脂肪细胞ATGL蛋白表达参与脂质代谢,同时增强脂肪细胞GLUT4的膜转移,促进葡萄糖吸收,改善胰岛素抵抗。Objective To investigate the effect of glucagon-like peptide-1 （GLP-1） on glycolipid metabolism in 3T3-L1 adipocytes and explore the mechanism. Methods 3T3-L1 adipocytes were treated with GLP-1, insulin, or both for 24 h, and Western blotting was used to analyze the expression levels of adipose triglyceride lipase （ATGL）, glucose transporter type 4 （GLUT4）, Aktl, Akt2 and phosphorylated Akt in the cells. Immunofluorescence was used to observe lipid content in 3T3-L1 adipocytes. Results Aktl and Akt2 were not activated by insulin stimulation in 3T3-L1 adipocytes. Akt was phosphorylated by GLP-1 stimulation, which inhibited the expression of ATGL and increased the translocation of GLUT4 from the intracellular membranes to plasma membranes. These changes were more obvious under the synergistic effect of insulin in 3T3-L1 adipocytes. Conclusion GLP-1 decreases lipolysis by inhibiting the expression of ATGL and improves insulin resistance by increasing the translocation of GLUT4 in 3T3-L1 adipocytes.

关 键 词：ATGL GLP-1 脂肪细胞 胰岛素抵抗 

分 类 号：R587.1[医药卫生—内分泌]