胰升糖素样肽1通过PKA途径促进3T3-L1脂肪细胞内脂素的表达  

Glucagon like peptide-1 increases visfatin expression in 3T3-L1 adipocytes via PKA pathway

作　　者：刘瑞[1] 彭永德[1] 董维平[1] 张爱芳[1] 王熠非[1] 丁晓颖[1] 

机构地区：[1]上海交通大学附属第一人民医院内分泌科,200080

出　　处：《中华内分泌代谢杂志》2013年第11期977-980,共4页Chinese Journal of Endocrinology and Metabolism

基　　金：国家自然科学基金资助项目（81070682,81200622）;上海卫生局面上项目（20124263）

摘　　要：目的检测胰升糖素样肽1（GLP-1）是否调节内脂素的合成，并探讨其作用机制。方法以3T3＋L1分化成熟脂肪细胞为模型，GLP—l干预后，提取总RNA定量检测内脂素转录水平，收集培养液酶联免疫法检测内脂素分泌水平：PKA通路抑制剂H89预处理30min，检测内脂素的转录水平。结果GLP-1呈剂量依赖性增加3T3-L1细胞表达内脂素，10^10mol／L时显著提高（P〈0．05），10^-9moL／L时达峰值（P〈0．01）：并呈时间依赖性，作用18h时内脂素显著升高（P〈0．05）。H89部分阻断GLP—I刺激的内脂素表达。结论GLP-1通过PKA途径提升脂肪细胞表达内脂素，进而可能提升胰岛功能和周围组织胰岛素敏感性。Objective To test whether glucagon like peptide-1 （ GLP-1 ） would regulate the expression of visfatin in adipocytes, and to explore the mechanism of this effect. Methods Fully differentiated 3T3-LI adipocytes were treated with GLP-1. Total RNA was extracted for analyzing the level of visfatin mRNA by quantitative RT-PCR. The media were collected for measuring the level of visfatin protein by enzyme linked immuno-assay （ELISA）. In order to test the involvement of PKA pathway, the adipocytes were pretreated with a specific pharmacological PKA inhibitor H89 for 30 rain before GLP-1 was added. Results GLP-1 increased visfatin expression in a time- and dose-dependent manner. The level of visfatin significantly increased at the concentration of 10-10 mol/L GLP-1 （ P〈0.05 ）, and reached the peak at 10-9 mol/L （ P〈0.01 ）. After incubation for 18 hours, GLP-1 dominantly increased the level of visfatin （ P〈0.05 ）. Inhibition of PKA pathway by H89 partially blocked the effect of GLP-1 on visfatin expression. Conclusions GLP-1 may enhance the expression of visfatin in 3T3-L1 adipocyte via the PKApathway, which might contribute to the improvement in glucose homeostasis.

关 键 词：胰升糖素样肽1 内脂素 脂肪细胞 糖尿病 

分 类 号：R587.1[医药卫生—内分泌]