Glucagon-like Peptide-1 Upregulates Visfatin Expression in 3T3-L1 Adipocytes
Glucagon-like Peptide-1 Upregulates Visfatin Expression in 3T3-L1 Adipocytes
复制标题
DOI：
10.1055/s-0033-1343472
复制
发表时间：
2013-09-01
影响因子：
2.2
通讯作者：
Peng, Y.
中科院分区：
文献类型：
--
作者：
Liu, R.;Ding, X.;Peng, Y.
肠促胰岛素激素胰高血糖素样肽-1（GLP-1）在控制葡萄糖稳态中发挥重要作用。许多研究已经揭示了GLP-1的分子靶点，但其对脂肪因子的影响尚未确定。内脂素是近年来发现的一种脂肪因子，它通过与胰岛素受体结合而减轻胰岛素抵抗。我们的研究表明，GLP-1诱导内脂素分泌到3 T3-L1脂肪细胞的培养基中，由于内脂素mRNA表达增加。此外，GLP-1对内脂素的作用具有剂量和时间依赖性。H89是一种蛋白激酶A抑制剂，可阻止GLP-1诱导内脂素表达。此外，通过PDTC抑制NF-B减少了基础内脂素释放，而对GLP-1的转录调节没有影响。此外，GLP-1还可减轻毒胡萝卜素诱导的内质网应激下visfatin mRNA表达的下降。综上所述，我们的研究表明，GLP-1通过PKA途径促进新型胰岛素样细胞因子脂内脂素的表达，并可能影响葡萄糖代谢。
The incretin hormone glucagon-like peptide-1 (GLP-1) exerts important functions in controlling glucose homeostasis. Many studies have revealed molecular targets of GLP-1, but its influence on adipokines has not been determined. Visfatin, a recently discovered adipokine, has been shown to attenuate insulin resistance by binding to insulin receptor. Our study shows that GLP-1 induced secretion of visfatin into the culture medium of 3T3-L1 adipocytes due to increased visfatin mRNA expression. Furthermore, the effect of GLP-1 on visfatin was dose- and time-dependent. H89, a protein kinase A inhibitor, prevented the induction of visfatin expression by GLP-1. Moreover, inhibition of NF-B by PDTC reduced the basal visfatin release while having no effect on the transcription regulation by GLP-1. In addition, GLP-1 alleviated the decrease of visfatin mRNA expression under endoplasmic reticulum stress induced by thapsigargin. Taken together, our study suggests that GLP-1 promotes the novel insulin-mimetic adipocytokine visfatin expression via the PKA pathway and might influence glucose metabolism.