Bacterial metabolite S-equol modulates glucagon-like peptide-1 secretion from enteroendocrine L cell line GLUTag cells via actin polymerization
Bacterial metabolite S-equol modulates glucagon-like peptide-1 secretion from enteroendocrine L cell line GLUTag cells via actin polymerization
复制标题
DOI：
10.1016/j.bbrc.2018.05.100
复制
发表时间：
2018-07-02
影响因子：
3.1
通讯作者：
Tsuboi, Takashi
中科院分区：
文献类型：
--
作者：
Harada, Kazuki;Sada, Shoko;Tsuboi, Takashi
雌马酚是由大豆异黄酮产生的肠道细菌代谢产物之一。虽然已知S-雌马酚促进葡萄糖诱导的胰岛素从胰腺β细胞分泌，但S-雌马酚是否影响胰高血糖素样肽-1（GLP-1）从肠内皮素L细胞分泌仍不清楚。在这里，我们评估了S-雌马酚对小鼠肠内分泌L细胞系GLUTag细胞的GLP-1分泌的影响。GLUTag细胞表达GPR 30和雌激素受体，它们是推定的S-雌马酚受体。S-雌马酚的应用通过GPR 30诱导细胞内Ca 2+水平增加。然而，S-雌马酚不增强GLP-1胞吐作用，并且S-雌马酚的长期处理抑制GLP-1分泌。此外，免疫细胞化学显示，S-雌马酚通过GPR 30下的G12113信号传导增加皮质肌动蛋白丝的密度。这些数据表明，S-雌马酚阻止GLP-1分泌的Ca 2+动员和肌动蛋白重组之间的竞争性调节的结果。(C)2018爱思唯尔公司All rights reserved.
S-equol is one of gut bacterial metabolites produced from soybean isoflavone daizein. While S-equol is known to promote glucose-induced insulin secretion from pancreatic beta cells, whether S-equol affects glucagon-like peptide-1 (GLP-1) secretion from enteroendoceine L cells remains unclear. Here we assessed the effect of S-equol on GLP-1 secretion from mouse enteroendocrine L cell line GLUTag cells. GLUTag cells expressed GPR30 and estrogen receptors, which are putative S-equol receptors. Application of S-equol induced an increase in intracellular Ca2+ levels via GPR30. However, S-equol did not enhance GLP-1 exocytosis, and long-term treatment of S-equol suppressed GLP-1 secretion. Moreover, immunocytochemistry revealed that S-equol increased the density of cortical actin filaments via G12113 signaling under GPR30. These data suggest that S-equol prevents GLP-1 secretion as a result of competing regulation between Ca2+ mobilization and actin reorganization. (C) 2018 Elsevier Inc. All rights reserved.