Bacterial metabolite S-equol modulates glucagon-like peptide-1 secretion from enteroendocrine L cell line GLUTag cells via actin polymerization

Biochemical and Biophysical Research Communications
Kazuki HaradaTakashi Tsuboi

Abstract

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 β 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 G12/13 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.

Citations

Jun 4, 2019·Biological & Pharmaceutical Bulletin·Takayuki MatsumotoTsuneo Kobayashi
Oct 28, 2019·International Journal of Molecular Sciences·Panida SittipoYun Kyung Lee
Feb 9, 2021·Briefings in Functional Genomics·Changlu QiLiang Cheng
Jan 16, 2021·Current Opinion in Endocrinology, Diabetes, and Obesity·Ming YangFiona M Gribble
Jun 26, 2021·Frontiers in Endocrinology·Rune E KuhreNatalia Petersen

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