2018
DOI: 10.1016/j.bbrc.2018.05.100
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Bacterial metabolite S-equol modulates glucagon-like peptide-1 secretion from enteroendocrine L cell line GLUTag cells via actin polymerization

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Cited by 16 publications
(11 citation statements)
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“…The anti-prostate cancer activity of equol in cell cultures has been proposed associated with activation of FOXO3a (one of the forkhead-family factors of transcription involved in apoptosis) via protein kinase B (Akt)-specific signaling transduction pathway, and with the inhibition of the expression of the MDM2 complex (a negative regulator of tumor suppressor p53) [186,187], plus the inhibition of the degradation of the androgen receptor [185]. Diabetes and other metabolic disorders may be influenced by equol via its preventing glucagon-like peptide 1 (GLP-1) secretion from the GLUTag cells [188]. The modulation of glucose-induced insulin secretion and the suppression of glucagon release (from the α- and β-pancreatic cells, respectively) by GLP-1 in response to the ingestion of nutrients have been firmly established [189].…”
Section: Mechanistic Mode Of Action Of Equolmentioning
confidence: 99%
“…The anti-prostate cancer activity of equol in cell cultures has been proposed associated with activation of FOXO3a (one of the forkhead-family factors of transcription involved in apoptosis) via protein kinase B (Akt)-specific signaling transduction pathway, and with the inhibition of the expression of the MDM2 complex (a negative regulator of tumor suppressor p53) [186,187], plus the inhibition of the degradation of the androgen receptor [185]. Diabetes and other metabolic disorders may be influenced by equol via its preventing glucagon-like peptide 1 (GLP-1) secretion from the GLUTag cells [188]. The modulation of glucose-induced insulin secretion and the suppression of glucagon release (from the α- and β-pancreatic cells, respectively) by GLP-1 in response to the ingestion of nutrients have been firmly established [189].…”
Section: Mechanistic Mode Of Action Of Equolmentioning
confidence: 99%
“…Enteroendocrine L cells express putative equol receptors, GPR30 and estrogen receptors. The interaction between equol and receptors leads to increased levels of intracellular Ca 2+ and actin reorganization, resulting in the suppression of GLP-1 secretion [146]. An in vitro study with Caco-2 cells showed that the ginsenoside metabolite compound K induces glucose uptake mediated by the Na(+)/glucose co-transporter 1 (SGLT1), which is essential to ameliorate intestinal inflammation.…”
Section: Microbial Metabolites: Messages From the Intestinal Micromentioning
confidence: 99%
“…For instance, small intestinal L-cells in humans (Sun et al, 2017) and rats (Kuhre et al, 2015) are sensitive to glucose, whereas in vitro colonic L-cells express bile receptors and receptors for short-chain fatty acids (Tolhurst et al, 2012). Bacterial metabolites such as indole (Chimerel et al, 2014), S-equol (Harada et al, 2018) and prebiotics (Gibson and Roberfroid, 1995;Cani et al, 2006) induce GLP-1 secretion, but conversely, GLP-1 is also elevated in germ-free mice (Wichmann et al, 2013). Although L-cells are classically described as endocrine cells, like enterochromaffin cells (Bellono et al, 2017), they can synapse directly with peripheral afferent and efferent neurons (Bohórquez et al, 2015), providing a direct neural pathway for bi-directional brain-gut communication (Kaelberer et al, 2018).…”
Section: Introductionmentioning
confidence: 99%