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The nuclear receptor FXR inhibits Glucagon-Like Peptide-1 secretion in response to microbiota-derived Short-Chain Fatty Acids.
Ducastel, Sarah; Touche, Véronique; Trabelsi, Mohamed-Sami; Boulinguiez, Alexis; Butruille, Laura; Nawrot, Margaux; Peschard, Simon; Chávez-Talavera, Oscar; Dorchies, Emilie; Vallez, Emmanuelle; Annicotte, Jean-Sébastien; Lancel, Steve; Briand, Olivier; Bantubungi, Kadiombo; Caron, Sandrine; Bindels, Laure B; Delzenne, Nathalie M; Tailleux, Anne; Staels, Bart; Lestavel, Sophie.
Afiliación
  • Ducastel S; Université de Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011- EGID, F-59000, Lille, France.
  • Touche V; Université de Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011- EGID, F-59000, Lille, France.
  • Trabelsi MS; Université de Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011- EGID, F-59000, Lille, France.
  • Boulinguiez A; Université de Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011- EGID, F-59000, Lille, France.
  • Butruille L; Université de Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011- EGID, F-59000, Lille, France.
  • Nawrot M; Université de Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011- EGID, F-59000, Lille, France.
  • Peschard S; Université de Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011- EGID, F-59000, Lille, France.
  • Chávez-Talavera O; Université de Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011- EGID, F-59000, Lille, France.
  • Dorchies E; Université de Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011- EGID, F-59000, Lille, France.
  • Vallez E; Université de Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011- EGID, F-59000, Lille, France.
  • Annicotte JS; Université de Lille, CNRS, CHU Lille, Institut Pasteur de Lille, UMR 8199 - EGID, F-59000, Lille, France.
  • Lancel S; Université de Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011- EGID, F-59000, Lille, France.
  • Briand O; Université de Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011- EGID, F-59000, Lille, France.
  • Bantubungi K; Université de Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011- EGID, F-59000, Lille, France.
  • Caron S; Université de Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011- EGID, F-59000, Lille, France.
  • Bindels LB; Metabolism and Nutrition Research Group, Louvain Drug Research Institute, Université Catholique de Louvain, 1200, Brussels, Belgium.
  • Delzenne NM; Metabolism and Nutrition Research Group, Louvain Drug Research Institute, Université Catholique de Louvain, 1200, Brussels, Belgium.
  • Tailleux A; Université de Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011- EGID, F-59000, Lille, France.
  • Staels B; Université de Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011- EGID, F-59000, Lille, France. bart.staels@pasteur-lille.fr.
  • Lestavel S; Université de Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011- EGID, F-59000, Lille, France.
Sci Rep ; 10(1): 174, 2020 01 13.
Article en En | MEDLINE | ID: mdl-31932631
The gut microbiota participates in the control of energy homeostasis partly through fermentation of dietary fibers hence producing short-chain fatty acids (SCFAs), which in turn promote the secretion of the incretin Glucagon-Like Peptide-1 (GLP-1) by binding to the SCFA receptors FFAR2 and FFAR3 on enteroendocrine L-cells. We have previously shown that activation of the nuclear Farnesoid X Receptor (FXR) decreases the L-cell response to glucose. Here, we investigated whether FXR also regulates the SCFA-induced GLP-1 secretion. GLP-1 secretion in response to SCFAs was evaluated ex vivo in murine colonic biopsies and in colonoids of wild-type (WT) and FXR knock-out (KO) mice, in vitro in GLUTag and NCI-H716 L-cells activated with the synthetic FXR agonist GW4064 and in vivo in WT and FXR KO mice after prebiotic supplementation. SCFA-induced GLP-1 secretion was blunted in colonic biopsies from GW4064-treated mice and enhanced in FXR KO colonoids. In vitro FXR activation inhibited GLP-1 secretion in response to SCFAs and FFAR2 synthetic ligands, mainly by decreasing FFAR2 expression and downstream Gαq-signaling. FXR KO mice displayed elevated colonic FFAR2 mRNA levels and increased plasma GLP-1 levels upon local supply of SCFAs with prebiotic supplementation. Our results demonstrate that FXR activation decreases L-cell GLP-1 secretion in response to inulin-derived SCFA by reducing FFAR2 expression and signaling. Inactivation of intestinal FXR using bile acid sequestrants or synthetic antagonists in combination with prebiotic supplementation may be a promising therapeutic approach to boost the incretin axis in type 2 diabetes.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Receptores Citoplasmáticos y Nucleares / Colon / Péptido 1 Similar al Glucagón / Ácidos Grasos Volátiles / Microbiota Límite: Animals Idioma: En Revista: Sci Rep Año: 2020 Tipo del documento: Article País de afiliación: Francia Pais de publicación: Reino Unido

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Receptores Citoplasmáticos y Nucleares / Colon / Péptido 1 Similar al Glucagón / Ácidos Grasos Volátiles / Microbiota Límite: Animals Idioma: En Revista: Sci Rep Año: 2020 Tipo del documento: Article País de afiliación: Francia Pais de publicación: Reino Unido