Enteroendocrine L Cells Sense LPS after Gut Barrier Injury to Enhance GLP-1 Secretion

• DOI: 10.1016/j.celrep.2017.10.008
• Publication Date: 2017-10-31T15:47:19Z
• Authors: Lorène J. Lebrun; Kaatje Lenaerts; Dorien Kiers; Jean-Paul Pais de...; Naig Le Guern; Jiri Plesnik; Charles Thomas; Thibaut Bourgeois; Cornelis H.C. Dejong; Matthijs Kox; Inca H.R. Hundscheid; Naim Akhtar Khan; Stéphane Mandard; Valérie Deckert; Peter Pickkers; Daniel J. Drucker; Laurent Lagrost; Jacques Grober
• Keywords: Enteroendocrine cell; Incretin; Proinflammatory cytokine

Glucagon-like peptide 1 (GLP-1) is a hormone released from enteroendocrine L cells. Although first described as glucoregulatory incretin hormone, GLP-1 also suppresses inflammation and promotes mucosal integrity. Here, we demonstrate that plasma levels are rapidly increased by lipopolysaccharide (LPS) administration in mice via Toll-like receptor 4 (TLR4)-dependent mechanism. Experimental manipulation of gut barrier integrity after dextran sodium sulfate treatment, or ischemia/reperfusion experiments mice, triggered rapid rise circulating GLP-1. This phenomenon was detected prior to measurable changes inflammatory status cytokine LPS levels. In human subjects, induced secretion. Furthermore, were following the induction ischemia intestine. These findings expand traditional concepts cell biology encompass sensing stimuli compromised integrity, linking glucagon-like secretion inflammation.