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

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Lebrun, Lorène J | Lenaerts, Kaatje | Kiers, Dorien | Pais de Barros, Jean-Paul | Le Guern, Naïg | Plesnik, Jiri | Thomas, Charles | Bourgeois, Thibaut | Dejong, Cornelis H.C. | Kox, Matthijs | Hundscheid, Inca H.R. | Khan, Naim Akhtar, Akhtar | Mandard, Stéphane | Deckert, Valérie | Pickkers, Peter | Drucker, Daniel, J. | Lagrost, Laurent | Grober, Jacques

Edité par CCSD ; Elsevier Inc -

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

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