Abstract
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.
Original language | English |
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Pages (from-to) | 1160-1168 |
Number of pages | 9 |
Journal | Cell Reports |
Volume | 21 |
Issue number | 5 |
DOIs | |
Publication status | Published - 31 Oct 2017 |
Keywords
- GLUCAGON-LIKE PEPTIDE-1
- INSULIN-SECRETION
- RECEPTOR AGONISTS
- MICE
- INFLAMMATION
- DISEASE
- LIPOPOLYSACCHARIDE
- MODEL
- PERMEABILITY
- PHYSIOLOGY