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Gut-derived glucagon-like peptides attenuate T cell-induced intestinal injury

Koehler JA, Baggio LL, Cao X, Shang R et al. · Cell reports. Medicine · Oct 20, 2026
DOI 10.1016/j.xcrm.2026.103115 · PubMed 42901164

Design: Animal study
Drugs: Semaglutide
Assessment: Facts extracted automatically · reviewed by Carrie Schluter, Nov 5, 2026 · added Nov 6, 2026

This study was added automatically, and its details were extracted by machine rather than read off the paper by a person. Carrie Schluter has reviewed the record, but that review did not re-extract those details, so the collection still publishes no population match, weight-loss explanation, study tier, findings, population or funding details for it: a check of automatically extracted details found too many errors to show them as fact. The abstract below is the source as retrieved.

01Source

The source, as retrieved

Abstract

Glucagon-like peptide-1 (GLP-1) and glucagon-like peptide-2 (GLP-2) are produced in enteroendocrine L cells and control energy homeostasis. GLP-1 receptor (GLP-1R) activation improves glucose homeostasis and induces satiety and weight loss, whereas GLP-2 receptor (GLP-2R) signaling promotes intestinal growth and nutrient absorption. GLP-1R and GLP-2R agonism also reduce intestinal damage in preclinical studies. Here, we demonstrate that endogenous GLP-1R and GLP-2R signaling are essential for protecting the intestine from T cell-mediated enteropathy. Gut injury induced by T cell activation is increased in Glp1r-/- and Glp2r-/- mice, as well as in mice with selective loss of intestinal proglucagon gene expression (GcgGut-/-). Conversely, the GLP-2R agonist teduglutide and the GLP-1R agonist semaglutide, administered separately or together, attenuate αCD3-induced intestinal damage in GcgGut-/- mice. Collectively, these findings demonstrate distinct biological roles for endogenous GLP-1R/GLP-2R activity in immune-mediated intestinal injury and highlight the therapeutic potential of glucagon-like peptides, alone or together, for ameliorating T cell-mediated mucosal injury.

Where this record came from

Source	Retrieved	Identifier
pubmed	Oct 25, 2026	42901164 first ingestion
pubmed	Oct 25, 2026	42901164 duplicate matched on doi
pubmed	Nov 1, 2026	42901164 duplicate matched on doi
pubmed	Nov 1, 2026	42901164 duplicate matched on doi
owner-review	Nov 6, 2026	reviewed_by set to Carrie Schluter (2026-11-05) on the owner's own confirmation. The assessment is unchanged and still the auto-classifier's, so its extracted values stay withheld under the 2026-10-18 decision.
reextract	Nov 6, 2026	manufacturer: 'Novo Nordisk, Eli Lilly, Lilly, AstraZeneca, Sanofi, Amgen, Pfizer, Roche, Zealand Pharma' -> None. Q-043: manufacturer and drug_details.dose re-extracted by auto-classifier-v1.2. manufacturer no longer reads companies named only in the authors' conflicts statement (IN-062) and refuses a multi-company roster; dose is tied to the GLP-1 agent by name, never reads a concentration, and records a multi-dose design whole. Every other value is carried forward unchanged. Owner decision IN-064 option 1, 2026-11-06.