Literature DB >> 24106731

A pilot study examining the relationship among Crohn disease activity, glucagon-like peptide-2 signalling and intestinal function in pediatric patients.

David L Sigalet, Dragan Kravarusic, Decker Butzner, Bolette Hartmann, Jens J Holst, Jon Meddings.   

Abstract

UNLABELLED: BACKGROUND⁄
OBJECTIVES: The relationship between the enteroendocrine hormone glucagon-like peptide 2 (GLP-2) and intestinal inflammation is unclear. GLP-2 promotes mucosal growth, decreases permeability and reduces inflammation in the intestine; physiological stimulation of GLP-2 release is triggered by nutrient contact. The authors hypothesized that ileal Crohn disease (CD) affects GLP-2 release.
METHODS: With ethics board approval, pediatric patients hospitalized with CD were studied; controls were recruited from local schools. Inclusion criteria were endoscopy-confirmed CD (primarily of the small intestine) with a disease activity index >150. Fasting and postprandial GLP-2 levels and quantitative urinary recovery of orally administered 3-O-methyl-glucose (active transport) and lactulosemannitol (passive) were quantified during the acute and remission phases.
RESULTS: Seven patients (mean [± SD] age 15.3 ± 1.3 years) and 10 controls (10.3 ± 1.6 years) were studied. In patients with active disease, fasting levels of GLP-2 remained stable but postprandial levels were reduced. Patients with active disease exhibited reduced glucose absorption and increased lactulosemannitol recovery; all normalized with disease remission. The change in the lactulosemannitol ratio was due to both reduced lactulose and increased mannitol absorption.
CONCLUSIONS: These findings suggest that pediatric patients with acute ileal CD have decreased postprandial GLP-2 release, reduced glucose absorption and increased intestinal permeability. Healing of CD resulted in normalization of postprandial GLP-2 release and mucosal functioning (nutrient absorption and permeability), the latter due to an increase in mucosal surface area. These findings have implications for the use of GLP-2 and feeding strategies as a therapy in CD patients; further studies of the effects of inflammation and the GLP-2 axis are recommended.

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Year:  2013        PMID: 24106731      PMCID: PMC3805340          DOI: 10.1155/2013/460958

Source DB:  PubMed          Journal:  Can J Gastroenterol        ISSN: 0835-7900            Impact factor:   3.522


  41 in total

Review 1.  Barrier dysfunction and Crohn's disease.

Authors:  J Meddings
Journal:  Ann N Y Acad Sci       Date:  2000       Impact factor: 5.691

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Authors:  Gary R Martin; Jonathan B Meddings; David L Sigalet
Journal:  JPEN J Parenter Enteral Nutr       Date:  2003 Jan-Feb       Impact factor: 4.016

3.  Use of enteral nutrition for the control of intestinal inflammation in pediatric Crohn disease.

Authors:  Jeff Critch; Andrew S Day; Anthony Otley; Cynthia King-Moore; Jonathan E Teitelbaum; Harohalli Shashidhar
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4.  Circulating levels of glucagon-like peptide-2 in human subjects with inflammatory bowel disease.

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5.  Glucagon-like peptide 2 decreases mortality and reduces the severity of indomethacin-induced murine enteritis.

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7.  Elevated plasma glucagon-like peptide 1 and 2 concentrations in ileum resected short bowel patients with a preserved colon.

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8.  3-0 methylglucose uptake as a marker of nutrient absorption and bowel length in pediatric patients.

Authors:  David L Sigalet; Gary R Martin; Jon B Meddings
Journal:  JPEN J Parenter Enteral Nutr       Date:  2004 May-Jun       Impact factor: 4.016

Review 9.  Direct and indirect mechanisms regulating secretion of glucagon-like peptide-1 and glucagon-like peptide-2.

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Authors:  Gary R Martin; Laurie E Wallace; David L Sigalet
Journal:  Am J Physiol Gastrointest Liver Physiol       Date:  2004-02-12       Impact factor: 4.052

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Review 3.  Gut microbiota: sculptors of the intestinal stem cell niche in health and inflammatory bowel disease.

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Review 4.  Bugs, genes, fatty acids, and serotonin: Unraveling inflammatory bowel disease?

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