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  • Halim, Abdul,1983-Uppsala universitet,Gastroenterologi/hepatologi (author)

Glucagon-like peptide-1 inhibits prandial gastrointestinal motility through myenteric neuronal mechanisms in humans

  • Article/chapterEnglish2018

Publisher, publication year, extent ...

  • 2017-11-21
  • The Endocrine Society,2018
  • printrdacarrier

Numbers

  • LIBRIS-ID:oai:DiVA.org:uu-334892
  • https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-334892URI
  • https://doi.org/10.1210/jc.2017-02006DOI
  • http://kipublications.ki.se/Default.aspx?queryparsed=id:137656881URI

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  • Language:English
  • Summary in:English

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  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

Notes

  • Context: Glucagon-like peptide-1 (GLP-1) secretion from L-cells and postprandial inhibition of gastrointestinal motility.Objective: Investigate whether physiological plasma concentrations of GLP-1 can inhibit human postprandial gastrointestinal motility; determine target mechanism of GLP-1 and analogue ROSE-010 action.Design: Single-blind parallel study.Setting: University research laboratory.Participants: Healthy volunteers investigated with antroduodenojejunal manometry. Human gastric, intestinal and colonic muscle strips.Interventions: Motility indices (MI) obtained before and during infusion of saline or GLP-1 were compared. Plasma GLP-1 and glucagon-like peptide-2 (GLP-2) measured by radioimmunoassay. Gastrointestinal muscle strips, pre-contracted with bethanechol/electric field stimulation (EFS), investigated for GLP-1- or ROSE-010-induced relaxation. GLP-1, GLP-2 and their receptors localized by immunohistochemistry. Action mechanisms studied employing exendin(9-39)amide, Lω-nitro-monomethylarginine (L-NMMA), 2´,5´-dideoxyadenosine (DDA), tetrodotoxin (TTX).Main outcome measures: Hypothesize postprandial gastric relaxation induced by GLP-1, the mechanism of which intrinsic neuronally-mediated.Results: Food intake increased MI to 6.4±0.3 (antrum), 5.7±0.4 (duodenum) and 5.9±0.2 (jejunum). GLP-1 administered intravenously raised plasma GLP-1, but not GLP-2. GLP-1 0.7 pmol/kg·min significantly suppressed MI to 4.6±0.2, 4.7±0.4 and 5.0±0.2, respectively, while 1.2 pmol/kg·min suppressed corresponding MI to 5.4±0.2, 4.4±0.3 and 5.4±0.3 (p<0.0001-0.005). GLP-1 and ROSE-010 prevented bethanechol- or EFS-induced muscle contractions (p <0.005-0.05). Inhibitory responses to GLP-1 and ROSE-10 were blocked by exendin(9-39)amide, L-NMMA, DDA or TTX (all p <0.005-0.05). GLP-1 and GLP-2 were localized to epithelial cells; GLP-1 also in myenteric neurons. GLP-1R and GLP-2R were localized at myenteric neurons but not muscle, GLP-1R also in epithelial cells.Conclusions: GLP-1 inhibits postprandial motility through GLP-1R at myenteric neurons, involving nitrergic and cAMP-dependent mechanisms.

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  • Degerblad, MarieKarolinska Institutet (author)
  • Sundbom, MagnusUppsala universitet,Gastrointestinalkirurgi(Swepub:uu)magsundb (author)
  • Karlbom, UrbanUppsala universitet,Gastrointestinalkirurgi(Swepub:uu)urbakarl (author)
  • Juul Holst, Jens (author)
  • Webb, Dominic-LucUppsala universitet,Gastroenterologi/hepatologi(Swepub:uu)domwe127 (author)
  • Hellström, Per M.,1954-Uppsala universitet,Gastroenterologi/hepatologi(Swepub:uu)perhe742 (author)
  • Uppsala universitetGastroenterologi/hepatologi (creator_code:org_t)

Related titles

  • In:Journal of Clinical Endocrinology and Metabolism: The Endocrine Society103:2, s. 575-5850021-972X1945-7197

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