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Involvement of endogenous glucagon-like peptide-1 in regulation of gastric motility and pancreatic endocrine secretion
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2011 (English)In: Scandinavian Journal of Gastroenterology, ISSN 0036-5521, Vol. 46, no 4, 428-435 p.Article in journal (Refereed) Published
Abstract [en]


To study the role of endogenous glucagon-like peptide-1 (GLP-1) on gastric emptying rates of a solid meal as well as postprandial hormone secretion and glucose disposal.

Material and methods.

In nine healthy subjects, gastric emptying of a 310-kcal radio-labelled solid meal and plasma concentrations of insulin, glucagon and glucose were measured during infusion of saline or the GLP-1 receptor antagonist exendin(9-39)amide (Ex(9-39)) at 300 pmol·kg−1·min−1.


Ex(9-39) infusion had no effect on the total gastric emptying curve, but changed the intra-gastric distribution of the meal. During infusion of Ex(9-39), more content stayed in the upper stomach (79.1 ± 2.5% of total during Ex(9-39) compared to 66.6 ± 5.7% during saline at 5 min). During Ex(9-39) infusion, higher concentrations of plasma glucagon were measured both before (after 40 min of Ex(9-39) infusion the glucagon level was 15.1 ± 0.7 pmol·L−1 compared to 5.4 ± 1.4 during saline) and after the meal, and postprandial GLP-1 levels increased. Basal insulin and glucose levels were not affected by Ex(9-39), but the postprandial rise of insulin and glucose enhanced during Ex(9-39).


Endogenous GLP-1 is involved in the regulation of gastric motility in relation to meal intake and also in the regulation of postprandial insulin and glucose levels. Furthermore, endogenous GLP-1 seems to tonically restrain glucagon secretion.

Place, publisher, year, edition, pages
2011. Vol. 46, no 4, 428-435 p.
Keyword [en]
Exendin 9-39, gastric emptying, GLP-1, glucagon, insulin
National Category
Medical and Health Sciences
URN: urn:nbn:se:uu:diva-157655DOI: 10.3109/00365521.2010.537680ISI: 000288170600007OAI: oai:DiVA.org:uu-157655DiVA: diva2:436159
Available from: 2011-08-22 Created: 2011-08-22 Last updated: 2012-05-11Bibliographically approved

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Hellström, Per Martin
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