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Apelin stimulation of duodenal bicarbonate secretion: feeding-dependent and mediated via apelin-induced release of enteric cholecystokinin
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Physiology.
University of Oulu, Oulu, Finland. (Physiology)
University of Oulu, Oulu, Finland. (Physiology)
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Physiology.
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2011 (English)In: Acta Physiologica, ISSN 1748-1708, E-ISSN 1748-1716, Vol. 201, no 1, 141-150 p.Article in journal (Refereed) Published
Abstract [en]

Aim: Apelin peptides is the endogenous ligand of the G protein-coupled receptor APJ. Proposed actions include involvement in control of cardiovascular functions, appetite and body metabolism. We have investigated effects of apelin peptides on duodenal bicarbonate secretion in vivo and the release of cholecystokinin (CCK) from acutely isolated mucosal cells and the neuroendocrine cell line STC-1. Methods: Lewis x Dark Agouti rats had free access to water and, unless fasted overnight, free access  to food. A segment of proximal duodenum was cannulated in situ in anesthetized animals. Mucosal bicarbonate secretion was titrated (pH stat) and apelin was administered to the duodenum by close intra-arterial infusion. Total RNA was extracted from mucosal specimens, reverse transcripted to cDNA and expression of the APJ receptor measured by quantitative real-time PCR. Apelin-induced release of CCK was measured using (i) cells prepared from proximal small intestine, and (ii) STC-1 cells. Results: Even the lowest dose of apelin-13 (6 pmol kg-1 h-1) caused a significant rise in bicarbonate secretion. Stimulation occurred only in continuously fed animals and even a 100-fold greater dose (600 pmol kg-1 h-1) of apelin was without effect in overnight food deprived animals. Fasting also induced a 8-fold decrease  in the expression of APJ receptor mRNA. Apelin induced significant release of CCK from both mucosal and STC-1 cells, and the CCKA receptor antagonist devazepide abolished bicarbonate secretory responses to apelin. Conclusions: Apelin-induced stimulation of duodenal electrolyte secretion is feeding dependent and mediated by local mucosal release of CCK


Place, publisher, year, edition, pages
Oxford: Wiley-Blackwell , 2011. Vol. 201, no 1, 141-150 p.
Keyword [en]
Apelin, bicarbonate secretion, cholecystokinin, devazepide, fasting, luzindole
National Category
Gastroenterology and Hepatology
Research subject
URN: urn:nbn:se:uu:diva-143171DOI: 10.1111/j.1748-1716.2010.02175.xISI: 000285153100015PubMedID: 20726845OAI: oai:DiVA.org:uu-143171DiVA: diva2:389539
Appetite-related hormones and intestinal secretion
Swedish Research Council, 3515
Available from: 2011-01-19 Created: 2011-01-19 Last updated: 2014-04-07Bibliographically approved

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