HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS REGISTER		Author Keyword(s) Vol Page [Advanced]

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this link to a friend Similar articles in this journal Similar articles in PubMed Add article to my folders Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Horowitz, M Articles by Nauck, M A Search for Related Content PubMed PubMed Citation Articles by Horowitz, M Articles by Nauck, M A Topic Collections Relevant Article

To be or not to be—an incretin or enterogastrone?

¹ University of Adelaide, Endocrine and Metabolic Unit, Royal Adelaide Hospital, Adelaide, South Australia 5005, Australia
² Internist/Gastroenterology/Endocrinology, Diabetology (DDG), Diabeteszentrum Bad Lauterberg, Kirchberg, Bad Lauterberg im Harz, Germany

Correspondence to:
Correspondence to:
Professor M Horowitz
Department of Medicine, North Terrace, Royal Adelaide Hospital, Adelaide, South Australia 5005, Australia; michael.horowitz@adelaide.edu.au

Keywords: glucagon-like peptide 1; exendin(9-39); incretin; enterogastrone; pyloric motility

The first 150 words of the full text of this article appear below.

Incretin hormones are gut derived peptides that augment the insulin releasing action of hyperglycaemia. In his seminal review, based on the 1978 Claude Bernard lecture, delivered at the European Association for the Study of Diabetes Meeting, Werner Creutzfeldt defined the term incretin as "an endocrine transmitter produced by the gastrointestinal tract which is: (a) released by nutrients, especially carbohydrates and (b) stimulates insulin secretion in the presence of glucose if exogenously infused in amounts not exceeding blood levels achieved after food ingestion".¹ At that time, the best characterised incretin candidate was glucose dependent insulinotropic polypeptide (GIP), although there was evidence that GIP was not the only incretin.^1,3 An incretin role for GIP was established, along the lines of Creutzfeldt’s definition,¹ by intravenous infusion in healthy subjects, both alone and in combination with glucose, and demonstrating that the insulinotropic property of GIP was dependent on a permissive rise in blood . . . [Full text of this article]

Relevant Article

Endogenous glucagon-like peptide 1 controls endocrine pancreatic secretion and antro-pyloro-duodenal motility in humans

J Schirra, M Nicolaus, R Roggel, M Katschinski, M Storr, H J Woerle, and B Göke
Gut 2006 55: 243-251. [Abstract] [Full Text] [PDF]

This article has been cited by other articles:

				K. Sutherland, R. L. Young, N. J. Cooper, M. Horowitz, and L. A. Blackshaw Phenotypic characterization of taste cells of the mouse small intestine Am J Physiol Gastrointest Liver Physiol, May 1, 2007; 292(5): G1420 - G1428. [Abstract] [Full Text] [PDF]