COMMENTARY

Incretin

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

M Horowitz¹, M A Nauck²

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

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Glucagon-like peptide 1 does not comfortably fulfil the criterion of a gut derived factor responsible for an enhanced meal related insulin response; it appears logical to add the definition of a "physiological incretin hormone"

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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]

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

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