Gastric inhibitory polypeptide and glucagon-like peptide-1 in the pathogenesis of type 2 diabetes.

Abstract:

:The incretin effect denominates the phenomenon that oral glucose elicits a higher insulin response than does intravenous glucose. The two hormones responsible for the incretin effect, glucose-dependent insulinotropic hormone (GIP) and glucagon-like peptide-1 (GLP-1), are secreted after oral glucose loads and augment insulin secretion in response to hyperglycemia. In patients with type 2 diabetes, the incretin effect is reduced, and there is a moderate degree of GLP-1 hyposecretion. However, the insulinotropic response to GLP-1 is well maintained in type 2 diabetes. GIP is secreted normally or hypersecreted in type 2 diabetes; however, the responsiveness of the endocrine pancreas to GIP is greatly reduced. In approximately 50% of first-degree relatives of patients with type 2 diabetes, similarly reduced insulinotropic responses toward exogenous GIP can be observed, without significantly changed secretion of GIP or GLP-1 after oral glucose. This opens the possibility that a reduced responsiveness to GIP is an early step in the pathogenesis of type 2 diabetes. On the other hand, this provides a basis to use incretin hormones, especially GLP-1 and its derivatives, to replace a deficiency in incretin-mediated insulin secretion in the treatment of type 2 diabetes.

journal_name

Diabetes

journal_title

Diabetes

authors

Nauck MA,Baller B,Meier JJ

doi

10.2337/diabetes.53.suppl_3.s190

subject

Has Abstract

pub_date

2004-12-01 00:00:00

pages

S190-6

eissn

0012-1797

issn

1939-327X

pii

53/suppl_3/S190

journal_volume

53 Suppl 3

pub_type

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