1: Mol Cell Endocrinol. 2007 Sep 30;276(1-2):18-23. Epub 2007 Jun 29.

GLUT2 and the incretin receptors are involved in glucose-induced incretin
secretion.

Cani PD, Holst JJ, Drucker DJ, Delzenne NM, Thorens B, Burcelin R, Knauf C.

Institut de Médecine Moléculaire de Rangueil, I(2)MR, IFR31, CHU Rangueil, BP
84225, 31432 Toulouse cedex 4, France; Unit of Pharmacokinetics, Metabolism,
Nutrition and Toxicology, Université catholique de Louvain, Av. E. Mounier 73/69,
1200 Brussels, Belgium.

Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide 
(GIP) are incretins secreted in response to oral glucose ingestion by intestinal 
L and K cells, respectively. The molecular mechanisms responsible for intestinal 
cell glucose sensing are unknown but could be related to those described for
beta-cells, brain and hepatoportal sensors. We determined the role of GLUT2,
GLP-1 or GIP receptors in glucose-induced incretins secretion, in the
corresponding knockout mice. GLP-1 secretion was reduced in all mutant mice,
while GIP secretion did not require GLUT2. Intestinal GLP-1 content was reduced
only in GIP and GLUT2 receptors knockout mice suggesting that this impairment
could contribute to the phenotype. Intestinal GIP content was similar in all mice
studied. Furthermore, the impaired incretins secretion was associated with a
reduced glucose-stimulated insulin secretion and an impaired glucose tolerance in
all mice. In conclusion, both incretins secretion depends on mechanisms involving
their own receptors and GLP-1 further requires GLUT2.

PMID: 17681422 [PubMed - as supplied by publisher]

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