GLUT2 and the incretin receptors are involved in glucose-induced incretin secretion
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GLUT2 and the incretin receptors are involved in glucose-induced incretin secretion. / Cani, Patrice D; Holst, Jens Juul; Drucker, Daniel J; Delzenne, Nathalie M; Thorens, Bernard; Burcelin, Rémy; Knauf, Claude.
In: Molecular and Cellular Endocrinology, Vol. 276, No. 1-2, 30.09.2007, p. 18-23.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - GLUT2 and the incretin receptors are involved in glucose-induced incretin secretion
AU - Cani, Patrice D
AU - Holst, Jens Juul
AU - Drucker, Daniel J
AU - Delzenne, Nathalie M
AU - Thorens, Bernard
AU - Burcelin, Rémy
AU - Knauf, Claude
PY - 2007/9/30
Y1 - 2007/9/30
N2 - 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.
AB - 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.
KW - Animals
KW - Gastric Inhibitory Polypeptide
KW - Glucagon-Like Peptide 1
KW - Glucose
KW - Glucose Intolerance
KW - Glucose Tolerance Test
KW - Glucose Transporter Type 2
KW - Intestines
KW - Mice
KW - Mice, Knockout
KW - Models, Biological
KW - Portal System
KW - Receptors, Gastrointestinal Hormone
KW - Receptors, Glucagon
U2 - 10.1016/j.mce.2007.06.003
DO - 10.1016/j.mce.2007.06.003
M3 - Journal article
C2 - 17681422
VL - 276
SP - 18
EP - 23
JO - Molecular and Cellular Endocrinology
JF - Molecular and Cellular Endocrinology
SN - 0303-7207
IS - 1-2
ER -
ID: 132049904