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Title: The effect of gastric inhibitory polypeptide on intestinal glucose absorption and intestinal motility in mice.
Authors: Ogawa, Eiichi
Hosokawa, Masaya
Harada, Norio  kyouindb  KAKEN_id
Yamane, Shunsuke  kyouindb  KAKEN_id
Hamasaki, Akihiro
Toyoda, Kentaro
Fujimoto, Shimpei
Fujita, Yoshihito  kyouindb  KAKEN_id
Fukuda, Kazuhito
Tsukiyama, Katsushi
Yamada, Yuichiro
Seino, Yutaka
Inagaki, Nobuya  kyouindb  KAKEN_id
Author's alias: 稲垣, 暢也
Keywords: GIP
Glucose absorption
Intestine
Issue Date: 7-Jan-2011
Publisher: Elsevier Inc.
Journal title: Biochemical and biophysical research communications
Volume: 404
Issue: 1
Start page: 115
End page: 120
Abstract: Gastric inhibitory polypeptide (GIP) is released from the small intestine upon meal ingestion and increases insulin secretion from pancreatic β cells. Although the GIP receptor is known to be expressed in small intestine, the effects of GIP in small intestine are not fully understood. This study was designed to clarify the effect of GIP on intestinal glucose absorption and intestinal motility. Intestinal glucose absorption in vivo was measured by single-pass perfusion method. Incorporation of [(14)C]-glucose into everted jejunal rings in vitro was used to evaluate the effect of GIP on sodium-glucose co-transporter (SGLT). Motility of small intestine was measured by intestinal transit after oral administration of a non-absorbed marker. Intraperitoneal administration of GIP inhibited glucose absorption in wild-type mice in a concentration-dependent manner, showing maximum decrease at the dosage of 50nmol/kg body weight. In glucagon-like-peptide-1 (GLP-1) receptor-deficient mice, GIP inhibited glucose absorption as in wild-type mice. In vitro examination of [(14)C]-glucose uptake revealed that 100nM GIP did not change SGLT-dependent glucose uptake in wild-type mice. After intraperitoneal administration of GIP (50nmol/kg body weight), small intestinal transit was inhibited to 40% in both wild-type and GLP-1 receptor-deficient mice. Furthermore, a somatostatin receptor antagonist, cyclosomatostatin, reduced the inhibitory effect of GIP on both intestinal transit and glucose absorption in wild-type mice. These results demonstrate that exogenous GIP inhibits intestinal glucose absorption by reducing intestinal motility through a somatostatin-mediated pathway rather than through a GLP-1-mediated pathway.
Rights: © 2010 Elsevier Inc.
この論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。This is not the published version. Please cite only the published version.
URI: http://hdl.handle.net/2433/134608
DOI(Published Version): 10.1016/j.bbrc.2010.11.077
PubMed ID: 21095180
Appears in Collections:Journal Articles

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