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Title: The effect of gastric inhibitory polypeptide on intestinal glucose absorption and intestinal motility in mice

Abstract

Research highlights: {yields} Exogenous GIP inhibits intestinal motility through a somatostatin-mediated pathway. {yields} Exogenous GIP inhibits intestinal glucose absorption by reducing intestinal motility. {yields} The GIP-receptor-mediated action in intestine does not involve in GLP-1-mediated pathway. -- Abstract: Gastric inhibitory polypeptide (GIP) is released from the small intestine upon meal ingestion and increases insulin secretion from pancreatic {beta} 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 [{sup 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 50 nmol/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 [{sup 14}C]-glucose uptake revealed that 100 nM GIP did not changemore » SGLT-dependent glucose uptake in wild-type mice. After intraperitoneal administration of GIP (50 nmol/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.« less

Authors:
 [1];  [1]; ; ; ; ; ; ;  [1]; ;  [1];  [1];  [1]
  1. Department of Diabetes and Clinical Nutrition, Graduate School of Medicine, Kyoto University (Japan)
Publication Date:
OSTI Identifier:
22204727
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 404; Journal Issue: 1; Other Information: Copyright (c) 2010 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ABSORPTION; AMINO ACIDS; CARBON 14; CONCENTRATION RATIO; GLUCAGON; GLUCOSE; IN VITRO; IN VIVO; INGESTION; INSULIN; MICE; ORAL ADMINISTRATION; PANCREAS; RECEPTORS; SMALL INTESTINE; SOMATOSTATIN

Citation Formats

Ogawa, Eiichi, Hosokawa, Masaya, Faculty of Human Sciences, Tezukayama Gakuin University, Osaka, Harada, Norio, Yamane, Shunsuke, Hamasaki, Akihiro, Toyoda, Kentaro, Fujimoto, Shimpei, Fujita, Yoshihito, Fukuda, Kazuhito, Tsukiyama, Katsushi, Yamada, Yuichiro, Department of Internal Medicine, Division of Endocrinology, Diabetes and Geriatric Medicine, Akita University School of Medicine, Akita, Seino, Yutaka, Kansai Electric Power Hospital, Osaka, Inagaki, Nobuya, and CREST of Japan Science and Technology Cooperation. The effect of gastric inhibitory polypeptide on intestinal glucose absorption and intestinal motility in mice. United States: N. p., 2011. Web. doi:10.1016/J.BBRC.2010.11.077.
Ogawa, Eiichi, Hosokawa, Masaya, Faculty of Human Sciences, Tezukayama Gakuin University, Osaka, Harada, Norio, Yamane, Shunsuke, Hamasaki, Akihiro, Toyoda, Kentaro, Fujimoto, Shimpei, Fujita, Yoshihito, Fukuda, Kazuhito, Tsukiyama, Katsushi, Yamada, Yuichiro, Department of Internal Medicine, Division of Endocrinology, Diabetes and Geriatric Medicine, Akita University School of Medicine, Akita, Seino, Yutaka, Kansai Electric Power Hospital, Osaka, Inagaki, Nobuya, & CREST of Japan Science and Technology Cooperation. The effect of gastric inhibitory polypeptide on intestinal glucose absorption and intestinal motility in mice. United States. https://doi.org/10.1016/J.BBRC.2010.11.077
Ogawa, Eiichi, Hosokawa, Masaya, Faculty of Human Sciences, Tezukayama Gakuin University, Osaka, Harada, Norio, Yamane, Shunsuke, Hamasaki, Akihiro, Toyoda, Kentaro, Fujimoto, Shimpei, Fujita, Yoshihito, Fukuda, Kazuhito, Tsukiyama, Katsushi, Yamada, Yuichiro, Department of Internal Medicine, Division of Endocrinology, Diabetes and Geriatric Medicine, Akita University School of Medicine, Akita, Seino, Yutaka, Kansai Electric Power Hospital, Osaka, Inagaki, Nobuya, and CREST of Japan Science and Technology Cooperation. 2011. "The effect of gastric inhibitory polypeptide on intestinal glucose absorption and intestinal motility in mice". United States. https://doi.org/10.1016/J.BBRC.2010.11.077.
@article{osti_22204727,
title = {The effect of gastric inhibitory polypeptide on intestinal glucose absorption and intestinal motility in mice},
author = {Ogawa, Eiichi and Hosokawa, Masaya and Faculty of Human Sciences, Tezukayama Gakuin University, Osaka and Harada, Norio and Yamane, Shunsuke and Hamasaki, Akihiro and Toyoda, Kentaro and Fujimoto, Shimpei and Fujita, Yoshihito and Fukuda, Kazuhito and Tsukiyama, Katsushi and Yamada, Yuichiro and Department of Internal Medicine, Division of Endocrinology, Diabetes and Geriatric Medicine, Akita University School of Medicine, Akita and Seino, Yutaka and Kansai Electric Power Hospital, Osaka and Inagaki, Nobuya and CREST of Japan Science and Technology Cooperation},
abstractNote = {Research highlights: {yields} Exogenous GIP inhibits intestinal motility through a somatostatin-mediated pathway. {yields} Exogenous GIP inhibits intestinal glucose absorption by reducing intestinal motility. {yields} The GIP-receptor-mediated action in intestine does not involve in GLP-1-mediated pathway. -- Abstract: Gastric inhibitory polypeptide (GIP) is released from the small intestine upon meal ingestion and increases insulin secretion from pancreatic {beta} 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 [{sup 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 50 nmol/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 [{sup 14}C]-glucose uptake revealed that 100 nM GIP did not change SGLT-dependent glucose uptake in wild-type mice. After intraperitoneal administration of GIP (50 nmol/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.},
doi = {10.1016/J.BBRC.2010.11.077},
url = {https://www.osti.gov/biblio/22204727}, journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 1,
volume = 404,
place = {United States},
year = {Fri Jan 07 00:00:00 EST 2011},
month = {Fri Jan 07 00:00:00 EST 2011}
}