Pancreatic and Extrapancreatic Effects of Gastric Inhibitory Polypeptide
- Yuichiro Yamada1,
- Kazumasa Miyawaki1,
- Katsushi Tsukiyama1,
- Norio Harada1,
- Chizumi Yamada1 and
- Yutaka Seino12
- 1Department of Diabetes and Clinical Nutrition, Kyoto University Graduate School of Medicine, Kyoto, Japan
- 2Kansai Electric Power Hospital, Kyoto, Japan
- Address correspondence and reprint requests to Yuichiro Yamada, MD, PhD, Department of Diabetes and Clinical Nutrition, Kyoto University Graduate School of Medicine, 54 Shogoin-Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan. E-mail: yamada{at}metab.kuhp.kyoto-u.ac.jp
Abstract
The hormonal factor(s) implicated as transmitters of signals from the gut to pancreatic β-cells is referred to as incretin, and gastric inhibitory polypeptide (GIP) is identified as one of the incretins. GIP is a gastrointestinal peptide hormone of 42 amino acids that is released from duodenal endocrine K-cells after absorption of glucose or fat and exerts its effects by binding to its specific receptor, the GIP receptor. By generating and characterizing mice with a targeted mutation of the GIP receptor gene, we have shown that GIP has not only an insulinotropic role, but also physiological roles on fat accumulation into adipose tissues and calcium accumulation into bone. We here propose a new acronym, GIP, for gut-derived nutrient-intake polypeptide.
Footnotes
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This article is based on a presentation at a symposium. The symposium and the publication of this article were made possible by an unrestricted educational grant from Servier.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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- Accepted May 3, 2006.
- Received March 23, 2006.
- DIABETES
