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Pancreatic and Extrapancreatic Effects of Gastric Inhibitory Polypeptide

¹ Department of Diabetes and Clinical Nutrition, Kyoto University Graduate School of Medicine, Kyoto, Japan
² Kansai 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

Abbreviations: DPP-IV, dipeptidyl peptidase-IV; GIP, gastric inhibitory polypeptide; GLP-1, glucagon-like peptide 1

The hormonal factor(s) implicated as transmitters of signals from the gut to pancreatic ß-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.

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