Glucose intolerance caused by a defect in the entero-insular axis: A study in gastric inhibitory polypeptide receptor knockout mice

• DOI: 10.1073/pnas.96.26.14843
• Publication Date: 2002-07-26T14:32:33Z
• Authors: Kazumasa Miyawaki; Yuichiro Yamada; Hideki Yano; Hitoshi Niwa; Nobuhiro Ban; Yu Ihara; Akira Kubota; Shinpei Fujimoto; Mariko Kajikawa; Akira Kuroe; Kinsuke Tsuda; Hiroyuki Hashimoto; Tokuyuki Yamashita; Takahito Jomori; Fumi Tashiro; Jun-ichi Miyazaki; Yutaka Seino
• Keywords: Gastric inhibitory polypeptide; Pathogenesis; Knockout mouse

Mice with a targeted mutation of the gastric inhibitory polypeptide (GIP) receptor gene (GIPR) were generated to determine role GIP as mediator signals from gut pancreatic beta cells. GIPR-/- mice have higher blood glucose levels impaired initial insulin response after oral load. Although meal ingestion are not increased by high-fat diet in GIPR+/+ because compensatory secretion, they significantly lack such enhancement. Accordingly, early secretion mediated determines tolerance load vivo, and plays an important enhancement produced high demand, defect this entero-insular axis may contribute pathogenesis diabetes.