Glucose intolerance caused by a defect in the entero-insular axis: A study in gastric inhibitory polypeptide receptor knockout mice
| Autor: | Mariko Kajikawa, Jun-ichi Miyazaki, Akira Kubota, Takahito Jomori, Nobuhiro Ban, Hitoshi Niwa, Yuichiro Yamada, Tokuyuki Yamashita, Fumi Tashiro, Yutaka Seino, Kinsuke Tsuda, Akira Kuroe, Yu Ihara, Kazumasa Miyawaki, S. Fujimoto, Hiroyuki Hashimoto, Hideki Yano |
|---|---|
| Rok vydání: | 1999 |
| Předmět: |
medicine.medical_specialty
medicine.medical_treatment Glucagon-Like Peptides Administration Oral Gastric Inhibitory Polypeptide Biology Models Biological Receptors Gastrointestinal Hormone Pathogenesis Islets of Langerhans Mice Gastric inhibitory polypeptide Glucagon-Like Peptide 1 In vivo Internal medicine Diabetes mellitus Glucose Intolerance Insulin Secretion medicine Animals Homeostasis Insulin Protein Precursors Receptor Mice Knockout Multidisciplinary Biological Sciences Glucose Tolerance Test Glucagon medicine.disease Dietary Fats Peptide Fragments Intestines Glucose Endocrinology Diabetes Mellitus Type 2 Knockout mouse Gastric inhibitory polypeptide receptor Insulin Resistance Injections Intraperitoneal |
| Zdroj: | Proceedings of the National Academy of Sciences. 96:14843-14847 |
| ISSN: | 1091-6490 0027-8424 |
| Popis: | Mice with a targeted mutation of the gastric inhibitory polypeptide (GIP) receptor gene ( GIPR ) were generated to determine the role of GIP as a mediator of signals from the gut to pancreatic β cells. GIPR −/− mice have higher blood glucose levels with impaired initial insulin response after oral glucose load. Although blood glucose levels after meal ingestion are not increased by high-fat diet in GIPR +/+ mice because of compensatory higher insulin secretion, they are significantly increased in GIPR −/− mice because of the lack of such enhancement. Accordingly, early insulin secretion mediated by GIP determines glucose tolerance after oral glucose load in vivo , and because GIP plays an important role in the compensatory enhancement of insulin secretion produced by a high insulin demand, a defect in this entero-insular axis may contribute to the pathogenesis of diabetes. |
| Databáze: | OpenAIRE |
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