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

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Abstract
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.

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