| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Outline of Final Research Achievements |
The purpose of this study was to identify an endogenous ligand for the sweet taste receptor expressed in pancreatic beta-cells and adipocytes. We initially searched for intracellular compounds which activate the receptor. During the course of the study, we found that glucose is an endogenous ligand for this receptor. We therefore designated this receptor "the glucose-sensing receptor". We investigated the function and physiological role of this receptor in the action of glucose in beta-cells. We found that glucose activates the receptor, facilitates the metabolism in mitochondria and enhances the production of ATP. Since blockade of the receptor results in reduction of insulin secretion, we conclude that glucose-sensing receptor is involved in the action of glucose on insulin secretion. We also studied the changes in the expression of the glucose-sensing receptor in pancreatic beta-cells. The expression of the receptor is markedly reduced after the meal and hyperglycemia.
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