| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Outline of Final Research Achievements |
In this study, we investigated the role of glutamate signaling in incretin-induced insulin secretion. The increase in glutamate content in insulin granules by GLP-1 was protein kinase A-dependent. Glutamate transport into insulin granules through vesicular glutamate transporter 1 was required for amplification of insulin secretion by incretin/cAMP signaling. Dimethyl-glutamate, a membrane-permeable glutamate precursor, augmented glucose-induced insulin granule exocytosis. The analyses using pancreatic islets from animal models of diabetes and obesity indicated that glutamate production by glucose metabolism is associated with incretin-responsiveness. These results suggest the significant role of glutamate signaling in the pathophysiology of diabetes.
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