2013 Fiscal Year Final Research Report
Role of crosstalk between peripheral circadian clock and NO-cGMP system of pancreatic beta-cells in the pathogenesis of diabetes
| Project/Area Number |
23590192
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Medical pharmacy
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| Research Institution | University of Shizuoka |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KANEKO Yukiko 静岡県立大学, 薬学部, 助教 (00381038)
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| Project Period (FY) |
2011 – 2013
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| Keywords | 糖尿病 / シグナル伝達 / 糖尿病 |
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| Research Abstract |
This study was aimed to investigate the relation between the regulation of NO-cGMP system by the endogenous NO synthase inhibitor ADMA and peripheral circadian clock in pancreatic beta-cells and the involvement of these systems in the pathogenesis of diabetes. We found that the expression of the ADMA metabolic enzyme DDAH2 in beta-cells is suppressed by high glucose, suggesting that the NO-cGMP system is down-regulated by the accumulation of ADMA in diabetes. Unfortunately, we could not obtain any evidence for a relation between the NO-cGMP system and peripheral circadian clock in beta-cells. On the other hand, melatonin, a circadian synchronizer, was suggested to inhibit insulin secretion from beta-cells in the presence of GLP-1 secreted from the gastrointestinal mucosa in response to a meal. Thus, the possibility is raised that some relation between food intake and circadian rhythm exists in the regulation of beta-cell functions.
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