| Project/Area Number |
26460396
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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 |
Pathological medical chemistry
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| Research Institution | Kyorin University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
AOYAGI Kyota 杏林大学, 医学部, 講師 (50453527)
NAGAMATSU Shinya 杏林大学, 医学部, 教授 (80231489)
OKAMURA Tadashi 独立行政法人 国立国際医療センター, 研究所, 室長 (00333790)
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | インスリン分泌 / 膵β細胞 / 妊娠糖尿病 / 糖尿病 / 妊娠 / 開口分泌 / 開口放出 |
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| Outline of Final Research Achievements |
In preparation for the metabolic demands of pregnancy, β cells in the maternal pancreatic islets increase both in number and in glucose-stimulated insulin secretion per cell. Mechanisms have been proposed for the increased β cell mass, but not for the increased glucose-stimulated insulin secretion. Here we show using knockout mice for P2X7-purinoreceptor and CDKAL1, a type 2 diabetes susceptibility gene that (i) ATP, acting in a paracrine/autocrine manner through P2X7 plays an essential role in the increased glucose-stimulated insulin secretion of pregnancy; (ii) the decreased expression of CDKAL1 is associated with reduced glucose-stimulated insulin secretion during pregnancy.
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