Molecular etiology of congenital anomalies caused by diabetes as an environmental factor
| Project/Area Number |
25670491
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Embryonic/Neonatal medicine
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| Research Institution | Kyushu University |
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Principal Investigator |
Meno Chikara 九州大学, 医学(系)研究科(研究院), 教授 (20311764)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 糖尿病 / 先天性心疾患 / 内臓錯位 / 左右軸 / 臓器錯位 / 左右軸形成 / 先天異常 / マウス |
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| Outline of Final Research Achievements |
Epidemiology has revealed that the risk of congenital anomalies is increased in offspring born from mothers with pregestational diabetes. The etiology of such congenital anomalies remains largely unknown, however. In this research, we examined the effect of hyperglycemia on left-right axis formation in mouse embryos, since pregestational diabetes increases the risk of heterotaxia in human. By analyzing streptozotocin-induced diabetic mice and embryos cultured in high glucose medium, we found that high glucose concentration inhibits the establishment of Nodal-Pitx2 expression in left lateral plate mesoderm. Right isomerism in human pregestational diabetes may be explained by this mechanism.
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Report
(4 results)
Research Products
(16 results)
