| Project/Area Number |
23591351
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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 |
Endocrinology
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| Research Institution | Nagoya University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
HAYASHI Yoshitaka 名古屋大学, 環境医学研究所, 准教授 (80420363)
TAKAGISHI Yoshiko 名古屋大学, 環境医学研究所, 助教 (50024659)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | グルカゴン / 膵島 / α細胞 / 転写因子 / ARX / 膵臓 / ランゲルハンス島 / 過形成 |
|---|
| Research Abstract |
A transcription factor, aristaless-related homeobox (ARX), is known to play a pivotal role in the development of pancreatic islet cells. However, its precise mechanism remains to be clarified. We recently found that a marked hyperplasia was associated with increased expression of ARX in the pancreatic islet in mice deficient in glucagon gene-derived peptides. In this study, we sought to elucidate the role of ARX in the hyperplasia of alpha cells through analyses of two Arx mutant alleles that have different levels of impairment of their function. The increase in islet size and number of alpha-like cells were reduced in those mutant mice, indicating that the alpha cell hyperplasia induced by the inactivation of glucagon gene is reduced by introduction of an Arx mutation. In addition, the reduction was correlated with severity of disrupted ARX function, showing that the function of ARX is one of the key modifiers for the proliferation of pancreatic alpha cells.
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