Project/Area Number |
25670432
|
Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
Allocation Type | Multi-year Fund |
Research Field |
Metabolomics
|
Research Institution | Gifu University |
Principal Investigator |
TAKEDA Jun 岐阜大学, 医学(系)研究科(研究院), 教授 (40270855)
|
Co-Investigator(Renkei-kenkyūsha) |
HORIKAWA Yukio 岐阜大学, 医学部附属病院, 准教授 (10323370)
IIDUKA Katsumi 岐阜大学, 医学部附属病院, 講師 (40431712)
|
Project Period (FY) |
2013-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
Keywords | インスリン分泌 / 遺伝性疾患 / 分子遺伝学 / 生活習慣 / 糖尿病 / ランゲルハンス島 / ゲノム / トランスクリプトーム / 組織特異性 / 再生医療 |
Outline of Final Research Achievements |
Functional defects of MODY-related transcription factors are associated with both functional and morphological abnormalities in endocrine pancreas. In order to understand the pathogenesis, we examined functional properties of the related cofactors, using LRH-1 and SHP deficient mice. In addition, establishment of molecular inventory of differentially expressed genes located downstream of the pancreatic MODY network was also performed. Both LRH-1 and SHP deficient mice represented no glucose intolerance, suggesting that these factors alone could not initiate any remodeling of endocrine cells. However, LRH-1 (-/+) mice showed significantly increased body weight, suggesting that MODY transcription network might include various metabolic pathways. The comprehensive survey of differentially expressed genes in various conditions resulted in the identification of eleven candidate genes, the analysis of which could lead to the better understanding of acquirement of the tissue-specificity.
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