| Project/Area Number |
21229013
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| Research Category |
Grant-in-Aid for Scientific Research (S)
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| Allocation Type | Single-year Grants |
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| Research Field |
Endocrinology
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| Research Institution | Kyoto University |
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Principal Investigator |
NAKAO Kazuwa 京都大学, 医学(系)研究科(研究院), 教授 (00172263)
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| Co-Investigator(Kenkyū-buntansha) |
EBIHARA Ken 京都大学, 医学研究科, 准教授 (70362514)
YASODA Akihiro 京都大学, 医学研究科, 講師 (50378642)
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| Co-Investigator(Renkei-kenkyūsha) |
HOSODA Kiminori 京都大学, 医学研究科, 教授 (40271598)
MUKOYAMA Masashi 京都大学, 医学研究科, 准教授 (40270558)
TAMURA Naohisa 京都大学, 医学研究科, 講師 (40314207)
MORI Kiyoshi 京都大学, 医学研究科, 准教授 (60343232)
KUWAHARA Koichiro 京都大学, 医学研究科, 講師 (30402887)
SONE Masakatsu 京都大学, 医学研究科, 講師 (40437207)
MIYAZAWA Takashi 京都大学, 医学研究科, 特定准教授 (30443500)
SAWAI Kazutomo 国立循環器病研究センター研究所, 生化学部, 特任研究員 (80393213)
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| Project Period (FY) |
2009-05-11 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥211,900,000 (Direct Cost: ¥163,000,000、Indirect Cost: ¥48,900,000)
Fiscal Year 2013: ¥36,400,000 (Direct Cost: ¥28,000,000、Indirect Cost: ¥8,400,000)
Fiscal Year 2012: ¥36,400,000 (Direct Cost: ¥28,000,000、Indirect Cost: ¥8,400,000)
Fiscal Year 2011: ¥36,400,000 (Direct Cost: ¥28,000,000、Indirect Cost: ¥8,400,000)
Fiscal Year 2010: ¥36,400,000 (Direct Cost: ¥28,000,000、Indirect Cost: ¥8,400,000)
Fiscal Year 2009: ¥66,300,000 (Direct Cost: ¥51,000,000、Indirect Cost: ¥15,300,000)
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| Keywords | 内分泌学 / 間葉系細胞由来ホルモン / ホルモン / 間葉系 / 内分泌 / レプチン / CNP / ナトリウム利尿ペプチド / レプシン / 軟骨 / 脂肪組織 / 脂肪委縮症 / 間葉系細胞 / 脂肪細胞 / 心血管構成細胞 / 肥満 / 脂肪萎縮症 / ANP / GC-B / レブチン |
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| Research Abstract |
We demonstrated that the BP of CNP ecKO mice is significantly elevated. Their vascular relaxation reaction of mesenteric artery was diminished significantly. We showed that circulating CNP rescues chondrodysplastic CNP ko mice from impaired skeletal growth. We revealed that GC-A protects podocytes from aldosterone-induced glomerular injury.
We demonstrated the insufficiency of postprandial suppression of food-related neural activity by fMRI and satiety feeling in lipodystrophic patients, which was restored by leptin, and that the beneficial effect of leptin /amylin coadministration on glucose and lipid metabolism in DIO mice. Owing to our investigator-initiated trial, marketing and manufacturing of recombinant human leptin for lipodystrophy were approved in 2013 in Japan. We demonstrated on adipogenic potential of human iPS/ES cells in vitro, and that these adipocytes can survive for at least 4 weeks after transplantation.
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| Assessment Rating |
Verification Result (Rating)
A
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