2006 Fiscal Year Final Research Report Summary
Physiological role and molecular mechanism of mTOR signaling as a sensor of nutrition
| Project/Area Number |
17590267
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Kobe University |
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Principal Investigator |
HARA Kenta Kobe University, Graduate school of Medicine, COE Postdoctoral Fellow, 大学院・医学系研究科, COE研究員 (70397826)
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| Co-Investigator(Kenkyū-buntansha) |
YOKONO Koichi Kobe University, Graduate school of Medicine, Professor, 大学院・医学系研究科, 教授 (50144580)
NAGATA Masao Kobe University, Graduate school of Medicine, Associate professor, 大学院・医学系研究科, 助教授 (70294220)
MORIYAMA Hiroaki Kobe University, Graduate school of Medicine, COE Postdoctoral Fellow, 大学院・医学系研究科, COE研究員 (70372646)
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| Project Period (FY) |
2005 – 2006
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| Keywords | Signal Transduction / mTOR / Energy Metabolism / Nutrition Sensor |
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| Research Abstract |
1. Identification of novel binding protein to raptor. We identified some proteins which bind to mTOR adaptor protein, raptor. One of them was found to be an anti-tumor protein that is known to be involved in oxygen sensing and regulating expression of a variety of genes. Another one was found to be a novel mTOR substrate whose function has been yet to be identified. These results have uncovered new aspects of mTOR signaling.
2. Analysis of mTOR-haploinsufficient mice. The mice showed resistant to obesity under high fat diet. The induction of mTOR-haploinsufficiency in KK-A^y mice, an established obese and diabetes mice model, also exhibited resistance to obesity. The weight of fat tissues and serum leptin levels were significantly lower in mTOR-haploinsufficient mice, whereas the mRNA expressions of genes involved in energy metabolism, such as PPARs, were not significantly different. We found that expression of phosphorylation of one of mTOR effectors, S6 were increased in obese mice, while these were reduced in mTOR-haploinsufficient mice. These results suggested that mTOR signal plays an important role in regulation of energy metabolism, and raised the possibility that nutrient-regulated mTOR signal could be a target for the treatment of metabolic syndrome.
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[Book] 最新医学2005
Author(s)
原 賢太
Total Pages
8
Publisher
最新医学社
Description
「研究成果報告書概要(和文)」より
