Project/Area Number |
26461369
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Metabolomics
|
Research Institution | Toho University |
Principal Investigator |
JIANG Meizi 東邦大学, 医学部, 非常勤研究生 (00624066)
|
Co-Investigator(Renkei-kenkyūsha) |
BUJO Hideaki 東邦大学, 医学部, 教授 (80291300)
|
Research Collaborator |
SHIMIZU Naomi 東邦大学, 医学部, 講師 (30375802)
HIGASHI Morihiko 埼玉医科大学, 医学部, 准教授 (00323395)
Antonio Vidal-Puig University of Cambridge, Addenbrooke's Hospital Metabolic Research Laboratories, 教授
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
Keywords | LR11 / エネルギー消費 / 褐色細胞 / 機能獲得 / 肥満 / 糖尿病 / 熱代謝 / 褐色分化 / インスリン抵抗性 / ノックアウトマウス / 褐色脂肪 / 可溶性LR11 / 皮下脂肪 |
Outline of Final Research Achievements |
This study was aimed to clarify the mechanism underlying the regulation for the functional transition from white adipocytes to brown adipocytes, and to propose a novel modulation therapy for diabetes and obesity. Cell biological analyses showed that LR11 played an important role as an inhibitor in the functional acquisition of brown adipocytes. Intracellular signal analyses showed that, in the inhibition activity of soluble LR11 for the browning differentiation, LR11 was thought to at least in part inhibit the BMP7-induced signal cascade by the complex formation with the receptor BMPR. Taken together, LR11 was an inhibitor for the functional acquisition of brown adipocytes, and is possibly applied for the novel therapy for obesity and diabetes.
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