2007 Fiscal Year Final Research Report Summary
Regulation of Bone Formation by Adiponectin
| Project/Area Number |
17591551
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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 |
Orthopaedic surgery
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| Research Institution | The University of Tokyo |
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Principal Investigator |
MATSUDAIRA Ko The University of Tokyo, Faculty of Medicine, Assistant Professor (10302697)
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| Co-Investigator(Kenkyū-buntansha) |
OGATA Naoshi The University of Tokyo, Faculty of Medicine, Visiting Assistant Professor (10361495)
IKEDA Tosiyuki The University of Tokyo, Faculty of Medicine, Visiting Assistant Professor (80322759)
MATSUBARA Takehiro The University of Tokyo, Faculty of Medicine, Intern Doctor (40361498)
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| Project Period (FY) |
2005 – 2007
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| Keywords | Adiponectin / bone / lipid / osteoporosis |
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| Research Abstract |
Since interaction between bone and lipid metabolism has been suggested, this study investigated the regulation of bone metabolism by adiponectin, a representative adipokine, by analyzing deficient and overexpressing transgenic mice. Weinitially confirmed that adiponectin and its receptors were expressed in osteoblastic and osteoclastic cells, indicating that adiponectin can act on bone not only through an endocrine pathway as a hormone secreted from fat tissue, but also through an autocrine/paracrine pathway. There was no abnormality in bone mass or turnover of adiponectin-deficient (Ad_/_) mice, possibly due to an equivalent balance of the two pathways. In the culture of bone marrow cells from the Ad_/_mice, osteogenesis was decreased compared to the wild-type (WT) cell culture, indicating a positive effect of endogenous adiponectin through the autocrine/paracrine pathway. To examine the endocrine action of adiponectin, we analyzed transgenic mice overexpressing adiponectin in the liver, and found no abnormality in the bone. Addition of recombinant adiponectin in cultured osteoprogenitor cells suppressed osteogenesis, suggesting that the direct action of circulating adiponectin was negative for bone formation. In the presence of insulin, however, this suppression was blunted, and adiponectin enhanced the insulin-induced phosphorylations of the main downstream molecule insulin receptor substrate-1 and Akt. These lines of results suggest three distinct adiponectin actions on bone formation: a positive action through the autocrine/paracrine pathway by locally produced adiponectin, a negative action through the direct pathway by circulating adiponectin, and a positive action through the indirect pathway by circulating adiponectin via enhancement of the insulin signaling.
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[Journal Article] Akt1 in osteoblasts and osteoclasts controls bone remodeling2007
Author(s)
Kawamura N, Kugimiya F, Oshima Y, Ohba S, Ikeda T, Saito T, Shinoda Y, Kawasaki Y, Ogata N, Hoshi K, Akiyama T, Tobe T, Kadowaki T, Azuma Y, Tanaka S, Nakamura K, Chung UI, and Kawaguchi H
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Journal Title
PLoS ONE 2(10)
Pages: e1058
Description
「研究成果報告書概要(欧文)」より
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[Journal Article] Regulation of bone formation by adiponectin through autocrine/paracrine and endocrine pathways2006
Author(s)
Shinoda Y, Yamaguchi M, Ogata N, Akune T, Kubota N, Yamauchi T, Terauchi Y, Kadowaki T, Takeuchi Y, Fukumoto S, Ikeda T, Hoshi K, Chung UI, Nakamura K, Kawaguchi H.
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Journal Title
J Cell Biochem 99(1)
Pages: 196-208
Description
「研究成果報告書概要(欧文)」より
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[Presentation] Regulation of bone formation by adiponectin through autocrine/paracrine and endocrine pathways2005
Author(s)
Shinoda Y, Yamaguchi M, Ogata. N, Akune T, Kadowaki T, Takeuchi Y, Fukumoto S, Hoshi K, Chung U, Nakamura K, Kawaguchi H
Organizer
27th annual meeting of the American Society for Bone and Mineral Research
Place of Presentation
Nashville, Tennessee, USA
Year and Date
20050923-27
Description
「研究成果報告書概要(欧文)」より
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