2012 Fiscal Year Final Research Report
Analyses of soluble factors produced by human brown adipocytes
| Project/Area Number |
24659447
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Metabolomics
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
MAZDA Osamu 京都府立医科大学, 大学院・医学研究科, 教授 (00271164)
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| Co-Investigator(Renkei-kenkyūsha) |
KAWAHITO Yutaka 京都府立医科大学, 医学研究科, 准教授 (50336731)
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| Project Period (FY) |
2012
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| Keywords | 細胞分化 / 再生医療 |
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| Research Abstract |
Unlike white adipocytes, brown adipocytes contribute to energy expenditure and non-shivering heat generation. However, the functions and roles of human brown adipocytes have not been fully understood, because the existence of brown adipocytes in adult human remained controversial until recently . It remains almost unknown whether some soluble factors are produced by brown adipocytes and play regulatory roles in systemic metabolism. Here, we attempted to analyze functions of soluble factors produced by human brown adipocytes Genome-wide gene expression analysis of brown and white adipocytes using DNA chips suggested some putative protein that may be selectively secreted by brown adipocytes. We constructed chimeric genes for the candidate proteins fused with FLAG, and transfected them to cultured cells via electroporation. Western blot analyses using anti-FLAG antibody demonstrated expression of the chimeric proteins in the lysates of the transfected cells. In contrast, we also knocked down expression of the uncoupling protein 1 (UCP1) in brown adipocytes by short interfering RNA, and subjected the cells to some functional analyses. The UCP1-knocked down cells retained some functions, albeit at a low level compared with wild type. Further analyses suggested that the function was possibly mediated through some soluble factors. Thus, brown adipocytes may exert UCP1-independent functions through producing soluble factors. The present results may have strong implications to understanding and control of diabetes mellitus and metabolic syndrome.
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[Journal Article] Mild electrical stimulation with heat stimulation increase heat shock protein 70 in articular chondrocyte2013
Author(s)
Hiraoka N, Arai Y, Takahashi KA, Mazda O, Kishida T, Honjo K, Tsuchida S, Inoue H, Morino S, Suico MA, Kai H, & Kubo T
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Journal Title
J Orthop Res
Volume: 31(6)
Pages: 894-900
DOI
Peer Reviewed
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