Possible control mechanism of adipogenic progenitor cell proliferation by adiponectin and CTRP11.

2018 Fiscal Year Final Research Report

• Project/Area Number: 16K08068
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Integrative animal science
• Research Institution: Hokkaido University
• Principal Investigator: Kimura Kazuhiro 北海道大学, 獣医学研究院, 教授 (30192561)
• Research Collaborator: OKAMATSU Yuko
• Project Period (FY): 2016-04-01 – 2019-03-31
• Keywords: 前駆脂肪細胞 / アディポネクチン / CTRP11 (C1QL4) / インスリン抵抗性 / 肥満 / NGF / VEGF

Outline of Final Research Achievements

The present study aimed to examine physical interaction between adiponectin (AN) and stroma-vascular fraction-derived factor and physiological importance of the interaction. I showed that AN bound to NGF, VEGF165, factor A, factor B, but not to VEGF 120, and that AN prevented NGF-induced neurite outgrowth in PC12 cells, but failed to influence VEGF165-induced tubulogenesis in endothelium. I also found that antibody against either factor A or factor B, but not to NGF, suppresses proliferation of adipogenic progenitors. Addition of recombinant factor A or factor B to the culture medium reverse the inhibition by corresponding antibody. As mRNA and protein were detected in the isolated preadipocytes, it is the most likely that factor A and factor B are endogenous preadipocyte growth factor. As two factors interacted with AN, further works are necessary to reveal physiological relevance of the interaction, and also interaction with CTRP11, an AN homologue.

Free Research Field

獣医生化学

Academic Significance and Societal Importance of the Research Achievements

アディポクチン(AN)の新規特性としてNGF、VEGF165、匿名の因子A, Bとの結合能とNGFの機能阻害能を示した。また因子A、Bが前駆脂肪細胞増殖因子であることを明らかにした。これらは学術的知見の蓄積に貢献するだけでなく、後者は前駆脂肪細胞を増やしてインスリン抵抗性になった組織等にインスリン感受性細胞を供給する系を活性化し、抗糖尿病効果を示すと考えられる。