Analysis of the effect of inseparable association of AIM with IgM on obesity-related diseases

Research Project

Project/Area Number	17H06624
Research Category	Grant-in-Aid for Research Activity Start-up
Allocation Type	Single-year Grants
Research Field	Pathological medical chemistry
Research Institution	The University of Tokyo
Principal Investigator	SUGISAWA Ryoichi 東京大学, 大学院医学系研究科(医学部), 特任助教 (70803568)
Research Collaborator	MIYAZAKI Toru ARAI Satoko
Project Period (FY)	2017-08-25 – 2018-03-31
Project Status	Completed (Fiscal Year 2017)
Budget Amount *help	¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000) Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Keywords	肥満 / 脂肪肝 / 肝癌 / AIM / ネコ / 病態医科学 / 免疫学 / 蛋白質
Outline of Final Research Achievements	Apoptosis inhibitor of macrophage (AIM) has been shown to have suppressive functions in a broad range of diseases including obesity, liver steatosis, hepatocellular carcinoma, and acute kidney injury (AKI). AIM is a circulating protein, associate with IgM pentamers under health states in the blood, and during AKI, AIM dissociates from IgM and gains disease repair activity. On the other hand, due to its extremely high binding affinity for IgM, feline AIM rarely dissociates from IgM and AIM-felinized mice (mice which mouse AIM was replaced with feline AIM) exhibited deficient AKI repair as in cats. In this study, we investigated whether AIM activation via its release from IgM is required to ameliorate other diseases. When fed a high-fat diet (HFD), AIM-felinized mice exhibited resulting in more prominent obesity and fatty liver than in wild-type mice. Thus, blood AIM released from IgM contributes to suppression of obesity and fatty liver as in AKI.