Obesity and liver diseases: towards clarification of mechanisms for NASH
Project/Area Number |
25253056
|
Research Category |
Grant-in-Aid for Scientific Research (A)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Gastroenterology
|
Research Institution | The University of Tokyo |
Principal Investigator |
Miyazaki Toru 東京大学, 医学(系)研究科(研究院), 教授 (30396270)
|
Co-Investigator(Renkei-kenkyūsha) |
ARAI Satoko 東京大学, 大学院医学系研究科, 准教授 (60422276)
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥44,200,000 (Direct Cost: ¥34,000,000、Indirect Cost: ¥10,200,000)
Fiscal Year 2015: ¥11,310,000 (Direct Cost: ¥8,700,000、Indirect Cost: ¥2,610,000)
Fiscal Year 2014: ¥13,000,000 (Direct Cost: ¥10,000,000、Indirect Cost: ¥3,000,000)
Fiscal Year 2013: ¥19,890,000 (Direct Cost: ¥15,300,000、Indirect Cost: ¥4,590,000)
|
Keywords | NASH / 脂肪肝 / 肝癌 / AIM / 生活習慣病 |
Outline of Final Research Achievements |
NASH is a liver disease involved with a steatosis, which can be a cause of a cirrhosis, thereby is sometimes followed by HCC. In this study, we found that HCC was significantly developed in AIM-deficient mice fed a high fat diet for 1 year whereas wild-type mice did not show any HCC development, demonstrating that AIM possesses an anti-NASH-derived HCC effect. AIM was incorporated into normal hepatocytes, in which AIM suppressed progress of fatty liver by interfering with accumulation of triglyceride. However, the states of inflammation or of fibrosis in response to a long-term high-fat diet were not altered in AIM-deficient mice as compared with wild-type mice. Thus, AIM appeared to eliminate the cancerized cells, rather than suppress a cancerization of hepatocytes. We also found that AIM eliminated the HCC by inducing cell death through activation of complement cascades which is prompted by the specific accumulation of AIM on the surface of the HCC.
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Report
(4 results)
Research Products
(43 results)
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[Journal Article] 1.Apoptosis inhibitor of macrophage protein enhances intraluminal debris clearance and ameliorates acute kidney injury in mice.2016
Author(s)
Arai S, Kitada K, Yamazaki T, Takai R, Zhang X, Tsugawa Y, Sugisawa R, Matsumoto A, Mori M, Yoshihara Y, Doi K, Maehara N, Kusunoki S, Takahata A, Noiri E, Suzuki Y, Yahagi N, Nishiyama A, Gunaratnam L, Takano T, Miyazaki T.
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Journal Title
Nature Medicine
Volume: 22
Issue: 2
Pages: 183-193
DOI
Related Report
Peer Reviewed / Int'l Joint Research
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[Journal Article] Circulating AIM Prevents Hepatocellular Carcinoma through Complement Activation2014
Author(s)
Maehara N, Arai S, Mori M, Iwamura Y, Kurokawa J, Kai T, Kusunoki S, Taniguchi K, Ikeda K, Ohara O, Yamamura K, Miyazaki T
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Journal Title
Cell Reports
Volume: 9
Issue: 1
Pages: 61-74
DOI
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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[Journal Article] Circulating AIM as an Indicator of Liver Damage and Hepatocellular Carcinoma in Humans2014
Author(s)
Yamazaki T, Mori M, Arai S, Tateishi R, Abe M, Ban M, Nishijima A, Maeda M, Asano T, Kai T, Izumino K, Takahashi J, Aoyama K, Harada S, Takebayashi T, Gunji T, Ohnishi S, Seto S, Yoshida Y, Hiasa Y, Koike K, Yamamura K, Inoue K, Miyazaki T
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Journal Title
PLOS ONE
Volume: 9
Issue: 10
Pages: e109123-e109123
DOI
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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[Journal Article] MafB promotes atherosclerosis by inhibiting foam-cell apoptosis2014
Author(s)
Hamada M, Nakamura M, Tran MT, Moriguchi T, Hong C, Ohsumi T, Dinh TT, Kusakabe M, Hattori M, Katsumata T, Arai S, Nakashima K, Kudo T, Kuroda E, Wu CH, Kao PH, Sakai M, Shimano H, Miyazaki T, Tontonz P, Takahashi S
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Journal Title
Nat Commun
Volume: 5
Issue: 1
Pages: 3147-3147
DOI
Related Report
Peer Reviewed / Open Access
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