2016 Fiscal Year Final Research Report
Analysis of GADD34 deficiency effects on obesity-inducetype 2 diabetes and fatty liver development with the aging
Project/Area Number |
26870257
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
General internal medicine(including psychosomatic medicine)
Applied health science
|
Research Institution | Nagoya City University (2015-2016) Nagoya University (2014) |
Principal Investigator |
NISHIO Naomi 名古屋市立大学, 大学院医学研究科, 研究員 (80513457)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Keywords | GADD34 / 老化 / 脂肪肝 / インスリンシグナル伝達系 / 炎症 |
Outline of Final Research Achievements |
In this report, we analyzed the role of GADD34 gene on fatty liver and typeⅡ diabetes using GADD34 -deficient mice. We found that GADD34-deficient mice developed the fatty liver and liver inflammation with aging. Then displayed liver damage, which could proceed to NAFLD/NASH with age, some mice extended for a cancer or typeⅡ diabetes. Furthermore GADD34 deficiency developed obesity by enhancement the adipocyte proliferation and differentiation. TNF-α produced by adipocytes inhibited IGF-1/Insulin signaling, then induced insulin resistance. This report concluded that Mechanism of fatty liver and typeⅡ diabetes in GADD34 KO mice may be mainly comes from the effect of GADD34 on insulin signaling which related to cell proliferation and aging. GADD34 suppress adipocyte differentiation by decreasing IGF-1/Insulin signaling and inhibited the fat accumulation.
|
Free Research Field |
免疫学、基礎老化学
|