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2020 Fiscal Year Final Research Report

Elucidation of new tissue and molecular bases causing obesity

Research Project

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Project/Area Number 18H02967
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypeSingle-year Grants
Section一般
Review Section Basic Section 57010:Oral biological science-related
Research InstitutionKyushu University

Principal Investigator

Jimi Eijiro  九州大学, 歯学研究院, 教授 (40276598)

Co-Investigator(Kenkyū-buntansha) 松田 美穂  九州大学, 歯学研究院, 准教授 (40291520)
高 靖  九州大学, 歯学研究院, 助教 (40585882)
溝上 顕子  九州大学, 歯学研究院, 准教授 (70722487)
片桐 岳信  埼玉医科大学, 医学部, 教授 (80245802)
Project Period (FY) 2018-04-01 – 2021-03-31
Keywords肥満 / 緩やかな炎症 / NF-κB
Outline of Final Research Achievements

Metabolic diseases caused by obesity significantly reduce quality of life and are accompanied by life-threatening complications. In recent years, it has been reported that phosphorylation of p65 plays an important role in the transcriptional regulation of NF-κB, and in particular, phosphorylation of the serine 534 (S534) residue at the C-terminal has been considered to be extremely important. Therefore, we generated S534A knock-in mice that are not phosphorylated. When S534A mice were maintained on a high-fat diet (HFD), body weight was gained by increasing both the amount of food and water consumed. Furthermore, it showed decreased glucose tolerance and insulin resistance. Histologically, fatty liver was exhibited when S534A mice were bred in HFD. Furthermore, when S534A mice were maintained over 20 weeks, renal and uterine edema was frequently observed regardless of whether they were maintained on a normal diet or HFD.

Free Research Field

生化学

Academic Significance and Societal Importance of the Research Achievements

我々の研究成果は、p65の安定性制御を介した持続的活性化がPara-Inflammationを意味することを示した。さらにp65のリン酸化制御が、生活習慣病の発症機序の解明とともに、予防法や治療法の開発につながることが期待できる。

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Published: 2022-01-27  

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