| Project/Area Number |
26870920
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Metabolomics
Pathological medical chemistry
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| Research Institution | Chubu University (2015)
National Center for Geriatrics and Gerontology (2014) |
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Principal Investigator |
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| Research Collaborator |
SUGIMOTO Masataka 国立長寿医療研究センター, 老化機構研究部, 室長 (50426491)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 細胞老化 / 2型糖尿病 / 生体イメージングシステム / トランスジェニックマウス / 分子病態学 / メタボリックシンドローム / ２型糖尿病 / 白色脂肪組織 / インビボイメージングシステム |
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| Outline of Final Research Achievements |
It is imperative to inhibit increased morbidity of type 2 diabetes in Japan. We then have to elucidate the pathogenic mechanism and establish the new effective therapy of that. Senescent cells accumulate in adipose tissue as animal’s age, and are considered to underlie several aging-associated pathologies such as type 2 diabetes. During cellular senescence, the tumor suppressor p19ARF play definitive roles in inducing and maintaining permanent cell cycle arrest. Accordingly, aging-associated type 2 diabetes may be improved by the clearance of p19ARF-expressing cells from adipose tissue. We herein demonstrated that glucose metabolism was reversibly restored by the partial elimination of p19ARF-expressing cells. The ablation of p19ARF-expressing cells using a toxin receptor-mediated cell-knockout system in adult transgenic mice ameliorated insulin resistance. These results suggest that the aging-associated decline in metabolic activity was recovered by eliminating senescent cells.
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