| Project/Area Number |
18K16201
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 54040:Metabolism and endocrinology-related
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| Research Institution | Kobe University |
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Principal Investigator |
Nishimoto Yuki 神戸大学, 医学研究科, 医学研究員 (20814320)
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| Project Period (FY) |
2018-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2018: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | オートファジー / FSP27 / 脂肪細胞 / リポファジー / 脂肪滴 |
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| Outline of Final Research Achievements |
We investigated the effects of autophagy in brown adipose tissue(BAT) and white adipose tissue(WAT) of ｗild type(WT) and FSP27 knockout(KO) mice. Food deprivation induced autophagy in BAT of WT mice, as well as in WAT of FSP27 KO mice, suggesting that enhanced autophagy is the characteristic of adipocytes with small multilocular lipid droplets(LDs). Pharmacological inhibition of autophagy attenuated the fasting induced loss of LD in adipocytes with small multilocular LDs (BAT of WT mice and WAT of FSP27 KO mice). Overexpression of FSP27α but not FSP27β inhibited autophagy induction by serum deprivation in COS cells.
These results showed that FSP27α inhibits autophagy and might contribute to the energy-storage function of white adipose tissue.
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| Academic Significance and Societal Importance of the Research Achievements |
多房性脂肪蓄積形態をとる脂肪細胞ではオートファジーが亢進しており、白色脂肪細胞における巨大脂肪滴の形成に重要なFSP27αは、オートファジーの活性化を制御していることを明らかにした。
オートファジーが仲介する脂肪分解は、肥満の発症に関与するエネルギー消費型脂肪細胞（褐色脂肪細胞）のエネルギー代謝の制御に関連していると考えられ、肥満発症の新たな病態基盤の解明や肥満治療を考える上でも意義深いと考える。
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