Elucidation of the mechanisms and pharmacological target for metabolic syndrome by analyzing endoplasmic reticulum stress, which is mediated through physiological factor and cell-to-cell communication
| Project/Area Number |
16K08271
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pharmacology in pharmacy
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| Research Institution | Hiroshima University |
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Principal Investigator |
Hosoi Toru 広島大学, 医歯薬保健学研究科(薬), 准教授 (40379889)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | レプチン / 小胞体ストレス / グリア細胞 / 神経細胞 |
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| Outline of Final Research Achievements |
Obesity is one of the risk factors of the metabolic syndrome, such as diabetes. Therefore, elucidation of the mechanisms of the obesity may be an important subject with respect to preventive medicine. In the present study, we investigated mechanisms of the endoplasmic reticulum (ER) stress-induced obesity and metabolic syndrome, and tried to elucidate the therapeutic target for the disease. In the present study, we found that saturation of neuronal membrane fatty acid may cause leptin resistance. Also, we found glial cell may play an important role in neuronal leptin signal transduction. Furthermore, we found possibility that flurbiprofen may attenuate diabetes, suggesting that reducing ER stress by flurbiprofen may be able to ameliorate metabolic syndrome.
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| Academic Significance and Societal Importance of the Research Achievements |
レプチンは、脂肪細胞から分泌され、体重を減少させるタンパク質である。一方、最近ではレプチン抵抗性が肥満の原因として問題視されている。従って、レプチン抵抗性の原因を明らかにすることは、肥満の治療に重要であると考えられる。そこで本研究では、レプチン抵抗性の形成機構の解明を目指して研究を行なった。その結果、神経細胞膜の脂肪酸の飽和化がレプチン抵抗性形成に関わる可能性が明らかになった。さらに私たちはグリア細胞が神経細胞におけるレプチンシグナルを制御する可能性も見いだした。これらの結果は、新しいレプチン抵抗性の形成機序の一端を示すもので、レプチン抵抗性による肥満発症機構解明に寄与できると考えられる。
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Report
(4 results)
Research Products
(18 results)
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[Journal Article] Endospanin 1 affects oppositely body weight regulation and glucose homeostasis by differentially regulating central leptin signaling.2017
Author(s)
Vauthier V., Roujeau C., Chen P., Sarkis C., Migrenne S., Hosoi T., Ozawa K., Rouille Y., Foretz M., Mallet J., Launay J., Magnan C., Jockers R. and Dam J.
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Journal Title
Molecular Metabolism
Volume: 6
Issue: 1
Pages: 159-172
DOI
Related Report
Peer Reviewed / Int'l Joint Research
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