Suppressive mechanism of pancreatic beta cell failure in obese/type 2 diabetes model mice by mulberry leaf intake
Project/Area Number |
26460121
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Natural medicines
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Research Institution | Kyoto Institute of Technology |
Principal Investigator |
Kamei Kaeko 京都工芸繊維大学, 分子化学系, 教授 (00214544)
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Co-Investigator(Kenkyū-buntansha) |
横出 正之 京都大学, 医学研究科, 教授 (20252447)
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Project Period (FY) |
2014-04-01 – 2017-03-31
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Project Status |
Completed (Fiscal Year 2016)
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Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | 糖尿病 / 耐糖能異常 / 膵β細胞 / 桑葉 / インスリン抵抗性 / アポトーシス / インスリン産生細胞 / 耐糖能 |
Outline of Final Research Achievements |
In this study, we assumed the improving mechanism of impaired glucose tolerance by mulberry leaf intake from the viewpoint of the suppressive effects on pancreatic beta cell failure. We analyzed the effect of mulberry leaves intake on the proliferation of pancreatic beta cells at the compensation stage, in which pancreatic beta cell volume and insulin secretion temporarily increase, and the effect on the pancreatic beta cell death at the incompensation stage, using obese/type 2 diabetes model mice (db/db mice). We also studied the effect of mulberry leaf extract on cultured beta cells. In db/db mice, the oral administration of mulberry leaf reduced ER stress and oxidative stress in pancreatic beta cells and suppressed cell death at the incompensation stage. We found cell proliferation promoting activity on cultured beta cells in mulberry leaves extract. Thus, we could clarify a part of glucose tolerance improvement mechanism by mulberry leaf intake.
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Report
(4 results)
Research Products
(14 results)
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[Journal Article] AMAP1 as a negative-feedback regulator of nuclear factor-κB under inflammatory conditions.2014
Author(s)
Tien, D.N., Kishihata, M., Yoshikawa, A., Hashimoto, A., Sabe, H., Nishi, E., Kamei, K., Arai, H., Kita, T., Kimura, T., Yokode, M. and Ashida, N.
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Journal Title
Sci Rep.
Volume: 4
Issue: 1
Pages: 5094-5094
DOI
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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[Presentation] Roles of IKKβ in fibrosis2014
Author(s)
Dat Nguyen-tien, Masako Kishihata, Megumi Nishio, Kaeko Kamei, Kenji Kabashima, Yoshiki Miyachi, Takeshi Kimura, Masayuki Yokode, Noboru Ashida
Organizer
第37回日本分子生物学会
Place of Presentation
パシフィコ横浜
Year and Date
2014-11-25 – 2014-11-27
Related Report
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