| Project/Area Number |
26460636
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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 |
Applied pharmacology
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| Research Institution | Kyoto Pharmaceutical University |
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Principal Investigator |
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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: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 糖尿病治療薬 / 膵β細胞保護薬 / 糖尿病予防 / 亜鉛錯体 / インスリン抵抗性改善 / Aｋｔリン酸化作用 / PTEN阻害作用 / GPCR作動作用 / Aktリン酸化作用 / インスリン様作用 / 糖尿病治療 / ホスファターゼ阻害 |
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| Outline of Final Research Achievements |
Diabetes mellitus is a disease mainly with hyperglycemia, and its patients are increasing year by year. Many types of anti-diabetic medicines are clinically used, however, severe side effects such as hypoglycemia have been reported, and especially there is no therapeutic medicines protecting the pancreatic beta cell in the present. Zinc (Zn) ion is well known to have the insulin-mimetic activity, and thus we primarily intended to elucidate the action mechanism of insulin-mimetic Zn-complexes in terms of relatively higher safety and effect of Zn-complexes. Zn-complexes were found to act independently from endogenous insulin as like supporting and enhancing insulin function, that is, Zn-complexes increased the cellular insulin-signal because they inhibited both the PTP1B and PTEN, and thus enhanced Akt phosphorylation in the insulin-signal transduction pathway after uptake into adipocytes.
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