Analysis of mechanism of insulin-like activity by isothiocyanate compounds
| Project/Area Number |
25450161
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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 |
Food science
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| Research Institution | Iwate University |
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Principal Investigator |
ITO YOSHIAKI 岩手大学, 農学部, 准教授 (50312517)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 糖尿病 / 食品機能 / イソチオシアネート / インスリン / 糖新生 / シグナル応答 |
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| Outline of Final Research Achievements |
To elucidate mechanism of the anti-diabetic effect of isothiocyanate compounds containing cruciferous vegetables, we examined which signaling pathways were induced by phenethyl isothiocyanate (PEITC) in rat H4IIE cells. PEITC induced the phosphorylation of Akt, ERK, and p38.When H4IIE cells were incubated in the presence of PEITC, the expression of G6Pase mRNA was suppressed. Suppressive effect of PEITC on G6Pase expression was abolished by inhibition of Akt or ERK. On the contrary, effect of PEITC on expression of G6Pase was enhanced by inhibition of p38. The changes in expression of G6Pase mRNA treated with inhibitors were consistent with activities of glucose release into medium from cells.These data demonstrate that PEITC has suppressive effect of gluconeogenesis through Akt and ERK pathway in H4IIE cells. Conversely, it is likely that activation of p38 by PEITC causes the opposite effect on regulation of gluconeogenesis by PEITC.
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Report
(4 results)
Research Products
(11 results)
