| Project/Area Number |
15K08630
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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 |
Laboratory medicine
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| Research Institution | Hyogo Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
吉原 大作 兵庫医科大学, 医学部, 助教 (00567266)
藤原 範子 兵庫医科大学, 医学部, 教授 (10368532)
崎山 晴彦 兵庫医科大学, 医学部, 講師 (30508958)
鈴木 敬一郎 兵庫医科大学, 医学部, 教授 (70221322)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 糖尿病 |
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| Outline of Final Research Achievements |
The purpose of this study was to investigate the function of nitrated IL-18 in diabetes, and evaluate as a disease marker. It was found that nitration of IL-18 attenuated sugar metabolism such as STAT3 phosphorylation in gluconeogenesis. Furthermore, nitrated IL-18 was found in the diabetes model mice. These results suggested that nitrated IL-18 maybe involved in the development of diabetes mellitus.
Also, NAD+ was identified as a target molecule of NO. It was found that a function of NAD+ decreased by nitration. It was also found that NO reduced the expression of glycosyltransferase, FUT8, by the induction of DNA methylation. Because NAD+ and oligosaccharide structures are molecules taking the important role in sugar metabolism, these modifications maybe involved in the development of diabetes.
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