| Project/Area Number |
15K09255
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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 |
Kidney internal medicine
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| Research Institution | Nagoya University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
丸山 彰一 名古屋大学, 医学系研究科, 教授 (10362253)
小杉 智規 名古屋大学, 医学部附属病院, 講師 (90584681)
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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 |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 塩分感受性高血圧 / フルクトース / ケトヘキソキナーゼ / 高血圧 / 塩分感受性 / フルクトキナーゼ / 慢性腎臓病 |
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| Outline of Final Research Achievements |
The aim of this study is to elucidate the role of fructose metabolism by the primary enzyme of fructose, ketohexokinase (KHK) in hypertension. In this study, by using KHK knockout mice (KHK-KO), we found that the combination of fructose and high salt induced the elevation of blood pressure with decrease of sodium excretion and increase of mRNA expression of NHE3 in kidney in wild type mice (WT), but not in KHK-KO mice, and that fructose stimulation increased NHE activity accompanied by a decrease in intracellular cAMP that is dependent on KHK. These results suggest that fructose metabolism by KHK is involved in the development of salt-sensitive hypertension through increases of renal sodium reabsorption by NHE3.
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