The effects to suppress SREBP-1 gene as a lipid synthetic transcription factor on atheroscrelotic model mice.
Project/Area Number |
23590453
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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 |
Experimental pathology
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Research Institution | University of Tsukuba |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
SHIMANO Hitoshi 筑波大学, 医学医療系, 教授 (20251241)
SUZUKI Hiroaki 筑波大学, 医学医療系, 准教授 (40344890)
YATOH Shigeru 筑波大学, 医学医療系, 講師 (50451703)
|
Project Period (FY) |
2011 – 2013
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | 肥満 / メタボリックシンドローム / リポ蛋白代謝 / 動物モデル / 転写因子 |
Research Abstract |
LDL receptor disrupted mice (LDLRKO) were known as a model of atherosclerosis with disturbance of lipoprotein clearance from blood. But when the syntheses of lipid were suppressed in LDLRKO mice, that the atherosclerosis would be improved or not were unknown. We investigated SREBP-1 knockout mice on the background of LDLRKO, as the model of suppressed lipid syntheses. When these models were fed Western diet, they revealed that SREBP-1 deficit could decrease in cholesterol or triglyceride levels, in plasma or VLDLs, and also suppress atherosclerosis formation or secrease in the particle size of VLDLs. These results suggest that suppression of SREBP-1 could be a therapeutic target of atherosclerosis, especially in those who intake excessive high-calorie diets.
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Report
(4 results)
Research Products
(3 results)