Hyperlipidemia and Atherosclerotic Lesion Development in Ldlr-Deficient Mice on a Long-Term High-Fat Diet
文献类型：期刊论文
| 作者 | Ma, Yanling1; Wang, Wenyi1; Zhang, Jie1; Lu, Youli2; Wu, Wenyu1; Yan, Hong1; Wang, Yiping1
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| 刊名 | PLOS ONE
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| 出版日期 | 2012-04-25 |
| 卷号 | 7期号:4 |
| ISSN号 | 1932-6203 |
| DOI | 10.1371/journal.pone.0035835 |
| 文献子类 | Article |
| 英文摘要 | Background: Mice deficient in the LDL receptor (Ldlr(-/-) mice) have been widely used as a model to mimic human atherosclerosis. However, the time-course of atherosclerotic lesion development and distribution of lesions at specific time-points are yet to be established. The current study sought to determine the progression and distribution of lesions in Ldlr(-/-) mice. Methodology/Principal Findings: Ldlr-deficient mice fed regular chow or a high-fat (HF) diet for 0.5 to 12 months were analyzed for atherosclerotic lesions with en face and cross-sectional imaging. Mice displayed significant individual differences in lesion development when fed a chow diet, whereas those on a HF diet developed lesions in a time-dependent and site-selective manner. Specifically, mice subjected to the HF diet showed slight atherosclerotic lesions distributed exclusively in the aortic roots or innominate artery before 3 months. Lesions extended to the thoracic aorta at 6 months and abdominal aorta at 9 months. Cross-sectional analysis revealed the presence of advanced lesions in the aortic sinus after 3 months in the group on the HF diet and in the innominate artery at 6 to 9 months. The HF diet additionally resulted in increased total cholesterol, LDL, glucose, and HBA1c levels, along with the complication of obesity. Conclusions/Significance: Ldlr-deficient mice on the HF diet tend to develop site-selective and size-specific atherosclerotic lesions over time. The current study should provide information on diet induction or drug intervention times and facilitate estimation of the appropriate locations of atherosclerotic lesions in Ldlr(-/-) mice. |
| WOS关键词 | PLASMA-CHOLESTEROL LEVELS ; RECEPTOR KNOCKOUT MICE ; REDUCES ATHEROSCLEROSIS ; INNOMINATE-ARTERY ; APOLIPOPROTEIN-E ; ATHEROGENESIS ; AGONIST ; EXPRESSION ; CHOLATE ; INSULIN |
| 资助项目 | Shanghai Committee of Science and Technology, China[11ZR1444800] ; National Basic Research Program of China[2009CB930300] |
| WOS研究方向 | Science & Technology - Other Topics |
| 语种 | 英语 |
| WOS记录号 | WOS:000305345200085 |
| 出版者 | PUBLIC LIBRARY SCIENCE |
| 源URL | [http://119.78.100.183/handle/2S10ELR8/278111]  |
| 专题 | 药理学第一研究室 中科院受体结构与功能重点实验室 新药研究国家重点实验室 |
| 通讯作者 | Ma, Yanling |
| 作者单位 | 1.Chinese Acad Sci, Shanghai Inst Mat Med, State Key Lab Drug Res, Shanghai 200031, Peoples R China; 2.Shanghai Xuhui Cent Hosp, Cent Lab, Shanghai, Peoples R China |
| 推荐引用方式 GB/T 7714 | Ma, Yanling,Wang, Wenyi,Zhang, Jie,et al. Hyperlipidemia and Atherosclerotic Lesion Development in Ldlr-Deficient Mice on a Long-Term High-Fat Diet[J]. PLOS ONE,2012,7(4). |
| APA | Ma, Yanling.,Wang, Wenyi.,Zhang, Jie.,Lu, Youli.,Wu, Wenyu.,...&Wang, Yiping.(2012).Hyperlipidemia and Atherosclerotic Lesion Development in Ldlr-Deficient Mice on a Long-Term High-Fat Diet.PLOS ONE,7(4). |
| MLA | Ma, Yanling,et al."Hyperlipidemia and Atherosclerotic Lesion Development in Ldlr-Deficient Mice on a Long-Term High-Fat Diet".PLOS ONE 7.4(2012). |
入库方式： OAI收割
来源：上海药物研究所
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