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膳食脂肪与多氯联苯相互作用,在低密度脂蛋白受体缺陷的小鼠中诱导脂质代谢变化。

Dietary fat interacts with PCBs to induce changes in lipid metabolism in mice deficient in low-density lipoprotein receptor.

作者信息

Hennig Bernhard, Reiterer Gudrun, Toborek Michal, Matveev Sergey V, Daugherty Alan, Smart Eric, Robertson Larry W

机构信息

Molecular and Cell Nutrition Laboratory, College of Agriculture and Graduate Center for Nutritional Sciences, University of Kentucky, Lexington, Kentucky 40536-0200, USA.

出版信息

Environ Health Perspect. 2005 Jan;113(1):83-7. doi: 10.1289/ehp.7280.

Abstract

There is evidence that dietary fat can modify the cytotoxicity of polychlorinated biphenyls (PCBs) and that coplanar PCBs can induce inflammatory processes critical in the pathology of vascular diseases. To test the hypothesis that the interaction of PCBs with dietary fat is dependent on the type of fat, low-density lipoprotein receptor-deficient (LDL-R(-/-)) mice were fed diets enriched with either olive oil or corn oil for 4 weeks. Half of the animals from each group were injected with PCB-77. Vascular cell adhesion molecule-1 (VCAM-1) expression in aortic arches was nondetectable in the olive-oil-fed mice but was highly expressed in the presence of PCB-77. PCB treatment increased liver neutral lipids and decreased serum fatty acid levels only in mice fed the corn-oil-enriched diet. PCB treatment increased mRNA expression of genes involved in inflammation, apoptosis, and oxidative stress in all mice. Upon PCB treatment, mice in both olive- and corn-oil-diet groups showed induction of genes involved in fatty acid degradation but with up-regulation of different key enzymes. Genes involved in fatty acid synthesis were reduced only upon PCB treatment in corn-oil-fed mice, whereas lipid transport/export genes were altered in olive-oil-fed mice. These data suggest that dietary fat can modify changes in lipid metabolism induced by PCBs in serum and tissues. These findings have implications for understanding the interactions of nutrients with environmental contaminants on the pathology of inflammatory diseases such as atherosclerosis.

摘要

有证据表明,膳食脂肪可改变多氯联苯(PCBs)的细胞毒性,且共平面多氯联苯可引发对血管疾病病理学至关重要的炎症过程。为了验证多氯联苯与膳食脂肪的相互作用取决于脂肪类型这一假说,给低密度脂蛋白受体缺陷(LDL-R(-/-))小鼠喂食富含橄榄油或玉米油的饲料,持续4周。每组动物中有一半注射PCB-77。在喂食橄榄油的小鼠中,主动脉弓中的血管细胞黏附分子-1(VCAM-1)表达无法检测到,但在存在PCB-77的情况下高度表达。PCB处理仅在喂食富含玉米油饲料的小鼠中增加了肝脏中性脂质并降低了血清脂肪酸水平。PCB处理在所有小鼠中均增加了参与炎症、凋亡和氧化应激的基因的mRNA表达。在PCB处理后,橄榄油和玉米油饮食组的小鼠均显示出参与脂肪酸降解的基因的诱导,但不同关键酶的上调情况不同。仅在喂食玉米油的小鼠中,PCB处理后参与脂肪酸合成的基因减少,而在喂食橄榄油的小鼠中,脂质转运/输出基因发生了改变。这些数据表明,膳食脂肪可改变多氯联苯在血清和组织中诱导的脂质代谢变化。这些发现对于理解营养素与环境污染物在动脉粥样硬化等炎症性疾病病理学上的相互作用具有重要意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/546c/1253714/c4f5a17353dc/ehp0113-000083f1.jpg

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