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首页> 外文期刊>The Journal of Nutritional Biochemistry >A mechanism by which dietary trans fats cause atherosclerosis.
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A mechanism by which dietary trans fats cause atherosclerosis.

机译：饮食中的反式脂肪引起动脉粥样硬化的机制。

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Dietary trans fats (TFs) have been causally linked to atherosclerosis, but the mechanism by which they cause the disease remains elusive. Suppressed transforming growth factor (TGF)- beta responsiveness in aortic endothelium has been shown to play an important role in the pathogenesis of atherosclerosis in animals with hypercholesterolemia. We investigated the effects of a high TF diet on TGF- beta responsiveness in aortic endothelium and integration of cholesterol in tissues. Here, we show that normal mice fed a high TF diet for 24 weeks exhibit atherosclerotic lesions and suppressed TGF- beta responsiveness in aortic endothelium. The suppressed TGF- beta responsiveness is evidenced by markedly reduced expression of TGF- beta type I and II receptors and profoundly decreased levels of phosphorylated Smad2, an important TGF- beta response indicator, in aortic endothelium. These mice exhibit greatly increased integration of cholesterol into tissue plasma membranes. These results suggest that dietary TFs cause atherosclerosis, at least in part, by suppressing TGF- beta responsiveness. This effect is presumably mediated by the increased deposition of cholesterol into cellular plasma membranes in vascular tissue, as in hypercholesterolemia. All rights reserved, Elsevier.
机译：饮食中的反式脂肪（TFs）与动脉粥样硬化有因果关系，但其引起疾病的机制仍然难以捉摸。研究表明，高胆固醇血症动物在动脉粥样硬化的发病机理中起着抑制作用，而在主动脉内皮中抑制了转化生长因子（TGF）-β的应答。我们调查了高TF饮食对主动脉内皮中TGF-β反应性和组织中胆固醇整合的影响。在这里，我们显示正常老鼠高TF饮食喂养24周表现出动脉粥样硬化病变并抑制了主动脉内皮的TGF-β反应。通过主动脉内皮中TGF-βI和II型受体的表达显着降低以及磷酸化Smad2（一种重要的TGF-β反应指示剂）的水平显着降低，可以证明TGF-β反应性受到抑制。这些小鼠表现出大大增加的胆固醇整合入组织质膜的能力。这些结果表明，饮食中的TF至少部分地通过抑制TGF-β反应来引起动脉粥样硬化。据推测，这种作用是由胆固醇向血管组织中细胞质膜的沉积增加所介导的，如高胆固醇血症。保留所有权利，Elsevier。

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