高脂肪加果糖的饮食会使大鼠的血管前列腺素发生改变

H. A. Peredo, H. Lee, A. S. Donoso, V. Andrade, N. Sánchez Eluchans, A. M. Puyó
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引用次数: 13

摘要

在大鼠中,高脂肪(HF)加果糖(F)的饮食会产生类似于人类代谢综合征的心血管和代谢变化。Prostanoids (PR)是环加氧酶衍生的花生四烯酸代谢物,具有血管活性并介导炎症。本研究旨在分析HF+F饮食对雄性Sprague-Dawley大鼠血压(BP)、代谢参数和肠系膜血管床PR生成的影响。四组研究时间为9周(每组n = 6):对照组(C)、标准饮食组(SD)和自来水饮用组;F+SD和10% w/v F溶液饮用;HF 50% (w/w)牛脂肪添加到SD和自来水中;和HFF,两种治疗方法。高效液相色谱法测定PR。所有实验组的血压都升高了。F和HF组甘油三酯血症、胰岛素血症和HOMA-IR升高。HF+F动物出现血糖、胰岛素、HOMA-IR和甘油三酯血症升高。F降低肠系膜血管床血管舒张剂前列腺素PGI2和PGE2。体重没有明显改变。在HFF中,PGE2、PGF2alpha和TXB2的产生升高。HF和HFF患者血压升高的部分原因可能是血管PR生成向血管收缩剂的不平衡。另一方面,这种饮食改变可能会引起炎症,这可以解释PGE2的升高。在F组,高血压可能与血管扩张剂pr降低有关。在大鼠体内同时施用HF和F产生的有害影响比单独施用时观察到的更大。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
A high-fat plus fructose diet produces a vascular prostanoid alterations in the rat

  1. In the rat, a high-fat (HF) plus fructose (F) diet produces cardiovascular and metabolic alterations that resemble human metabolic syndrome. Prostanoids (PR), cyclo-oxygenase-derived arachidonic acid metabolites, have vasoactive properties and mediate inflammation.
  2. The aim of this study was to analyse the effect of a HF+F diet on blood pressure (BP), metabolic parameters and mesenteric vascular bed PR production in male Sprague–Dawley rats.
  3. Four groups were studied over 9 weeks (n = 6 each): control (C), standard diet (SD) and tap water to drink; F+SD and 10% w/v F solution to drink; HF 50% (w/w) bovine fat added to SD and tap water; and HFF, both treatments. PR were determined by HPLC.
  4. Blood pressure was elevated in all experimental groups. Triglyceridaemia, insulinaemia and HOMA-IR were increased in the F and HF groups. HF+F animals showed elevated glycaemia, insulinaemia, HOMA-IR and triglyceridaemia. F decreased the vasodilator prostanoids PGI2 and PGE2 in the mesenteric vascular bed. Body weight was not significantly altered. In HFF, production of PGE2, PGF2alpha and TXB2 was elevated.
  5. The increased BP in HF and HFF could be partly attributed to the imbalance in vascular PR production towards vasoconstrictors. On the other hand, this dietary modification could induce inflammation, which would explain the elevation of PGE2. In the F group, hypertension could be related to decreased vasodilator PRs.
  6. The simultaneous administration of HF and F in the rat produces deleterious effects greater than observed when treatments are applied separately.
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