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Nitro-oleic acid and epoxyoleic acid are not altered in obesity and type 2 diabetes: Reply

机译:肥胖和2型糖尿病患者的硝酸-油酸和环氧油酸没有改变:回复

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We appreciate the interest in our recent study of the in vivo signalling actions of electrophilic fatty acid nitroalkenes, including the commentary from Tsikas et al. This study is based on a high-fat diet (HFD)-induced obesity murine model that displays the canonical features of metabolic syndrome, including glucose tolerance, vascular dysfunction, increased inflammation, adipokine dysfunction, and most notably development of pulmonary hypertension. We tested the pharmacological actions of synthetic 10-nitro-octadec-9.-enoic acid (OA-NO_2) and reported potent protective actions of OA-NO2 in this murine model of HFD-induced obesity and pulmonary hypertension. First and foremost, we stress that under no circumstance did we state or imply the existence of any link between obesity and decreased OA-NO2 biosynthesis. This is an incorrect and misleading interpretation of the data presented in our manuscript.
机译:我们赞赏对亲电子脂肪酸硝基烯烃的体内信号传导作用的最新研究的兴趣,包括Tsikas等人的评论。这项研究基于高脂饮食(HFD)诱导的肥胖小鼠模型,该模型显示了代谢综合征的典型特征,包括葡萄糖耐量,血管功能障碍,炎症增加,脂肪因子功能障碍,以及最明显的肺动脉高压发展。我们测试了合成的10-硝基-十八烷基-9.-烯酸(OA-NO_2)的药理作用,并报道了在这种HFD诱导的肥胖和肺动脉高压鼠模型中OA-NO2的有效保护作用。首先,我们强调,在任何情况下,我们都没有声明或暗示肥胖与OA-NO2生物合成减少之间存在任何联系。这是对我们手稿中提供的数据的错误和误导性解释。

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