首页> 外文会议>International Study Group for Tryptophan Research >Interpretation of kynurenine pathway metabolism in osteoporosis
【24h】

Interpretation of kynurenine pathway metabolism in osteoporosis

机译:解释骨质疏松症的Kynurenine途径新陈代谢

获取原文

摘要

Recent evidence that oxidative stress may contribute to the development or progress of osteoporosis may indicate an underlying, or accompanying state of inflammation.In general, inflammatory conditions are associated with the activation of immune-competent cells in which activation of the kynurenine pathway occurs in parallel with the generation and release of cytokines and oxidative stress. We have therefore measured the levels of kynurenine pathway metabolites as well as peroxidation products and inflammatory markers such as neopterin, in patients with osteoporosis before and after two years of drug treatment. At diagnosis, patients showed much higher levels of anthranilic acid than control subjects, but less 3-hydroxy-anthranilic acid. There were also high levels of lipid peroxidation products. All these parameters normalised over two years of treatment, together with a significant improvement in bone density assessed by dual energy X-ray absorptiometry (DEXA) scans. Here, we hypothesise that there may be a causal link between these factors.
机译:最近的证据表明,氧化应激可能有助于开发或骨质疏松症的进展可能表明炎症的潜在或伴随状态。一般来说,炎症病症与免疫富集细胞的激活有关,在这种情况下平行激活犬留蛋白途径的激活随着细胞因子和氧化应激的产生和释放。因此,我们测量尿氨酸途径代谢物的水平,以及过氧化产物和炎症标志物如蝶呤,骨质疏松症患者前两年的药物治疗后。在诊断中,患者显示出比对照对象更高水平的蒽酸,但较少3-羟基 - 苯二甲酸。还有高水平的脂质过氧化产物。所有这些参数在两年内归一化的治疗,以及通过双能X射线吸收测定(DEXA)扫描评估的骨密度的显着改善。在这里,我们假设这些因素之间可能存在因果关系。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号