• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Genes and Nutrition >Suppressed hepcidin expression correlates with hypotransferrinemia in copper-deficient rat pups but not dams
【24h】

Suppressed hepcidin expression correlates with hypotransferrinemia in copper-deficient rat pups but not dams

机译：缺铁大鼠幼崽中抑制的铁调素表达与低铁蛋白血症相关，但与大坝无关

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Copper deficiency leads to anemia but the mechanism is unknown. Copper deficiency also leads to hypoferremia, which may limit erythropoiesis. The hypoferremia may be due to limited function of multicopper oxidases (MCO) hephaestin in enterocytes or GPI-ceruloplasmin in macrophages of liver and spleen whose function as a ferroxidase is thought essential for iron transfer out of cells. Iron release may also be limited by ferroportin (Fpn), the iron efflux transporter. Fpn may be lower following copper deficiency because of impaired ferroxidase activity of MCO. Fpn is also dependent on the liver hormone hepcidin as Fpn is degraded when hepcidin binds to Fpn. Anemia and hypoferremia both down regulate hepcidin by separate mechanisms. Current studies confirmed and extended earlier studies with copper-deficient (CuD) rats that suggested low hepicidin resulted in augmented Fpn. However, current studies in CuD dams failed to confirm a correlation that hepcidin expression was associated with low transferrin receptor 2 (TfR2) levels and also challenged the dogma that holotransferrin can explain the correlation with hepcidin. CuD dams exhibited hypoferremia, low liver TfR2, anemia in some rats, yet no depression in Hamp expression, the hepcidin gene. Normal levels of GDF-15, the putative erythroid cytokine that suppresses hepcidin, were detected in plasma of CuD and iron-deficient (FeD) dams. Importantly, FeD dams did display greatly lower Hamp expression. Normal hepcidin in these CuD dams is puzzling since these rats may need extra iron to meet needs of lactation and the impaired iron transfer noted previously.
机译：铜缺乏会导致贫血，但机制尚不清楚。铜缺乏还会导致低铁血症，这可能会限制红细胞生成。低铁血症可能是由于肠细胞中多铜氧化酶（MCO）肝素的功能有限，或肝和脾巨噬细胞中的GPI-铜蓝蛋白的功能有限所致，这些功能被认为对铁转运出细胞至关重要。铁释放也可能受到铁外排转运蛋白铁转运蛋白（Fpn）的限制。缺铜后Fpn可能会降低，因为MCO的亚铁氧化酶活性受损。 Fpn还依赖于肝激素hepcidin，因为当hepcidin与Fpn结合时Fpn会降解。贫血和低铁血症都通过单独的机制下调Hepcidin。当前的研究证实并扩展了对缺铜（CuD）大鼠的早期研究，这些研究表明低的Hepicidin导致Fpn增强。然而，目前在CuD大坝中的研究未能证实铁调素表达与低转铁蛋白受体2（TfR2）水平相关的相关性，也挑战了全铁传递蛋白可以解释与铁调素相关性的教条。 CuD大坝在某些大鼠中表现出低铁血症，低肝脏TfR2，贫血，但hepcidin基因Hamp表达却没有降低。在CuD和铁缺乏（FeD）坝的血浆中检测到正常水平的GDF-15（一种抑制hepcidin的类红细胞因子）。重要的是，FeD大坝确实显示出大大降低的Hamp表达。这些CuD大坝中的正常铁调素令人困惑，因为这些大鼠可能需要额外的铁来满足泌乳和铁转移受损的需求。

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