Iida Akio, Matsushita Mutsuyoshi, Ohta Takeshi, Yamada Takahisa
Biological/Pharmacological Laboratories, Central Pharmaceutical Research Institute, Japan Tobacco Inc., 1-1 Murasaki-cho, Takatsuki, Osaka 569-1125, Japan.
Department of Agrobiology, Faculty of Agriculture, Niigata University, 2-8050 Igarashi, Nishiku, Niigata 950-2181, Japan.
J Vet Med Sci. 2020 Mar 24;82(3):379-386. doi: 10.1292/jvms.19-0641. Epub 2020 Jan 29.
Ferric citrate is an oral iron-based phosphate binder, being known to affect iron status and improve iron deficiency anemia (IDA) in chronic kidney disease (CKD) patients. We examined whether oral administration of ferric citrate could change iron status and improve anemia without affecting phosphorus metabolism in iron deficiency anemia rats. In Normal rat study, normal rats were fed a diet containing 0.3 or 3% ferric citrate for 11 days for setting the dose and administration period of ferric citrate. The effects of ferric citrate on iron status- and phosphorus metabolism-related parameters were evaluated using blood and urine samples. Next, an iron deficiency anemia was induced by feeding iron-depleted diet in rats. After 7 days of starting the iron-depleted diet, 0.3% ferric citrate was administered for 7 days by dietary admixture. Iron status- and phosphorus metabolism-related parameters were evaluated with blood and urine samples. In Normal rat study, 3% ferric citrate treatment increased serum iron level and transferrin saturation (TSAT), and decreased serum phosphorus level, intact fibroblast growth factor 23 (iFGF23) level, and urinary phosphorus excretion, but 0.3% ferric citrate treatment showed no effects. On the other hand, in Iron deficiency anemia rat study, 0.3% ferric citrate treatment increased iron status-related parameters and improved anemia, but did not show any apparent changes in phosphorus metabolism-related parameters. In conclusion, ferric citrate could have hematopoietic effects without affecting phosphorus metabolism, and could be a potential option for the treatment of IDA in patients without CKD.
柠檬酸铁是一种口服铁基磷酸盐结合剂,已知其会影响铁状态并改善慢性肾脏病(CKD)患者的缺铁性贫血(IDA)。我们研究了口服柠檬酸铁是否能改变缺铁性贫血大鼠的铁状态并改善贫血,同时不影响其磷代谢。在正常大鼠研究中,正常大鼠喂食含0.3%或3%柠檬酸铁的饮食11天,以确定柠檬酸铁的剂量和给药期。使用血液和尿液样本评估柠檬酸铁对铁状态和磷代谢相关参数的影响。接下来,通过给大鼠喂食缺铁饮食诱导缺铁性贫血。在开始缺铁饮食7天后,通过饮食混合给予0.3%柠檬酸铁7天。用血液和尿液样本评估铁状态和磷代谢相关参数。在正常大鼠研究中,3%柠檬酸铁处理可提高血清铁水平和转铁蛋白饱和度(TSAT),并降低血清磷水平、完整成纤维细胞生长因子23(iFGF23)水平和尿磷排泄,但0.3%柠檬酸铁处理无此效果。另一方面,在缺铁性贫血大鼠研究中,0.3%柠檬酸铁处理可提高与铁状态相关的参数并改善贫血,但在磷代谢相关参数方面未显示任何明显变化。总之,柠檬酸铁可在不影响磷代谢的情况下产生造血作用,可能是治疗非CKD患者IDA的一个潜在选择。