Buys S S, Martin C B, Eldridge M, Kushner J P, Kaplan J
Department of Medicine, University of Utah School of Medicine, Salt Lake City, 84132.
Blood. 1991 Dec 15;78(12):3288-90.
We used a unique animal model, the hypotransferrinemic (Htx) mouse, to examine the role of transferrin (Tf) in gastrointestinal iron uptake. Despite the absence of Tf, Htx animals hyperabsorb iron. Transfusion of red blood cells sufficient to normalize the hematocrit and reticulocyte count resulted in a return of iron absorption to normal values. These studies indicate that Tf does not play an obligate role in iron absorption, either as a carrier or as a humoral signal regulating absorption. Transfer of plasma or whole blood from Htx mice or from other animal models of iron hyperabsorption to normal mice did not cause an increase in iron absorption in recipient animals. Using the plasma or blood transfer approach, we have been unable to detect a humoral regulator of gastrointestinal iron absorption.
我们使用了一种独特的动物模型——低转铁蛋白血症（Htx）小鼠，来研究转铁蛋白（Tf）在胃肠道铁吸收中的作用。尽管缺乏Tf，但Htx动物会过度吸收铁。输注足以使血细胞比容和网织红细胞计数恢复正常的红细胞会导致铁吸收恢复到正常值。这些研究表明，Tf在铁吸收中既不作为载体，也不作为调节吸收的体液信号发挥必要作用。将Htx小鼠或其他铁吸收过多动物模型的血浆或全血输注到正常小鼠体内，并未导致受体动物铁吸收增加。使用血浆或血液输注方法，我们未能检测到胃肠道铁吸收的体液调节因子。
