Said H M, Vaziri N D, Kariger R K, Hollander D
Acta Vitaminol Enzymol. 1984;6(4):339-46.
Folate deficiency and megaloblastic anemia occur in chronic renal failure. However, the possible role of intestinal malabsorption as a cause of the reported deficiency has not been investigated. Therefore, we examined the intestinal absorption of 5-methyltetrahydrofolate in rats made uremic by subtotal nephrectomy using in vivo perfusion technique and in vitro everted sac technique. The results were compared with those obtained in a group of sham-operated rats with normal renal function. The amount of 5-methyltetrahydrofolate absorbed in vivo was significantly lower in the uremic animals as compared to the control group. In contrast, no significant difference was found in the absorption of 5-methyltetrahydrofolate in vitro in the two groups. To mimic the uremic environment, the in vitro studies were repeated using jejunal sacs from normal animals filled with either buffer solution, or sera from uremic patients before and after dialysis. Their results showed a marked suppression of 5-methyltetrahydrofolate absorption with predialysis sera and a significant improvement with post dialysis sera. We conclude that intestinal absorption of 5-methyltetrahydrofolate is impaired in uremia. The results of the in vitro experiments suggest that the observed transport defect is due to some influence of uremic environment rather than to an acquired intrinsic defect of enterocytes in uremia.
叶酸缺乏和巨幼细胞贫血发生于慢性肾衰竭。然而，肠道吸收不良作为所报道的缺乏症病因的可能作用尚未得到研究。因此，我们采用体内灌注技术和体外翻转肠囊技术，检测了经次全肾切除造成尿毒症的大鼠对5-甲基四氢叶酸的肠道吸收情况。将结果与一组肾功能正常的假手术大鼠所得结果进行比较。与对照组相比，尿毒症动物体内吸收的5-甲基四氢叶酸量显著降低。相反，两组在体外对5-甲基四氢叶酸的吸收未发现显著差异。为模拟尿毒症环境，使用来自正常动物的空肠囊，分别填充缓冲溶液或尿毒症患者透析前后的血清，重复进行体外研究。结果显示，透析前血清显著抑制5-甲基四氢叶酸的吸收，而透析后血清则显著改善其吸收。我们得出结论，尿毒症时5-甲基四氢叶酸的肠道吸收受损。体外实验结果表明，观察到的转运缺陷是由于尿毒症环境的某些影响，而非尿毒症时肠细胞获得性内在缺陷所致。
