Dept. of Neuroscience, Physiology, and Pharmacology, Univ. College London Medical School, UK.
Am J Physiol Renal Physiol. 2010 Aug;299(2):F285-96. doi: 10.1152/ajprenal.00508.2009. Epub 2010 Jun 9.
Transport of phosphate across intestinal and renal epithelia is essential for normal phosphate balance, yet we know less about the mechanisms and regulation of intestinal phosphate absorption than we do about phosphate handling by the kidney. Recent studies have provided strong evidence that the sodium-phosphate cotransporter NaPi-IIb is responsible for sodium-dependent phosphate absorption by the small intestine, and it might be that this protein can link changes in dietary phosphate to altered renal phosphate excretion to maintain phosphate balance. Evidence is also emerging that specific regions of the small intestine adapt differently to acute or chronic changes in dietary phosphate load and that phosphatonins inhibit both renal and intestinal phosphate transport. This review summarizes our current understanding of the mechanisms and control of intestinal phosphate absorption and how it may be related to renal phosphate reabsorption; it also considers the ways in which the gut could be targeted to prevent, or limit, hyperphosphatemia in chronic and end-stage renal failure.
肠上皮和肾上皮细胞的磷酸盐转运对于维持正常的磷酸盐平衡至关重要，但我们对肠道磷酸盐吸收的机制和调节的了解还不如对肾脏磷酸盐处理的了解多。最近的研究提供了强有力的证据表明，钠-磷酸盐协同转运蛋白 NaPi-IIb 负责小肠的钠依赖性磷酸盐吸收，而且这种蛋白质可能可以将饮食磷酸盐的变化与肾脏磷酸盐排泄的改变联系起来，以维持磷酸盐平衡。也有证据表明，小肠的特定区域对饮食磷酸盐负荷的急性或慢性变化有不同的适应方式，而且磷酸酯酶可以抑制肾和肠道的磷酸盐转运。这篇综述总结了我们目前对肠道磷酸盐吸收的机制和控制的理解，以及它与肾脏磷酸盐重吸收的关系；还考虑了肠道可能被靶向以防止或限制慢性和终末期肾衰竭中的高磷酸盐血症的方法。
