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Intestinal phosphate transport refers to the absorption of dietary inorganic phosphate ions in the small intestine via two principal mechanisms: a dominant passive paracellular pathway (~65–80% of absorption), which is poorly characterized at the molecular level, and an active transcellular pathway mediated by sodium-dependent phosphate cotransporters, primarily NaPi-IIb (SLC34A2). This process is regulated by hormones such as parathyroid hormone, FGF-23, and vitamin D, forming part of a complex gut–renal axis critical to overall phosphate homeostasis. Dysregulation of intestinal phosphate absorption contributes to hyperphosphatemia, especially in chronic kidney disease, increasing cardiovascular risk. Novel therapeutics target these pathways either by binding luminal phosphate or inhibiting relevant transporters, making intestinal phosphate absorption a clinically important target, though "gastrointestinal phosphate" itself is not a specific molecule or receptor.
Physical binding of phosphate in the gut lumen (phosphate binders); Inhibition of paracellular absorption by altering tight junction permeability (tenapanor); Inhibition of sodium-dependent cotransport (experimental NaPi-IIb inhibitors)
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