Abstract
There has recently been significant interest in the concept of directly targeting intestinal phosphate transport to control hyperphosphatemia in patients with chronic kidney disease. However, we do not have a complete understanding of the cellular mechanisms that govern dietary phosphate absorption. Studies in the 1970s documented both active and passive pathways for intestinal phosphate absorption. However, following the cloning of the intestinal SLC34 cotransporter, NaPi-IIb, much of the research focused on the role of this protein in active transcellular phosphate absorption and the factors involved in its regulation. Generation of a conditional NaPi-IIb knockout mouse has demonstrated that this protein is critical for the maintenance of skeletal integrity during periods of phosphate restriction and that under normal physiological conditions, the passive sodium-independent pathway is likely be the more dominant pathway for intestinal phosphate absorption. The review aims to summarise the most recent developments in our understanding of the role of the intestine in phosphate homeostasis, including the acute and chronic renal adaptations that occur in response to dietary phosphate intake. Evidence regarding the overall contribution of the transcellular and paracellular pathways for phosphate absorption will be discussed, together with the clinical benefit of inhibiting these pathways for the treatment of hyperphosphatemia in chronic kidney disease.
Highlights
The regulation of phosphate homeostasis is achieved via complex interactions between the kidney, intestine and bone, and several endocrine factors [7]
The majority of the research focus with regard to understanding the cellular mechanisms and regulation of phosphate transport has concentrated on the processes that occur in the proximal tubule
This review aims to present evidence that NaPi-IIb is critical for intestinal phosphate absorption during periods of phosphate restriction or during ontogenesis, but that during adulthood under normal physiological conditions, the sodiumindependent pathway would play a more dominant role
Summary
The regulation of phosphate homeostasis is achieved via complex interactions between the kidney, intestine and bone, and several endocrine factors [7]. It is widely accepted that the kidneys play the major role in maintaining extracellular phosphate concentrations within their narrow limits. The majority of the research focus with regard to understanding the cellular mechanisms and regulation of phosphate transport has concentrated on the processes that occur in the proximal tubule. Less is known about the cellular pathways that govern intestinal phosphate absorption. With the desire to develop novel drugs to diminish dietary phosphate
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