title: The role of the gastrointestinal tract in phosphate homeostasis in health and chronic kidney disease.
abstract: OBJECTIVE
  For a number of years, there has been increasing interest in the concept of directly targeting intestinal phosphate transport to control hyperphosphatemia in chronic kidney disease. However, progress has been slow due to the paucity of information on the mechanisms involved in intestinal phosphate absorption. This editorial highlights the most recent developments in our understanding of this process and the role of the intestine in the maintenance of phosphate balance.
  
  
  RESULTS
  Recent studies in NaPi-IIb knockout mice have confirmed that this transport protein plays a significant role in intestinal phosphate absorption and is critical in the proposed feed-forward mechanism between the small intestine and kidney, which helps to maintain normal phosphate balance and steady-state plasma phosphate concentrations. In addition, renal failure-induced hyperphosphatemia is attenuated in NaPi-IIb knockout mice, confirming that NaPi-IIb is a suitable target in the prevention and treatment of hyperphosphatemia.
  
  
  CONCLUSIONS
  Recent findings suggest that consumption of processed foods containing phosphate preservatives may lead to excessive phosphate exposure (if not overload), toxicity, and cardiovascular disease in the general population, as well as in patients with declining renal function. Therefore, establishing more effective ways of targeting the intestine to limit dietary phosphate absorption could have wide-reaching health benefits.
authors.affiliation: London Epithelial Group, Department of Neuroscience, Physiology & Pharmacology, University College London Medical School, London, UK. joanne.marks@ucl.ac.uk
authors.forename: Joanne
authors.initials: J
authors.lastname: Marks
authors.forename: Edward S
authors.initials: ES
authors.lastname: Debnam
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Unwin
mesh_terms: D000818:Animals; D005520:Food Preservatives / Q000009:adverse effects / Q000378:metabolism*; D006706:Homeostasis; D006801:Humans; D054559:Hyperphosphatemia / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology / Q000628:therapy; D007408:Intestinal Absorption; D007413:Intestinal Mucosa / Q000378:metabolism*; D007422:Intestines / Q000503:physiopathology; D051379:Mice; D018345:Mice, Knockout; D010710:Phosphates / Q000009:adverse effects / Q000378:metabolism*; D016226:Phosphorus, Dietary / Q000009:adverse effects / Q000378:metabolism*; D051436:Renal Insufficiency, Chronic / Q000378:metabolism* / Q000503:physiopathology / Q000628:therapy; D050614:Sodium-Phosphate Cotransporter Proteins, Type IIb / Q000235:genetics / Q000378:metabolism
chemical_list: D005520:Food Preservatives; D010710:Phosphates; D016226:Phosphorus, Dietary; C493558:Slc34a2 protein, mouse; D050614:Sodium-Phosphate Cotransporter Proteins, Type IIb