Phosphate sensing.
OBJECTIVE
To discuss findings suggesting the presence of a phosphate-sensing mechanism in the various organs and the presence of a novel intestinal effector that alters renal phosphate excretion after the ingestion of a phosphate-containing meal.


RESULTS
Although phosphate homeostasis is controlled by a variety of hormones (such as parathyroid hormone and 1,25-dihydroxyvitamin D), peptides (the phosphatonins - fibroblast growth factor 23, secreted frizzled-related protein-4, matrix extracellular phosphoglycoprotein) and small molecules (dopamine) that regulate the efficiency of phosphate absorption in the intestine and phosphate excretion in the renal tubule, recent data suggest that postcibal changes in renal phosphate excretion following a meal containing phosphate are mediated by signals generated within the intestine that alter the efficiency of phosphate excretion in the kidney. The intestine detects luminal phosphate and signals to the kidney via the release of the mediator that increases renal phosphate excretion.


CONCLUSIONS
Such information would imply the existence of a phosphate-sensing mechanism within the intestine and the presence of intestinal factors that influence renal phosphate handling.
Departments of Medicine, Biochemistry and Molecular Biology, Division of Nephrology and Hypertension, Mayo Clinic and Foundation, Rochester, Minnesota 55905, USA. rkumar@mayo.edu
Rajiv
R
Kumar
D000818:Animals; D006706:Homeostasis; D006801:Humans; D007413:Intestinal Mucosa / Q000378:metabolism; D007668:Kidney / Q000378:metabolism*; D010281:Parathyroid Hormone / Q000502:physiology; D010710:Phosphates / Q000008:administration & dosage / Q000378:metabolism*
D010281:Parathyroid Hormone; D010710:Phosphates