cholecalciferol and Potassium-Deficiency

Homeostasis of inorganic phosphate (P(i)) is primarily an affair of the kidneys. Reabsorption of the bulk of filtered P(i) occurs along the renal proximal tubule and is initiated by apically localized Na(+)-dependent P(i) cotransporters. Tubular P(i) reabsorption and therefore renal excretion of P(i) is controlled by a number of hormones, including phosphatonins, and metabolic factors. In most cases, regulation of P(i) reabsorption is achieved by changing the apical abundance of Na(+)/Pi cotransporters. The regulatory mechanisms involve various signaling pathways and a number of proteins that interact with Na(+)/P(i) cotransporters.

Topics: Acidosis; Animals; Cholecalciferol; Circadian Rhythm; Diet; Fibroblast Growth Factor-23; Fibroblast Growth Factors; Gene Expression Regulation; Glucuronidase; Gonadal Steroid Hormones; Homeostasis; Humans; Ion Transport; Kidney Tubules, Proximal; Klotho Proteins; Parathyroid Hormone; Phosphates; Phosphoproteins; Potassium Deficiency; Signal Transduction; Sodium-Hydrogen Exchangers; Sodium-Phosphate Cotransporter Proteins; Sodium-Phosphate Cotransporter Proteins, Type IIa; Sodium-Phosphate Cotransporter Proteins, Type IIc