Phosphate

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Phosphate
2D structure for Phosphate
Chemical Name	phosphate
Chemical Formula	O₄P
CAS Number	14265-44-2
Chemical Information	HMDB01429
Biochemical Taxonomy	Inorganic Ions and Gases
Functional Taxonomy	Not Available
Nutritional Taxonomy	Not Available
Metabolic Pathways	Oxidative Phosphorylation Photosynthesis
Biofluid Location	Blood
Tissue Location	Not Available
Normal Biofluid Concentrations	Blood: 263-474 uM
Normal Tissue Concentrations	Not Available
Diseases / Conditions Related to Nutrition	Hemodialysis patients moderate hypophosphatemia with respiratory illness severe hypophosphatemia
Other (Monogenic Disorders)	25-@hydroxyvitamin D3 deficiency, selective OMIM: 600081 Carbamoyl phosphate synthetase i deficiency, hyperammonemia due to OMIM: 237300 Central core disease of muscle OMIM: 117000 Congenital disorder of glycosylation, type IA OMIM: 212065 Congenital disorder of glycosylation, type IB OMIM: 602579 Congenital disorder of glycosylation, type IC OMIM: 603147 Congenital hemidysplasia with ichthyosiform erythroderma and limb OMIM: 308050 Fabry disease OMIM: 301500 Fanconi-bickel syndrome OMIM: 227810 Friedreich ataxia 1 OMIM: 229300 Galactokinase deficiency OMIM: 230200 Galactose epimerase deficiency OMIM: 230350 Galactosemia OMIM: 230400 Glycine encephalopathy OMIM: 605899 Glycogen storage disease ib OMIM: 232220 Glycogen storage disease ic OMIM: 232240 Glycogen storage disease v OMIM: 232600 Glycogen storage disease vII OMIM: 232800 Hexokinase deficiency hemolytic anemia OMIM: 235700 Homocysteinemia OMIM: 603174 Hurler syndrome OMIM: 607014 Hyperornithinemia-hyperammonemia-homocitrullinuria syndrome OMIM: 238970 Hyperoxaluria, primary, type I OMIM: 259900 Hypoparathyroidism, familial isolated OMIM: 146200 Hypophosphatasia, infantile OMIM: 241500 Hypophosphatemic rickets with hypercalciuria, hereditary OMIM: 241530 Hypophosphatemic rickets, autosomal dominant OMIM: 193100 Hypophosphatemic rickets, x-linked dominant OMIM: 307800 Infantile sialic acid storage disorder OMIM: 269920 Inflammatory bowel disease 1 OMIM: 266600 Lactic acidosis, congenital infantile OMIM: 245400 Lowe oculocerebrorenal syndrome OMIM: 309000 Malignant hyperthermia, susceptibility to, 1 OMIM: 145600 Mannosidosis, alpha b, lysosomal OMIM: 248500 Mccune-albright syndrome OMIM: 174800 Menkes disease OMIM: 309400 Mucolipidosis II OMIM: 252500 N-acetylglutamate synthase deficiency OMIM: 237310 Ornithine transcarbamylase deficiency, hyperammonemia due to OMIM: 311250 Pulmonary hypertension, familial persistent, of the newborn OMIM: 265380 Pyridoxamine 5-prime-phosphate oxidase deficiency OMIM: 610090 Rhizomelic chondrodysplasia punctata, type 1 OMIM: 215100 Rhizomelic chondrodysplasia punctata, type 3 OMIM: 600121 Ribose 5-phosphate isomerase deficiency OMIM: 608611 Vitamin d-dependent rickets, type I OMIM: 264700 Vitamin d-dependent rickets, type II OMIM: 277440 Zellweger syndrome OMIM: 214100
Abnormal Biofluid Concentrations	Blood (Hemodialysis patients): 653.0+/- 126.0 umol/L Blood (moderate hypophosphatemia with respiratory illness): 105 - 263 uM Blood (severe hypophosphatemia): < 105 uM
Abnormal Tissue Concentrations	Not Available
Physiological Processes	Not Available

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Introduction

guidelines
Phosphate (Pi) is an essential component of life. In classical endocrine regulation, low serum phosphate induces the renal production of the seco-steroid hormone 1,25-dihydroxyvitamin D3 (1,25(OH)2D3).This active metabolite of vitamin D acts to restore circulating mineral levels by increasing absorption in the intestine, reabsorption in the kidney, and mobilization of calcium and phosphate from bone. Thus, chronic renal failure is associated with hyperparathyroidism, which in turn contributes to osteomalacia. Another complication of chronic renal failure is hyperphosphatemia. Fibroblast growth factor 23 (FGF-23) has recently been recognized as a key mediator of phosphate homeostasis, its most notable effect being promotion of phosphate excretion. FGF-23 was discovered to be involved in diseases such as autosomal dominant hypophosphatemic rickets, X-linked hypophosphatemia, and tumor-induced osteomalacia in which phosphate wasting was coupled to inappropriately low levels of 1,25(OH)2D3. FGF-23 is regulated by dietary phosphate in humans: phosphate restriction decreased FGF-23, and phosphate loading increased FGF-23. Phosphate must be actively transported into cells against its electrochemical gradient. In vertebrates, two unrelated families of Na+-dependent Pi transporters carry out this task. Remarkably, the two families transport different Pi species: whereas type II Na+/Pi cotransporters (SCL34) prefer divalent HPO4(2), type III Na+/Pi cotransporters (SLC20) transport monovalent H2PO4. The SCL34 family comprises both electrogenic and electroneutral members that are expressed in various epithelia and other polarized cells. Through regulated activity in apical membranes of the gut and kidney, they maintain body Pi homeostasis, and in salivary and mammary glands, liver, and testes they play a role in modulating the Pi content of luminal fluids. Hyperphosphatemia is a prevalent condition in the dialysis population and is associated with increased risk of mortality. Hypophosphatemia (hungry bone syndrome) has been associated to postoperative electrolyte aberrations and after parathyroidectomy. (PMID: 17581921, 11169009, 11039261, 9159312, 17625581)