Status
Please wait ...
EndoNet
The information resource about the endocrine network in human.
Search
Search a component
Browse
Browse pathways
Browse hormones
Browse hormones functions
Browse hormone classification
Browse receptors
Network
Load network
Path analysis
Process network
Help
Help
Statistic
About
Details for phenotype: tumor-induced osteomalacia
Top
General information
Triggers
Toolbox
Click to access the toolbox
Top
General information
Triggers
Toolbox
Click to access the toolbox
EndoNet ID: ENP00118
Add to network
Name
tumor-induced osteomalacia
General information
This phenotype is not pathologic
Links to other resources
GO
vitamin D3 receptor activity
Medline Plus
000376
Disease database
9351
Phenotype triggers
VDR
ui-button
in
bone
ui-button
Ectopic overproduction of FGF23 overwhelms its processing and degradation, leading to TIO.
[1]
Administration of recombinant FGF23 in normal and parathyroidectomized animals induced a decrease in serum phosphate levels, phosphaturia accompanied by a reduction in renal mRNA and protein levels for sodium-phosphate cotransport activites in the kidney, a decrease in renal mRNA for 25-hydroxyvitamin D-1{alpha}-hydroxylase, and an increase in 25-hydroxyvitamin D-24-hydroxylase, the cytochrome P-450 enzymes that generate and inactivate 1,25(OH)2D3 hormone, respectively
[1]
Mice implanted with FGF23-expressing Chinese hamster ovary (CHO) cells showed more severe hypophosphatemia, osteomalacia, and decreased 1,25(OH)2D3 levels.
[1]
Reference
