Contents
- 1 PTH enhances urinary phosphate excretion by downregulating
- 2 Fibroblast growth factor-23 (FGF23) is a bone-derived hormone
- 3 Fibroblast growth factor-23 is a
- 4 FGF23 suppress which of the following enzyme reducing its ability to activate vitamin D?
- 5 At the very early stages of chronic kidney disease levels of FGF23
- 6 Which of the following activates FGF23?
- 7 Principal action of FGF23
- 8 FGF23 is associated with Non-nutritional diseases of hypophosphatemia
- 9 FGFR mediating the suppressive effects of FGF23 on renal tubular 1,25(OH)2D3 synthesis
- 10 Klotho
PTH enhances urinary phosphate excretion by downregulating
A. Upregulating K+Cl− Symporter
B. Upregulating NPT2a cotransporter
C. Downregulating NPT2a cotransporter
D. Downregulating K+Cl− Symporter
Fibroblast growth factor-23 (FGF23) is a bone-derived hormone
A. Decrease phosphate reabsorption and vitamin D hormone synthesis in the kidney
B. Increase phosphate reabsorption and vitamin D hormone synthesis in the kidney
C. Increase phosphate reabsorption and decrease vitamin D hormone synthesis in the kidney
D. Decrease phosphate reabsorption and Increase vitamin D hormone synthesis in the kidney
Fibroblast growth factor-23 is a
A. Lipoprotein
B. Glycoprotein
C. Carbohydrate
D. Phospholipid
FGF23 suppress which of the following enzyme reducing its ability to activate vitamin D?
A. Prolyl 3-Hydroxylase
B. Lysyl Hydroxylase
C. Prolyl 4-hydroxylase
D. 1-alpha-hydroxylase
At the very early stages of chronic kidney disease levels of FGF23
A. Increase significantly
B. Decrease significantly
C. Not affected
D. Mild variation seen
Which of the following activates FGF23?
A. α-klotho
B. Calciferol
C. Titin
D. alpha-hydroxylase
Principal action of FGF23
The principal action of FGF23 on mineral metabolism that led to its discovery as a hormone is the
Suppressive effect on phosphate reabsorption from the urine.
FGF23 suppresses the synthesis of the vitamin D hormone, 1α,25-dihydroxyvitamin D3 [1,25(OH)2D3], in the kidney.
Diseases characterized by excessive blood concentrations of intact FGF23 lead to
- Renal phosphate wasting
- Inappropriately low-circulating 1,25(OH)2D3 levels in patients with a normal kidney function
FGF23 is associated with Non-nutritional diseases of hypophosphatemia
FGF23 is associated with Non-nutritional diseases of hypophosphatemia:
- Autosomal dominant hypophosphatemic rickets
- X-linked hypophosphatemia
- Autosomal recessive hypophosphatemic rickets type 1, 2, and 3,
- Tumor-induced osteomalacia
- Hypophosphatemic rickets with hypercalciuria
FGFR mediating the suppressive effects of FGF23 on renal tubular 1,25(OH)2D3 synthesis
FGFR1c is probably the predominant FGFR mediating the suppressive effects of FGF23 on renal tubular 1,25(OH)2D3 synthesis
Klotho
α-klotho is highly expressed in the brain, liver and kidney.
β-klotho is predominantly expressed in the liver.
γ-klotho is expressed in the skin.
| klotho | Highly expressed in | |
| 1 | α-klotho | brain, liver and kidney. |
| 2 | β-klotho | liver |
| 3 | γ-klotho | skin |
