Cell Signaling Vitamin D3 Flashcards
Where do we get most of our vitamin D?
the sun and our diet
Children with vitamin D deficiency tend to have …
cavities
Which step of vitamin D3 synthesis does the sun catalyze?
Pro (7-dehydrocholesterol) to previtamin D3
What is the biologically active form of vitamin D3?
1,25(OH)2D3
What organ provides the majority of the circulating 1,25(OH)2D3?
kidney
Serum levels measure what vitamin D molecule?
25(OH)D3 because it is the main circulatory form
What protein usually binds thing in the blood?
Albumin
What is another name for 1,25(OH)2D3?
calcitriol
What is another name for vitamin D2?
Ergocalciferol
What is another name for vitamin D3?
cholecalciferol
Vitamin D2
Plant/fungi form; most commonly found in dietary supplements and fortified foods. Less absorbable, less potent, shorter acting.
Vitamin D receptor (VDR)
- Transcription factor widely distributed in the body
- Upon binding 1,25-(OH)2D3, VDR forms a heterodimeric complex with other nuclear hormone receptors, particularly the Retinoid-X-Receptor.
Vitamin D3 is modified by what organ before the kidney?
Liver
Vitamin D3 is required for proper ____ and ____ absorption needed to build strong bones and teeth.
calcium; phosphorus
Vitamin D metabolites are transported in the blood bound to?
Vitamin D binding protein and serum albumin
Vitamin D3 induces what in the gut?
Calcium absorption
Calmodulin
Binding protein that helps calcium be absorbed into the body.
Vitamin D Receptor affects:
- Genes regulating Ca transport (TRPV6)
- Genes needed to form bone
- RANKL/ osteoclast formation
- Antimicrobial peptides like defensins/cathelicidin
Name an antimicrobial peptide that is vitamin D3 dependent
defensins and cathelicidin
Rickets
- Vitamin D/calcium/phosphate deficiency
- Most common in countries that do not fortify their foods and have low exposure to sunlight
- Prominence of the costochondrial junction, deformities of the back, bowing of the legs, parietal flattening, delayed eruption of the permeant dentition and enamel defects
Type I rickets
- Manifests by age 2, usually by 6mo
- Low circulating 1,25(OH)2D3
- Defect in 1-hydrolase
Type II Rickets
- Normal at birth, bone disease before age 2
- Normal or high circulating levels of 1,25(OH)2D3
- Due to mutations in VDR receptor
- Alopecia
Osteomalacia
Similar to rickets; Softening of the bones due to inadequate levels of calcium and phosphate which are most commonly due to vitamin D deficiency
Vitamin D resistant rickets
caused by an inactivating mutation in the nuclear vitamin D receptor.
