So far, I haven’t seen so much work about epigenetic regulation of vitamin D. There was already a paper in 2005 that showed how treatment with the
methylation inhibitor 5-aza-2′-deoxycytidine together with the deacetylation inhibitor trichostatin A resulted in elevation of both CYP27B1 and CYP24 mRNA expression demonstrating that even in normal human prostate cells expression of Vitamin D hydroxylases may be under epigenetic control
A recent review confirmed somewhere hidden in the text that
… treatment with 1alpha,25(OH)2D3 induced DNA methylation at CpG sites in the promotor and exon regions of the CYP27B1 gene (data not shown).
As no details are given I am plotting here the human CYP27B1 region (chr12:56,442,385-56,447,243) with additional +1500 bp on both sides by means of the EBI server.
which confirms the assumed CpG islands.
The situation is much clearer with an excellent paper on the rodent CYP24A1 that identified two CpG islands
Here is the EBI plot from the human CYP24A1 sequence
Using bisulfite sequencing, there was convincing evidence that both islands were hypermethylated in tumor derived endothelial cells; treatment with 5-aza-2′-deoxycytidine restored CYP24A1 promotor activity.
I do not know, if or when the human vitamin hydroxylases are being methylated but given the large variation of human 25-OH-D3 serum levels (under comparable environmental conditions) there could be an early conditioning of these enzymes.