The kidneys very tightly regulate
calcitriol production because too much from any source leads to high blood calcium, also known as hypercalcemia.
Understanding the function of non-kidney
calcitriol production and its connection to inflammatory diseases, ranging from multiple sclerosis to arthritis, is of great interest to a number of biomedical researchers, who would like to know whether and how vitamin D could potentially be used to treat these diseases.
Importantly, deleting these regions affected the response of vitamin D activation to hormones, but not to inflammation - related molecules, indicating that these regions were key to allowing researchers to separately study the two types of
calcitriol production.
Calcitriol production is carried out by the enzyme CYP27B1, but the genomic regions that the team deleted in the experimental mice are far away from the gene encoding this enzyme.
Not exact matches
In these non-kidney sites,
calcitriol seems to serve an altogether different purpose: it appears to play no role in regulation of minerals, and its
production is induced by inflammation rather than by the hormones that control
calcitriol synthesis in the kidneys.
Calcitriol, the hormonally active form of vitamin D, accumulates in the adrenals, and this stimulates the
production of the gene for tyrosine hydroxylase, which is involved in serotonin
production.
It controls the
calcitriol hormone which causes fat
production.