Hypothetically, can the body use the 25(OH)vitamine D derived from skin and sunlight (initially D3, then processed in liver) and that is further metabolized by CYP27B1 to active-D-vit - if you have no PTH?
From Pubmed PMID: 17656568 Parathyroid hormone regulates histone deacetylases in osteoblasts Emi Shimizu, Nagarajan Selvamurugan, Jennifer J Westendorf, Nicola C Partridge:
Vitamin D undergoes two enzymatic steps to form the active compound 1,25-dihydroxyvitamin D3 (1,25(OH)2D3).2 CYP27B1 is a cytochrome P450 enzyme that performs the second step in this process, metabolizing 25-hydroxyvitamin D3 to 1,25(OH)2D3 (1, 2), and thus controls the biological activity of vitamin D.
CYP27B1 is tightly regulated. A primary signal in mediating induction of 1,25(OH)2D3 in the kidney is elevated parathyroid hormone (PTH). This was demonstrated in early animal studies in which thyroparathyroidectomy resulted in reduced production of 1,25(OH)2D3, whereas administration of parathyroid extract restored 1,25(OH)2D3 production almost to control levels (5).
1,25(OH)2D3 is known to regulate its own production by inhibiting CYP27B1. In addition to 1,25(OH)2D3, the phosphaturic factor fibroblast growth factor 23 (FGF23), which acts as an endocrine factor, also suppresses expression of renal CYP27B1 (1, 2) (Fig. 1). But, what are the molecular mechanisms connecting these hormones to CYP27B1 and each other? Some initial hints have emerged. Early studies showed that 1,25(OH)2D3 treatment could suppress Cyp27b1 expression in both thyroparathyroidectomy and sham-operated rats, suggesting that activation by PTH and suppression by 1,25(OH)2D3 are two distinct events (6). It was suggested that 1,25(OH)2D3-mediated suppression may not be based on direct binding of the vitamin D receptor to a consensus vitamin D response element in the Cyp27b1 gene but rather may be indirect (7).
The answer is probably less if the reviews of surgical hypoparathyroidism are anything to go by. In this review they only mention treatment with any one of the available Vit D analogues....see https://iv.iiarjournals.org/content/30/3/171.long
"In patients with PHypo, vitamin D2 or D3, (ergocalciferol or cholecalciferol, respectively) or vitamin D metabolites, (calcitriol or 1,25-(OH)2 vitamin D or 1 alpha-OH vitamin D), are usually required. Calcitriol is the active metabolite of vitamin D with rapid action and is frequently used for primary therapy as it maintains serum calcium, in part, by improving the efficiency of intestinal calcium absorption (50). Calcitriol is administered over a wide dosing range (0.25-2.0 μg/day) (51) and can rise serum calcium levels significantly within 3 days (52, 53). The analog alfacalcidol (1-alpha-hydroxyvitamin D3), which is quickly converted to 1,25(OH)2D3 in vivo, can be useful in clinical practice (54). Vitamin D therapy can be related to hyperphosphatemia, since active vitamin metabolites and analogs also increase intestinal phosphate absorption (48). In such cases, the hyperphosphatemia may be reduced by lessening dietary intake of phosphate (e.g., in meats, eggs, dairy products and cola b"
The answer is probably less .... should read The answer is probably yes
Apologies for the typo!
Thank you Thomas! I believe we came to the same conclusion when we discussed the matter at a conference, there doesn't seem to be enough research ATM to fully answer the question.
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