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Diabetes changes liver genes so as to destroy (catabolize) Vitamin D – May 2016

Expression pattern of CYP24 in liver during ageing in long-term diabetes

Acta Histochemica. Available online 9 May 2016, doi:10.1016/j.acthis.2016.05.001
Ana Vuicaa, Katarina Vukojevića, b, Lejla Ferhatović Hamzićc, Milka Jerića, Livia Puljakc, Ivica Grkovića, Natalija Filipovića, b, ,


This is why diabetes seems to consume vitamin D, it distroys it.
It seems that CYP24A1 is associated with the Kidney, but the Liver may have it as well
I am confused about differences between CYP24 and CYP24A1
Genetics category listing contains the following

318 articles in the Genetics category

see also

Vitamin D blood test misses a lot
Blood Test Misses a lot (VDW 3439)

  • Vitamin D from coming from tissues (vs blood) was speculated to be 50% in 2014, and by 2017 was speculated to be 90%
  • Note: Good blood test results (> 40 ng) does not mean that a good amount of Vitamin D actually gets to cells
  • A Vitamin D test in cells rather than blood was feasible (2017 personal communication)
  •    Commercially available 2019
    • However, test results would vary in each tissue due to multiple genes
  • Good clues that Vitamin D is being restricted from getting to the cells
    1) A vitamin D-related health problem runs in the family
    2) Slightly increasing Vitamin D shows benefits (even if conventional Vitamin D test shows an increase)
    3) Vitamin D Receptor test (<$30) scores are difficult to understand in 2016
    • easier to understand the VDR 23andMe test results analyzed by FoundMyFitness in 2018

    4) Back Pain

Chart from the web shows that CYP24A1 (which destroys Vitamin D)
is normally activated by diabetes (2),
but is deactivated by addition of Vitamin D (3) in rats


 Download the PDF from Sci-Hub via VitaminDWiki

Association of liver calcitriol (active vitamin D metabolite) catabolism with osteomalacia during prolonged use of certain drugs was reported in several recent studies. To examine whether the increased calcitriol catabolism could be a potential link between ageing/diabetes mellitus (DM) and bone loss, we studied the dynamic of expression of CYP24, the main calcitriol catabolising enzyme in the liver of rats during ageing and a long-term experimental DM1. DM1 model was induced with intraperitoneally injected streptozotocin (STZ) (55 mg/kg). Sprague-Dawley rats were sacrificed 6 and 12 months after the DM1 induction. The immunohistochemical analyses of CYP24 and transforming growth factor ß 1 (TGF-ß1) expression in the liver were performed. We found that ageing and long-term DM1 resulted in a significantly increased expression of CYP24 in hepatocytes, as well as in non-hepatocyte liver cells (Kupffer cells, hepatic stellate cells and sinusoidal endothelial cells). Ageing and long-term DM1 resulted in an increased expression of TGF-ß1 as well. Expression of CYP24 coexisted with the expression of TGF-ß1 in all types of hepatic cells.

We concluded that liver has the capacity for an active vitamin D catabolism in different populations of liver cells, especially in sinusoidal endothelial cells, through an expression of CYP24. That capacity is substantially increased during ageing and long-term diabetes mellitus. Increased liver calcitriol catabolism could be one of the mechanisms of the bone metabolism impairment related to ageing and diabetes.

Attached files

ID Name Comment Uploaded Size Downloads
13183 CYP24A1 unexpressed by addtion of Vitamin D.jpg admin 18 Dec, 2019 23:21 32.53 Kb 336
13182 CYP24 liver sci-hub.pdf admin 18 Dec, 2019 23:14 695.10 Kb 430