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Obesity cut semi-activation of Vitamin D in half (mice) – Jan 2019

Obesity Decreases Hepatic 25‐Hydroxylase Activity Causing Low Serum 25‐Hydroxyvitamin D

Journal of Bone Mineral Research https://doi.org/10.1002/jbmr.3686
Jeffrey D Roizen Caela Long Alex Casella Lauren O'Lear Ilana Caplan Meizan Lai Issac Sasson Ravinder Singh Andrew J Makowski … See all authors

Vitamin D Life

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Genetics category listing contains the following

266 articles in the Genetics category

see also

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

  • Snapshot of the literature by Vitamin D Life as of early 2019
  • 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 show 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

Overview Obesity and Vitamin D contains the following summary


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  • Normal weight     Obese     (50 ng = 125 nanomole)

Report on this study

/How does a high-fat diet influence vitamin D metabolism?
"Obesity reduces the ability of the liver to convert vitamin D into calcidiol"

 Download the PDF from Sci-Hub via Vitamin D Life
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Normal vitamin D homeostasis is critical for optimal health; nevertheless, vitamin D deficiency is a worldwide public health problem. Vitamin D insufficiency is most commonly due to inadequate cutaneous synthesis of cholecalciferol and/or insufficient intake of vitamin D, but can also arise as a consequence of pathological states such as obesity. Serum concentrations of 25(OH)D (calcidiol) are low in obesity, and fail to increase appropriately after vitamin D supplementation.

Although sequestration of vitamin D in adipose tissues or dilution of ingested or cutaneously synthesized vitamin D in the large fat mass of obese patients has been proposed to explain these findings, here we investigate the alternative mechanism that reduced capacity to convert parent vitamin D to 25(OH)D due to decreased expression of CYP2R1, the principal hepatic vitamin D 25‐hydroxylase.

To test this hypothesis, we isolated livers from female mice of 6 to 24 weeks of age, weaned onto either a normal chow diet or a high‐fat diet, and determined the abundance of Cyp2r1 mRNA using digital droplet‐quantitative PCR. We observed a significant (p < 0.001) decrease in Cyp2r1 mRNA in the liver of high‐fat diet–fed mice relative to lean‐chow–fed female mice. Moreover, there was a significant (p < 0.01) relationship between levels of Cyp2r1 mRNA and serum 25(OH)D concentrations as well as between Cyp2R1 mRNA and the ratio of circulating 25(OH)D3 to cholecalciferol (p < 0.0001).
Using linear regression we determined a curve with 25(OH)D3/cholecalciferol versus normalized Cyp2R1 mRNA abundance with an R2 value of 0.85. Finally, we performed ex vivo activity assays of isolated livers and found that obese mice generated significantly less 25(OH)D3 than lean mice (p < 0.05). Our findings indicate that expression of CYP2R1 is reduced in obesity and accounts in part for the decreased circulating 25(OH)D.


Created by admin. Last Modification: Monday June 17, 2019 15:37:46 GMT-0000 by admin. (Version 12)

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11443 Obese mice F4.jpg admin 22 Feb, 2019 14:35 17.09 Kb 191
11442 Obese mice.pdf PDF 2019 admin 22 Feb, 2019 14:35 680.67 Kb 254
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