Toggle Health Problems and D

Glucocorticoid treatment reduces Vitamin D getting to cells via 3 or 4 genes

Examples include beclomethasone, betamethasone, budesonide, cortisone, dexamethasone, hydrocortisone, methylprednisolone, prednisolone, prednisone, triamcinolone


Notice Glucocorticoid and Vitamin D References:
Reference #1: discusses 3 genes, only one of which affects blood test
Reference #2 discusses another Vitamin D gene (VDR) - not affect a blood test
Reference #3 discusses only blood test

Glucocorticoids reduces Vitamin D getting to cells via 3 genes – 2017

Glucocorticoid exposure induces preeclampsia via dampening 1,25-dihydroxyvitamin D3.
Hypertens Res. 2017 Nov 2. doi: 10.1038/hr.2017.98. [Epub ahead of print]
Zhang D1,2, biozdx at 163.com Zeng J1, Miao X1, Liu H3, Ge L4, Huang W2, Jiao J2, Ye D2.

  • 1 Department of Clinical Laboratory, Puai Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
  • 2 Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
  • 3 Department of Internal Medicine, Puai Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
  • 4 Department of Gynecology and Obstetrics, Puai Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

The pathogenesis of preeclampsia (PE) involves a number of biological processes that may be directly or indirectly affected by glucocorticoid (GC) and vitamin D. GC exposure increases the risk of PE, and 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) deficiency may result in PE. The purpose of the present study was to confirm the involvement of GC/1,25-(OH)2D3 axis in the pathogenesis of PE. In the study, cortisol levels of PE patients were found to be higher than that of non-complicated pregnancies, while 1,25-(OH)2D3 were decreased in both PE women and GC-induced PE rats.
Mechanically, GC reduced 1,25-(OH)2D3 levels via disturbing its biosynthetic and catabolic enzymes, including

  • Cyp3a1,
    especially enhancing the expressions of Cyp3a1, the dominant enzyme for vitamin D degeneration
  • Cyp24a1 and
  • Cyp27b1

Moreover, replenishing 1,25-(OH)2D3 ameliorated the symptoms and placental oxidative stress of GC-induced rat PE. The protective actions of 1,25-(OH)2D3 might be explained by its roles in antagonizing the effects of GC on trophoblast proliferation and apoptosis. Together, these findings suggest that GC exposure could lead to PE via dampening 1,25-(OH)2D3 biosynthesis, and GC/1,25-(OH)2D3 axis might represent a common pathway through which PE occurs.

PMID: 29093562 DOI: 10.1038/hr.2017.98
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Glucocorticoid regulation of the vitamin D receptor – 2010

J Steroid Biochem Mol Biol. 2010 Jul;121(1-2):372-5. doi: 10.1016/j.jsbmb.2010.03.081. Epub 2010 Apr 14.
Hidalgo AA1, Trump DL, Johnson CS.

Many studies indicate calcitriol has potent anti-tumor activity in different types of cancers. However, high levels of vitamin D can produce hypercalcemia in some patients. Glucocorticoids are used to ameliorate hypercalcemia and to enhance calcitriol anti-tumor activity. Calcitriol in combination with the glucocorticoid dexamethasone (Dex) increased vitamin D receptor (VDR) protein levels and ligand binding in squamous cell carcinoma VII (SCC). In this study we found that both calcitriol and Dex induce VDR- and glucocorticoid receptor (GR)-mediated transcription respectively, indicating both hormone receptors are active in SCC. Pre-treatment with Dex increases VDR-mediated transcription at the human CYP24A1 promoter. Whereas, pre-treatment with other steroid hormones, including dihydrotestosterone and R1881, has no effect on VDR-mediated transcription. Real-time PCR indicates treatment with Dex increases Vdr transcripts in a time-dependent manner, suggesting Dex may directly regulate expression of Vdr. Numerous putative glucocorticoid response elements (GREs) were found in the Vdr gene. Chromatin immuno-precipitation (ChIP) assay demonstrated GR binding at several putative GREs located within the mouse Vdr gene. However, none of the putative GREs studied increase GR-mediated transcription in luciferase reporter assays. In an attempt to identify the response element responsible for Vdr transcript regulation, future studies will continue to analyze newly identified GREs more distal from the Vdr gene promoter.

PMID: 20398752 PMCID: PMC2907065 DOI: 10.1016/j.jsbmb.2010.03.081
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Glucocorticoid use increases risk by 2X of vitamin D < 10 ng – 2011

Association of glucocorticoid use and low 25-hydroxyvitamin D levels: results from the National Health and Nutrition Examination Survey (NHANES): 2001-2006
J Clin Endocrinol Metab. 2011 Dec;96(12):3838-45. doi: 10.1210/jc.2011-1600. Epub 2011 Sep 28.
Skversky AL1, Kumar J, Abramowitz MK, Kaskel FJ, Melamed ML.

CONTEXT: In many disorders requiring steroid therapy, there is substantial decrease in bone mineral density. The association between steroid use and 25-hydroxyvitamin D [25(OH)D] deficiency has not been confirmed in large population-based studies, and currently there are no specific vitamin D recommendations for steroid users.

OBJECTIVE: The aim of the study was to evaluate the association of serum 25(OH)D deficiency [defined as 25(OH)D <10 ng/ml] with oral steroid use.

DESIGN: Cross-sectional analysis was performed using NHANES 2001-2006.

SETTING: We analyzed a nationally representative sample of U.S. children and adults.

PARTICIPANTS: The study sample consisted of children, adolescents, and adults from NHANES 2001-2006 (n = 22,650), representative of 286 million U.S. residents, with serum 25(OH)D levels and data on other potential confounders.

MAIN OUTCOME MEASURE: We measured serum 25(OH)D levels below 10 ng/ml.

RESULTS: A total of 181 individuals (0.9% of the population) used steroids within the past 30 d. Overall, 5% of the population had 25(OH)D levels below 10 ng/ml. Among steroid users, 11% had 25(OH)D levels below 10 ng/ml, compared to 5% among steroid nonusers (P = 0.009). The odds of having 25(OH)D deficiency were 2-fold higher in those who reported steroid use compared to those without steroid use [odds ratio (OR), 2.36; 95% confidence interval (CI), 1.25, 4.45]. This association remained after multivariable adjustment (OR, 2.21; 95% CI, 1.01, 4.85) and in a multivariable model using NHANES III data (OR, 1.88; 95% CI, 1.01, 3.48).

CONCLUSION: Steroid use is independently associated with 25(OH)D deficiency in this nationally representative cohort limited by cross-sectional data. It suggests the need for screening and repletion in patients on chronic steroids.

PMID: 21956424 PMCID: PMC3232615 DOI: 10.1210/jc.2011-1600
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Created by admin. Last Modification: Friday August 21, 2020 00:14:37 GMT-0000 by admin. (Version 15)

Attached files

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13461 Gluco 2017.pdf admin 07 Feb, 2020 03:07 1.06 Mb 324
8630 Association of glucocorticoid use.pdf admin 03 Nov, 2017 15:13 368.19 Kb 487
8629 Glucocorticoid regulation of the vitamin D receptor.pdf admin 03 Nov, 2017 15:13 234.86 Kb 512
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