Financiado en parte por Pfizer
Genetic variants in CYP2R1, CYP24A1, and VDR modify the efficacy of vitamin D3 supplementation for increasing serum 25-hydroxyvitamin D levels in a randomized controlled trial
Barry EL, Rees JR, Peacock JL, Mott LA, Amos CI, Bostick RM, Figueiredo JC, Ahnen DJ, Bresalier RS, Burke CA, Baron JA
The Journal of clinical endocrinology and metabolism · 122 citas
Etiquetas de revisión
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Cómo se estudió
- Diseño
- Ensayo controlado aleatorizado (indexado por PubMed)
- Estudiado en
- Personas
- Resultado principal
- Marcadores de salud y funcionamiento
Quién lo pagó
- Financiación
- Financiado por la industria
- Empresa
- Pfizer
- Gobierno
- National Institutes of Health
- Universidad u hospital
- Audrey and Theodor Geisel School of Medicine at Dartmouth
- Gobierno
- National Cancer Institute
- Gobierno
- National Institute of General Medical Sciences
- Gobierno
- NCI NIH HHS
- Gobierno
- NIGMS NIH HHS
- Subvenciones
- National Cancer Institute (CA159360); National Institute of General Medical Sciences (P20GM103534); National Cancer Institute (P30CA023108); National Cancer Institute (R01CA098286); National Cancer Institute (CA098286); National Cancer Institute (R03 CA159360)
Según 7 financiadores declarados.
Publicación
- Publicado
- 2014-07-29 · J Clin Endocrinol Metab · vol. 99 · número 10 · págs. E2133–E2137
- Editorial
- Oxford University Press
- Citado
- 157 citas · más que el 99% de estudios similares · 9.6× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 12 trabajos
- Acceso
- Acceso abierto (copia en repositorio)
- Áreas de investigación
- Vitamin D Research Studies · Nutrition, Genetics, and Disease · Genetic Associations and Epidemiology
- Palabras clave
- 25-hydroxyvitamin D, single nucleotide polymorphisms, CYP2R1, CYP24A1, vitamin D receptor, genetic susceptibility, calcium carbonate
- MeSH
- humans, vitamin d deficiency, calcium carbonate, cholecalciferol, vitamin d, receptors, calcitriol, treatment outcome, linear models, drug resistance, genotype, polymorphism, single nucleotide, aged, middle aged, female, male, genetic variation, cholestanetriol 26-monooxygenase, vitamin d3 24-hydroxylase, cytochrome p450 family 2
11 autores
- Elizabeth L. Barry🇺🇸🇬🇧 · autor de correspondenciaUniversity of Southern California; Emory University; King's College London
- Judy R. Rees
- Janet L. Peacock🇬🇧National Health Service; King's College London; National Institute for Health and Care Research
- Leila A. Mott
- Christopher Ian Amos
- Roberd M. Bostick🇺🇸Emory University
- Jane C. Figueiredo🇺🇸University of Southern California
- Dennis J. Ahnen🇺🇸Veterans Health Administration; Denver VA Medical Center; University of Colorado Anschutz; University of Colorado Denver
- Robert S. Bresalier🇺🇸The University of Texas MD Anderson Cancer Center
- Carol Ann Burke🇺🇸Cleveland Clinic
- John A. Baron🇺🇸Dartmouth College; University of North Carolina at Chapel Hill
Resumen
El texto original del estudio, en el idioma en que se publicó.
Context
Adequate serum 25-hydroxyvitamin D concentrations, [25(OH)D], are required for optimal bone health, and low levels are associated with chronic diseases.
Objective
We investigated whether 41 candidate single nucleotide polymorphisms (SNPs) in vitamin D and calcium pathway genes (GC, DHCR7, CYP2R1, CYP27B1, CYP24A1, VDR, and CASR) are associated with [25(OH)D] or modify the increase in [25(OH)D] from vitamin D3 supplementation.
Design and setting
Baseline and year 1 [25(OH)D] measurements from a randomized controlled trial conducted at 11 clinical centers in the United States.
Participants
A total of 1787 healthy non-Hispanic white participants aged 45-75 years.
Interventions
Vitamin D3 (1000 IU/d), calcium carbonate (1200 mg/d elemental), both, or placebo.
Main outcome measures
Genotype main effects and interactions with vitamin D3 treatment estimated using multiple linear regression.
Results
The baseline serum [25(OH)D] was 25.4 ± 8.7 ng/mL (mean ± SD). Associations with baseline levels were discovered for SNPs in CYP24A1 (rs2209314, rs2762939) and confirmed for SNPs in GC and CYP2R1. After 1 year, [25(OH)D] increased on average by 6.1 ± 8.9 ng/mL on vitamin D3 treatment and decreased by 1.1 ± 8.4 ng/mL on placebo. The increase in [25(OH)D] due to vitamin D3 supplementation was modified by genotypes at rs10766197 near CYP2R1, rs6013897 near CYP24A1, and rs7968585 near VDR.
Conclusions
The increase in [25(OH)D] attributable to vitamin D3 supplementation may vary according to common genetic differences in vitamin D 25-hydroxylase (CYP2R1), 24-hydroxylase (CYP24A1), and the vitamin D receptor (VDR) genes. These findings have implications for achieving optimal vitamin D status and potentially for vitamin D-related health outcomes.
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