Financiado en parte por Eli Lilly and Company, Pfizer, GlaxoSmithKline, Sanofi, Servier, Johnson and Johnson
Association of vitamin D with risk of type 2 diabetes: A Mendelian randomisation study in European and Chinese adults
Lu L, Bennett DA, Millwood IY, Parish S, McCarthy MI, Mahajan A, Lin X, Bragg F, Guo Y, Holmes MV, Afzal S, Nordestgaard BG, Bian Z, Hill M, Walters RG, Li L, Chen Z, Clarke R
PLoS medicine · 93 citas
Etiquetas de revisión
Vínculos de autores con la industriaFinanciado por la industriaDatos neutrales que nuestra revisión registró sobre cómo se hizo este estudio. Describen el método, nunca si nos gusta el resultado.
Cómo se estudió
- Diseño
- Metaanálisis (indexado por PubMed)
- Estudiado en
- Personas
- Resultado principal
- Eventos clínicos como enfermedad o muerte
Quién lo pagó
- Financiación
- Financiado por la industria
- Empresa
- Eli Lilly and Company
- Empresa
- Pfizer
- Empresa
- GlaxoSmithKline
- Empresa
- Sanofi
- Organización sin fines de lucro
- Wellcome Trust
- Organización sin fines de lucro
- Cancer Research UK
- Gobierno
- National Institute for Health and Care Research
- Organización sin fines de lucro
- British Heart Foundation
- Universidad u hospital
- University of Oxford
- Gobierno
- National Natural Science Foundation of China
- Gobierno
- Ministry of Science and Technology of the People's Republic of China
- Gobierno
- Chinese Center for Disease Control and Prevention
- Empresa
- Servier
- Organización sin fines de lucro
- Kadoorie Charitable Foundation
- Gobierno
- Centers for Disease Control and Prevention
- Empresa
- Johnson and Johnson
- Gobierno
- Medical Research Council
- Gobierno
- Ministry of Science and Technology of the People’s Republic of China
- Gobierno
- National Institute for Health Research (NIHR)
- Autores
- Al menos un autor declara un vínculo económico con la industria
- Subvenciones
- Medical Research Council (MC_PC_13049); National Natural Science Foundation of China (81390544); Wellcome Trust (212946/Z/18/Z); Wellcome Trust (202922); National Natural Science Foundation of China (104085/Z/14/Z); British Heart Foundation (104085/Z/14/Z); Wellcome Trust (104085); Medical Research Council (MC_PC_14135); Wellcome Trust (202922/Z/16/Z, 104085/Z/14/Z, 088158/Z/09/Z); University of Oxford (104085/Z/14/Z); Wellcome Trust (81390544); Medical Research Council (104085/Z/14/Z); Cancer Research UK (088158/Z/09/Z); Wellcome Trust (202922/Z/16/Z); Ministry of Science and Technology of the People's Republic of China (202922/Z/16/Z); Wellcome Trust (098381); Ministry of Science and Technology of the People's Republic of China (2011BAI09B01); Kadoorie Charitable Foundation (81390541); National Natural Science Foundation of China (81390541); British Heart Foundation (PG/12/32/29544); National Natural Science Foundation of China (202922/Z/16/Z); Medical Research Council (088158/Z/09/Z); Kadoorie Charitable Foundation (2011BAI09B01); Medical Research Council (202922/Z/16/Z); Wellcome Trust (088158/Z/09/Z); Cancer Research UK (14135); National Natural Science Foundation of China (088158/Z/09/Z); Ministry of Science and Technology of the People's Republic of China (088158/Z/09/Z); National Natural Science Foundation of China (81390540); Ministry of Science and Technology of the People's Republic of China (81390544); University of Oxford (202922/Z/16/Z); National Natural Science Foundation of China (81390540, 81390541, 81390544); Ministry of Science and Technology of the People's Republic of China (81390541); British Heart Foundation (088158/Z/09/Z); Wellcome Trust (104085/Z/14/Z); Wellcome Trust (088158); Kadoorie Charitable Foundation (202922/Z/16/Z); Medical Research Council (MC_PC_17228); National Institute for Health and Care Research (NF-SI-0611-10099); Cancer Research UK (104085/Z/14/Z); National Natural Science Foundation of China (2011BAI09B01); Ministry of Science and Technology of the People's Republic of China (81390540); Cancer Research UK (81390540); Kadoorie Charitable Foundation (088158/Z/09/Z); Kadoorie Charitable Foundation (104085/Z/14/Z); Kadoorie Charitable Foundation (81390544); Cancer Research UK (202922/Z/16/Z); Ministry of Science and Technology of the People's Republic of China (104085/Z/14/Z); British Heart Foundation (81390540); Medical Research Council (MC_PC_14135); Medical Research Council (81390540); Wellcome Trust (81390540); Medical Research Council (MC_PC_13049); British Heart Foundation (202922/Z/16/Z); Wellcome Trust (2011BAI09B01); National Institute for Health and Care Research (NF-SI-0617-10090); British Heart Foundation (FS/18/23/33512); Kadoorie Charitable Foundation (81390540); University of Oxford (088158/Z/09/Z); Wellcome Trust (81390541)
Según 19 financiadores declarados y la declaración de financiación del texto completo.
Publicación
- Publicado
- 2018-05-02 · PLoS Med · vol. 15 · número 5 · pág. e1002566
- Editorial
- Public Library of Science
- Citado
- 111 citas · más que el 98% de estudios similares · 8.2× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 36 trabajos
- Acceso
- Acceso abierto (revista) · CC-BY
- Áreas de investigación
- Vitamin D Research Studies · Genetic Associations and Epidemiology · Nutrition, Genetics, and Disease
- Palabras clave
- type 2 diabetes, 25-hydroxyvitamin D, vitamin D, causal relationship, genetic variants, DHCR7, CYP2R1, CYP24A1, vitamin D synthesis, vitamin D transport, vitamin D catabolism, genetic score, China Kadoorie Biobank
- MeSH
- humans, diabetes mellitus, type 2, vitamin d, linear models, logistic models, risk factors, genotype, polymorphism, single nucleotide, adult, aged, middle aged, china, europe, female, male, mendelian randomization analysis
18 autores
- Ling Lu🇨🇳🇬🇧Chinese Academy of Sciences; University of Oxford; Shanghai Institutes for Biological Sciences
- Derrick Bennett🇬🇧University of Oxford
- Iona Y. Millwood🇬🇧University of Oxford; MRC Population Health Research Unit
- Sarah Parish🇬🇧University of Oxford; MRC Population Health Research Unit
- Mark I. McCarthy🇬🇧Centre for Human Genetics; University of Oxford; Oxford Centre for Diabetes, Endocrinology and Metabolism
- Anubha Mahajan🇬🇧Centre for Human Genetics; University of Oxford
- Xu Lin🇨🇳Chinese Academy of Sciences; Shanghai Institutes for Biological Sciences
- Fiona Bragg🇬🇧University of Oxford
- Canqing Yu🇨🇳Chinese Academy of Medical Sciences & Peking Union Medical College
- Michael Vaclav Holmes🇬🇧University of Oxford; MRC Population Health Research Unit
- Shoaib Afzal🇩🇰University of Copenhagen; Herlev Hospital; Copenhagen University Hospital; Gentofte Hospital
- Børge Grønne Nordestgaard🇩🇰University of Copenhagen; Herlev Hospital; Copenhagen University Hospital; Gentofte Hospital
- Zheng Bian🇨🇳Chinese Academy of Medical Sciences & Peking Union Medical College
- Michael Hill🇬🇧University of Oxford
- Robin G. Walters🇬🇧University of Oxford
- Liming Li🇨🇳Chinese Academy of Medical Sciences & Peking Union Medical College; Peking University
- Zhengming Chen🇬🇧University of Oxford
- Robert Clarke🇬🇧 · autor de correspondenciaUniversity of Oxford
Resumen
El texto original del estudio, en el idioma en que se publicó.
Background
Observational studies have reported that higher plasma 25-hydroxyvitamin D (25[OH]D) concentrations are associated with lower risks of diabetes, but it is unclear if these associations are causal. The aim of this study was to test the relevance of 25(OH)D for type 2 diabetes using genetically instrumented differences in plasma 25(OH)D concentrations.
Methods and findings
Data were available on four 25(OH)D single nucleotide polymorphisms (SNPs; n = 82,464), plasma 25(OH)D concentrations (n = 13,565), and cases with diabetes (n = 5,565) in the China Kadoorie Biobank (CKB). The effects on risk of diabetes were assessed by a genetic score using two 25(OH)D synthesis SNPs (DHCR7-rs12785878 and CYP2R1-rs10741657), with and without the addition of SNPs affecting the transport (GC/DBP-rs2282679) and catabolism (CYP24A1-rs6013897) of 25(OH)D. The CKB results were combined in a meta-analysis of 10 studies for the 2 synthesis SNPs (n = 58,312 cases) and 7 studies for all 4 SNPs (n = 32,796 cases). Mean (SD) 25(OH)D concentration was 62 (20) nmol/l in CKB, and the per allele effects of genetic scores on 25(OH)D were 2.87 (SE 0.39) for the synthesis SNPs and 3.54 (SE 0.32) for all SNPs. A 25-nmol/l higher biochemically measured 25(OH)D was associated with a 9% (95% CI: 0%-18%) lower risk of diabetes in CKB. In a meta-analysis of all studies, a 25-nmol/l higher genetically instrumented 25(OH)D concentration was associated with a 14% (95% CI: 3%-23%) lower risk of diabetes (p = 0.01) using the 2 synthesis SNPs. An equivalent difference in 25(OH)D using a genetic score with 4 SNPs was not significantly associated with diabetes (odds ratio 8%, 95% CI: -1% to 16%, lower risk, p = 0.07), but had some evidence of pleiotropy. A limitation of the meta-analysis was the access only to study level rather than individual level data.
Conclusions
The concordant risks of diabetes for biochemically measured and genetically instrumented differences in 25(OH)D using synthesis SNPs provide evidence for a causal effect of higher 25(OH)D for prevention of diabetes.
Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial (CC BY).
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