6–8 DBP gene spans 35 kilobase pairs and contains 13 exons and 12 introns, and maps to the long arm of chromosome 4 (4q12–q13).5 9 There are

two major polymorphisms in DBP which were studied. kinase inhibitor A nucleotide exchange (GAT to GAG) in position 416 contributes to an Asp to Glu exchange. Additionally, the ACG to AAG in position 420 changes Thr to Lys.10 A few previous studies have been carried out to access the association between DBP polymorphisms and risk of T2DM in different populations; however, the results are inconsistent and inconclusive.11–16 Therefore, it remains uncertain if DBP polymorphisms are really associated with an increased risk of T2DM. The purpose of this study was to assess the

association of DBP polymorphisms with T2DM by conducting a systematic review and meta-analysis from individual data sets of all relevant studies published to date. Materials and methods Literature and search strategy The study was performed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) statement.17 A computerised literature search was conducted using the Cochrane, Pubmed, ISI, CNKI (Chinese) and Wanfang (Chinese) databases for relevant articles published in English and Chinese before the end of March 2014. The search terms were as follows: “vitamin D binding protein or group-specific component protein (DBP or Gc)” and “polymorphism or variant” and “type 2 diabetes mellitus (T2DM)”. In addition, the reference lists of original and review articles were also researched to identify any additional relevant articles using the previous databases. The included studies must meet the following criteria: (1) the design had to be a case-control or correlation

study; (2) there is a description of DBP genotype frequencies in cases and controls provided; (3) the study evaluated the association between DBP polymorphisms and T2DM; (4) there were sufficient data for estimating an OR with 95% CI. In all the studies, genomic Carfilzomib DNA from people was extracted from blood and DBP status was determined by analysis of the gene through PCR single strand conformation polymorphism (PCR-SSCP), PCR restriction fragment length polymorphisms (PCR-RFLP), PCR-based denaturing high-performance liquid chromatography (DHPLC), conforming two-pair primers (CTPP) or biochip. Data extraction Data were extracted and entered into a database by two investigators (GW and YL) independently. For conflicting evaluations, an agreement was reached following a discussion.