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http://purl.uniprot.org/citations/16752173http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16752173http://www.w3.org/2000/01/rdf-schema#comment"

Aims/hypothesis

Impaired beta cell function is the hallmark of gestational diabetes mellitus (GDM) and MODY. In addition, women with MODY gene mutations often present with GDM, but it is not known whether common variants in MODY genes contribute to GDM.

Subjects and methods

We genotyped five common variants in the glucokinase (GCK, commonly known as MODY2), hepatocyte nuclear factor 1-alpha (HNF1A, commonly known as MODY3) and 4-alpha (HNF4A commonly known as MODY1) genes in 1,880 Scandinavian women (648 women with GDM and 1,232 pregnant non-diabetic control women).

Results

The A allele of the GCK -30G-->A polymorphism was more common in GDM women than in control subjects (odds ratio [OR] 1.28 [95% CI 1.06-1.53], p=0.008, corrected p value, p=0.035). Under a recessive model [AA vs GA+GG], the OR increased further to 2.12 (95% CI 1.21-3.72, p=0.009). The frequency of the L allele of the HNF1A I27L polymorphism was slightly higher in GDM than in controls (1.16 [95% CI 1.001-1.34], p=0.048, corrected p value, p=0.17). However, the OR increased under a dominant model (LL+IL vs II; 1.31 [95% CI 1.08-1.60], p=0.007). The rs2144908, rs2425637 and rs1885088 variants, which are located downstream of the primary beta cell promoter (P2) of HNF4A, were not associated with GDM.

Conclusions/interpretation

The -30G-->A polymorphism of the beta-cell-specific promoter of GCK and the I27L polymorphism of HNF1A seem to increase the risk of GDM in Scandinavian women."xsd:string
http://purl.uniprot.org/citations/16752173http://purl.org/dc/terms/identifier"doi:10.1007/s00125-006-0258-8"xsd:string
http://purl.uniprot.org/citations/16752173http://purl.uniprot.org/core/author"Karlsson E."xsd:string
http://purl.uniprot.org/citations/16752173http://purl.uniprot.org/core/author"Groop L."xsd:string
http://purl.uniprot.org/citations/16752173http://purl.uniprot.org/core/author"Almgren P."xsd:string
http://purl.uniprot.org/citations/16752173http://purl.uniprot.org/core/author"Parikh H."xsd:string
http://purl.uniprot.org/citations/16752173http://purl.uniprot.org/core/author"Lernmark A."xsd:string
http://purl.uniprot.org/citations/16752173http://purl.uniprot.org/core/author"Ivarsson S."xsd:string
http://purl.uniprot.org/citations/16752173http://purl.uniprot.org/core/author"Lynch K."xsd:string
http://purl.uniprot.org/citations/16752173http://purl.uniprot.org/core/author"Shaat N."xsd:string
http://purl.uniprot.org/citations/16752173http://purl.uniprot.org/core/author"Berntorp K."xsd:string
http://purl.uniprot.org/citations/16752173http://purl.uniprot.org/core/date"2006"xsd:gYear
http://purl.uniprot.org/citations/16752173http://purl.uniprot.org/core/name"Diabetologia"xsd:string
http://purl.uniprot.org/citations/16752173http://purl.uniprot.org/core/pages"1545-1551"xsd:string
http://purl.uniprot.org/citations/16752173http://purl.uniprot.org/core/title"Common variants in MODY genes increase the risk of gestational diabetes mellitus."xsd:string
http://purl.uniprot.org/citations/16752173http://purl.uniprot.org/core/volume"49"xsd:string
http://purl.uniprot.org/citations/16752173http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/16752173
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http://purl.uniprot.org/uniprot/#_E0YMK3-mappedCitation-16752173http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16752173
http://purl.uniprot.org/uniprot/#_E0YMI7-mappedCitation-16752173http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16752173
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http://purl.uniprot.org/uniprot/#_E0YMJ0-mappedCitation-16752173http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16752173