Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2014) 35 P388 | DOI: 10.1530/endoabs.35.P388

ECE2014 Poster Presentations Diabetes (epidemiology, pathophysiology) (63 abstracts)

What is the contribution of MODY gene polymorphisms in the development of gestational diabetes mellitus?

Duygu Ilke Cikman 1 , Muzaffer Seyhan Cikman 3 , Tomris Erbas 1 , Mehmet Alikasifoglu 2 & Selcuk Dagdelen 1

1Department of Endocrinology and Metabolism, School of Medicine, Hacettepe University, Ankara, Turkey; 2Department of Genetics, School of Medicine, Hacettepe University, Ankara, Turkey; 3Zekai Tahir Burak Women’s Health Training and Research Hospital, Ankara, Turkey.

Objective: Gestational diabetes mellitus (GDM) is the consequence of increased insulin resistance during pregnancy in predisposed individuals who already have impaired insulin secretion due to beta-cell dysfunction as in maturity onset diabetes of young (MODY) cases. Here we aimed to document the association between MODY subtypes and GDM to understand the pathogenesis of GD.

Design: Matched, case-control study.

Method: Ninety-three patients with the diagnosis of GDM according to the diagnostic criteria of 2011 ADA and 89 healthy pregnant non-diabetic subjects participated in this study. Patients with T1DM or T2DM diagnosis before pregnancy or with organ failure were excluded. Peripheric blood samples were obtained from all the participants to study the genetic polymorphims of GCK (rs1799884), HNF1A (rs1169288) and HNF4A (rs2144908) genes. The association between GDM and gene polymorphisms were examined.

Results: HNF1A (rs1169288) gene polymorphism was positively correlated with GDM which was statistically significant (P=0.038). Although IGF2BP2 (rs1470579) and GCK (rs1799884) gene polymorhisms were more frequent in GDM group, this association was not statistically significant. There was no association between GDM and HNF1A (rs1169288) gene polymorphism. Besides these, as the number of the risk allelles of the three genes, included in our study, increasing; the risk of GDM increased as well (P=0.012). In addition to this, individuals with the risk allels of GCK gene have had higher HbA1c and post-OGTT glucose levels (P=0.028 and P=0.010 respectively).

Conclusions: The risk of GDM is related to the additive effect of these three genes (GCK (rs1799884), HNF1A (rs1169288) and HNF1A (rs1169288)) rather than a single gene effect which was firstly described here in our study.

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