The role of selenoprotein P and selenium in the etiopathogenesis of gestational diabetes mellitus: Association with selenoprotein P1 gene (rs3877899) polymorphism

摘要

Objective: The aim of this study was to investigate the role of selenoprotein P (SeP) and selenium in the etiopathogenesis of gestational diabetes mellitus (GDM) and their association with a common selenoprotein P1 (rs3877899) single nucleotide polymorphism (SNP) in pregnant women with GDM. Materials and methods: Eighty-six pregnant women with GDM and 90 healthy pregnant women from the same geographic region were included in the study. Fasting glucose, insulin HOMA-IR, and HbA1c were compared. Serum selenium levels were measured by graphite-furnace atomic absorption spectrophotometer. Plasma SeP levels were determined by ELISA. Allele-specific polymerase chain reaction (ASPCR) analysis was used to identify polymorphisms of the selenoprotein P1 gene (SEPP1) (rs3877899). Results: The biochemical parameters of GDM such as fasting glucose, insulin, HOMA-IR, and HbA1c were higher in pregnant women with GDM compared to healthy pregnant women. Maternal selenium levels (mu g/L) were 77.99 +/- 7.21 and 76.04 +/- 7.77 in GDM and healthy pregnant women, respectively (p 0.05). However, SeP levels (ng/mL) were found to be significantly lower in GDM (35.29 +/- 3.00) compared to control subjects (46.98 +/- 4.59) (p 0.01). Although there was no significant difference in the distribution of the SEPP1 genotypes and alleles between two groups, SeP levels were higher in the GG genotype of the gene compared to their respective control (p 0.001). Conclusion: Although frequency of SEPP1 polymorphism and selenium levels did not differ significantly between diabetic and healthy pregnant women, SeP levels increased in pregnant women with GDM suggesting SeP plays a role in the etiopathogenesis of GDM. Moreover, the GG genotype of SEPP1 gene polymorphism may be involved in the development of GDM with a different mechanism. It should be clarified with further studies in larger populations.