Is there any link between severe pre-eclampsia and defined polymorphisms in leptin and adiponectin genes?

Aim:  The pathophysiology of pre‐eclampsia, one of the leading causes of maternal mortality worldwide, still remains unclear. Recently, it has been suggested that impaired regulation of complex interactions among various adipokines plays an important role in the development of pre‐eclampsia. The aim...

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Published in:The journal of obstetrics and gynaecology research 2008-10, Vol.34 (5), p.858-864
Main Authors: Bienertová-Vašků, Julie, Dostálová, Zuzana, Kaňková, Kateřina, Bienert, Petr, Vašků, Anna, Unzeitig, Vít
Format: Article
Language:English
Subjects:
adiponectin
Adiponectin - genetics
Adult
Case-Control Studies
Cohort Studies
Female
Genetic Predisposition to Disease
Humans
Infant, Newborn
leptin
Leptin - genetics
polymorphism
Polymorphism, Single Nucleotide
pre-eclampsia
Pre-Eclampsia - genetics
Pregnancy
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Summary:Aim:  The pathophysiology of pre‐eclampsia, one of the leading causes of maternal mortality worldwide, still remains unclear. Recently, it has been suggested that impaired regulation of complex interactions among various adipokines plays an important role in the development of pre‐eclampsia. The aim of this study was to investigate whether the two common polymorphisms of the leptin (LEP) and adiponectin (APM1) genes are associated with the development of pre‐eclampsia and its related traits (gestational hypertension, proteinuria and various measures of reduced fetal growth ) in the Czech pre‐eclamptic population. Methods:  The case–control study comprised a total of 123 pre‐eclamptic women and 150 healthy controls of similar age and parity distribution. They were genotyped for the LEP −2548G/A (5′‐untranslated region) and APM1 T94G (exon 2) polymorphisms using polymerase chain reaction. Results:  The allele frequency of the LEP −2548G polymorphism was 0.541 in the pre‐eclamptic group versus 0.583 in the control group (P = 0.578); the frequency of the APM1 94G polymorphism was 0.073 and 0.079 (P = 0.628), respectively. No significant associations were detected between either of the two single nucleotide polymorphisms or any of the parameter biomarkers related to pre‐eclampsia, such as gestational hypertension or proteinuria. However, the APM1 T94G polymorphism was significantly associated with a low birth weight in pre‐eclamptic pregnancies, with mothers carrying the T‐allele having an almost three‐fold increase in the likelihood of giving birth to a child with a low birth weight for its gestational age (odds ratio, 2.7; 95% confidence interval, 0.18–5.9; P = 0.004). Conclusions:  The APM1 T94G and LEP −2548G/A polymorphisms do not seem to be major genetic determinants of susceptibility to pre‐eclampsia in the Czech Caucasian population. However, evidence has been provided for possible APM1 T94G involvement in controlling the birth weight of children from pre‐eclamptic pregnancies, thus supporting the hypothesis of T94G involvement in controlling the birth weight of newborns.
ISSN:1341-8076
1447-0756
DOI:10.1111/j.1447-0756.2008.00794.x