Zuzana Dostálová

ASSOCIATION OF LEPTIN GENETIC POLYMORPHISM -2548 G/A WITH GESTATIONAL DIABETES MELLITUS

The aim of this study was to investigate possible associations of -2548 G/A polymorphism in leptin gene promoter and pregnancy-associated diseases with abnormal fetal growth such as preeclampsia and gestational diabetes. The study was also focused on whether it is rather maternal or fetal variants that determines the pathological growth status. Peripheral or cord blood samples obtained from 49 preeclamptic women and their 39 newborns, 53 healthy controls and their 53 healthy newborns and 48 patients with gestational diabetes mellitus were evaluated for leptin gene (LEP) locus -2548 genotypes. The significantly higher risk for gestational diabetes mellitus was observed in the presence of an allele (AA and AG genotypes) against carriers of GGgenotype(OR=2.84, 95%CI1.14–7.07,p=0.02). Thereisa significant risk of diabetes mellitus associated to A allele (OR=1.79, 95%CI 1.02–3.14, p=0.03). Furthermore, evaluations of preeclamptic patients’ data revealed a significant association of genotype distribution and delivery and spontaneous abortion rate, where the GG carriers performed the highest pregnancy rate while the AG carriers performed the lowest spontaneous abortion rate. Our results support the hypothesis for -2548 G/A leptin gene polymorphism involvement in ethiopathogenesis of pregnancy-associated diseases with abnormal fetal growth, especially gestational diabetes mellitus.

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 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.

Visfatin is secreted into the breast milk and is correlated with weight changes of the infant after the birth

INTRODUCTION Visfatin is a recently identified adipokine with numerous metabolic and immunoregulatory properties that has been implicated in the regulation of the white adipose tissue (WAT) and significant changes in visfatin levels were reported during pregnancy. The aim of the study was to investigate dynamics of visfatin levels in maternal serum and human breast milk during a 180-d period after the delivery. MATERIALS AND METHODS : Breast milk and venous blood samples were obtained from 24 healthy lactating women with uncomplicated, physiological pregnancy and appropriate-for-gestational age neonates and serum-milk sample duos were collected at the time of birth, at the 1-3, 12-14, 28-30, 88-90 and 178-180 postpartum. RESULTS Our study demonstrates that (1) visfatin is abundantly secreted into breast milk in humans, reaching approx. 100× higher concentrations compared to maternal serum; (2) visfatin concentrations in maternal serum show significant variations after the delivery and (3) visfatin concentration in colostrum could be used for prediction of the subsequent weight development (less/more severe weight loss during first 3 days after the birth) of the infant. DISCUSSION Our data suggest that visfatin could play an important role in regulation of adiposity of the infant after the birth.

A common variation in the cannabinoid 1 receptor (CNR1) gene is associated with pre-eclampsia in the Central European population.

OBJECTIVE Recently it has been proposed that tightly regulated levels of endogenous cannabinoids play a fundamental role in early placental development. The aim of this study was to investigate associations of three single-nucleotide polymorphisms (SNPs) in the cannabinoid 1 receptor (CNR1) gene (rs1049353, rs12720071 and rs806368) and their inferred haplotypes with pre-eclampsia, a severe pregnancy-associated condition characterized by abnormal development and remodeling of spiral decidual arteries. STUDY DESIGN The case-control study comprised a total of 115 pre-eclamptic women and 145 healthy pregnant controls, all originating from the Central-European Czech population. Using PCR-based methods, we tested rs1049353, rs12720071 and rs806368 in the CNR1 gene and haplotypes were constructed. RESULTS Statistically significant difference in genotype distributions of rs806368 (p(g)<10(-3)) was observed when comparing the cases and the controls; the cases presenting with significantly lower proportion of CC homozygotes. In multivariate modeling, the rs806368 served as a predictor for pre-eclampsia development (β=0.15; p=0.04). Haplotype analysis revealed presence of four common haplotypes; the CAA haplotype being less frequent in pre-eclamptic cases compared to the controls (p<0.008). Analysis of regression models confirmed the independent prediction role of AAC haplotype for pre-eclampsia onset (β=-0.18; p=0.03). CONCLUSION This is the first study focusing on the relationship between SNPs in the CNR1 gene and pre-eclampsia risk. Although limited by a relatively small sample size, the study indicates that rs806368 in the CNR1 gene may act as a susceptibility marker for pre-eclampsia in humans.

Comparison of agouti-related peptide levels in peripheral blood of postpartum pre-eclamptic and non pre-eclamptic women and in umbilical cord blood from their pregnancies

Plasma levels of agouti-related peptide (AgRP) were reported to continuously rise during ongoing pregnancy in rats. The aim of the study was to investigate the maternal pre-partum peripheral plasma levels of AgRP and levels in umbilical cord blood in pre-eclamptic and physiological pregnancies in humans.