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Placental expressions and serum levels of adiponectin, visfatin, and omentin in GDM. | LitMetric
Aims : Adiponectin, visfatin, and omentin have been shown to be associated with insulin sensitivity and might have a role in the pathophysiology of gestational diabetes mellitus (GDM). This study aimed to (1) compare adiponectin, visfatin, and omentin mRNA expressions in placenta and their serum levels between normal pregnancy (NP) and GDM class A1 (GDMA1) pregnancy and (2) determine correlations between placental gene expressions as well as serum levels with maternal and neonatal clinical parameters in all, NP, and GDM subjects.Methods : NP subjects (n = 37), who had normal medical history during their pregnancies without diagnosis of any abnormalities and GDMA1 subjects (n = 37), who were diagnosed since they had antenatal care, were recruited when they were in labor with a gestational age of at least 34 weeks. Clinical parameters and serum adiponectin, visfatin, and omentin levels were measured in the delivery room.Results : GDMA1 subjects had higher serum visfatin and plasma glucose levels, but lower serum omentin levels (p < 0.05 all) compared to controls, with comparable levels of placental adiponectin, visfatin, and omentin expressions, plasma insulin, and indices of insulin sensitivity and insulin resistance. Serum visfatin was negatively correlated with neonatal weight and length in the GDM group (p < 0.05 all). Serum omentin was negatively correlated with pre-pregnancy body mass index and waist circumference only in the NP group (p < 0.05 all). Serum adiponectin was negatively correlated with maternal age and HOMA-IR in the NP group (p < 0.05 all) and with placental weight and serum omentin in the GDM group (p < 0.05 all).Conclusions : In conclusion, in GDMA1, increased serum visfatin, which has insulin-mimetic effect, might be associated with a compensatory mechanism that improves the impaired insulin function. Decreased serum omentin in GDMA1, which is normally found in visceral obesity, might lead to insulin resistance and contribute to the pathophysiology of GDM.
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