Placental expressions and serum levels of adiponectin, visfatin, and omentin in GDM
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.
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.
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).
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.
KeywordsGDM Insulin resistance Obesity Adiponectin Visfatin Omentin
We thank the nurses and residents of the Department of Obstetrics and Gynecology, Faculty of Medicine, Siriraj Hospital, Mahidol University, for subject recruitment, data, blood, and placenta collection. We thank Pailin Maikaew for the management of financial documents. This work was supported by the Faculty of Medicine Siriraj Hospital Research Fund (Grant Number [IO] R015934008). X. Souvannavong-Vilivong and R. Klinjampa were supported by the Siriraj Graduate Scholarship, Faculty of Medicine Siriraj Hospital, Mahidol University. C. Sitticharoon was supported by the Chalermprakiat Grant.
All authors participated in the design, interpretation of the studies and analysis of the data and review of the manuscript; XS-V, CS, RK, CS, and IK conducted the experiments. XS-V and CS wrote the manuscript.
Compliance with ethical standards
Conflict of interest
The authors declare no potential conflicts of interest.
The study has been approved by the the Siriraj Institutional Review Board (COA no. Si.545/2015) of the Faculty of Medicine Siriraj Hospital, Mahidol University, Thailand and has been performed in accordance with the Declaration of Helsinki.
Written informed consents were obtained from all subjects prior to the study.
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