Archives of Gynecology and Obstetrics (2018) 297:885–889
Maternal and neonatal omentin‑1 levels in gestational diabetes
· Mariella Polterauer
· Stephanie Springer
· Lorenz Kuessel
· Peter Haslinger
· Christof Worda
Received: 28 September 2017 / Accepted: 20 December 2017 / Published online: 15 January 2018
© The Author(s) 2018. This article is an open access publication
Purpose To evaluate the eﬀect of gestational diabetes on omentin-1 in maternal and cord plasma. As a potent mediator of
insulin resistance, Omentin-1, an adipokine derived from human adipose and placental tissue, may be an important player
in the pathophysiology of gestational diabetes.
Methods This was a prospective case–control study. The study included 96 women with gestational diabetes and 96 pregnant
women without. Omentin-1 was measured at the time of the oral glucose tolerance test, at 32 weeks in maternal plasma and
right after delivery in umbilical cord blood by ELISA assay.
Results Over a period of 2 years, 200 patients were enrolled. Omentin-1 levels did not signiﬁcantly diﬀer between both groups
throughout the pregnancy: omentin-1 levels were 157 ± 83 ng/ml in women with gestational diabetes and 158 ± 93 ng/ml
in women without gestational diabetes (p = 0.94) at time of the oral glucose tolerance test and 118 ± 77 ng/ml in women
with diabetes and 150 ± 89 ng/ml in women without (p = 0.12) at 32 weeks, respectively. Both groups showed a decrease in
omentin-1 levels throughout pregnancy, with a more pronounced decrease in diabetic women (13 ± 53 versus 4 ± 48 ng/ml;
p = 0.5). Neonatal omentin-1 levels were signiﬁcantly lower in oﬀspring of diabetic mothers: 106 ± 61 versus 134 ± 45 ng/
ml (p = 0.03).
Conclusions There was no signiﬁcant diﬀerence in omentin-1 levels between healthy and diabetic mothers throughout the
pregnancy. However, we found signiﬁcantly lower omentin-1 levels in oﬀspring of diabetic mothers. This may indicate a
risk for the development of insulin resistance in later life.
Keywords Omentin-1 · Gestational diabetes · Adipokines · Insulin resistance
In each pregnancy, a physiological insulin resistance syn-
drome occurs to ensure that the fetus is suﬃciently supplied
with glucose. Despite this physiological insulin resistance,
most women stay normoglycemic throughout the pregnancy
because of adequate β-cell function. If this physiological
compensation fails, gestational diabetes occurs.
Gestational diabetes is one of the most common preg-
nancy-associated diseases with a prevalence of 5–10%
of all pregnancies and its prevalence is increasing [1, 2].
It includes facets of type 2 diabetes (DM2) like insulin
resistance and up to 50% of women with GDM develop DM2
within the following 10 years after pregnancy [3, 4]. Ges-
tational diabetes is associated with severe hazards to both
mother and fetus such as macrosomia, plexus palsy, prema-
ture delivery, and intrauterine death [5, 6]. Furthermore, the
exact pathogenesis of GDM is not completely understood;
however, increased insulin resistance is a well-demonstrated
A recent study suggests that not only hyperglycemia but
also altered maternal lipid metabolism may constitute a risk
factor for macrosomia in GDM .
It has been described that adipokines, which are proteo-
hormones secreted mainly from adipose tissue, could play
an important role in the development of diabetes and also
gestational diabetes . Adipokines inﬂuence metabolic
processes through various pathways like appetite control,
inﬂammation, regulation of adipogenesis, and alter insulin
sensitivity and secretion . Since several adipokines like
* Katharina Worda
Department of Obstetrics and Gynecology, Medical
University of Vienna, Währinger Gürtel 18-20, 1090 Vienna,