16 iul. 2018 THE ROLE OF ADIPOKINES IN THE DIAGNOSIS OF GESTATIONAL DIABETES
Andreea Florian, Gh. Cruciat, D. Mureşan, F. Stamatian
Department of Obstetrics and Gynecology ”Iuliu Haţieganu” University of Medicine and
Pharmacy, Cluj-Napoca, Romania
Abstract
Gestational diabetes (GD) is one of the most common complications of pregnancy and can lead to significant
risks to the mother and fetus. Gestational diabetes is defined as glucose intolerance that develops or is diagnosed
during pregnancy. The incidence of this disease varies from 0.6 to 20%, depending on the diagnostic criteria used,
with an increasing trend over the past years. GD occurs when an inadequate secretion of the beta-pancreatic cells
fails to compensate for the decrease in peripheral insulin sensitivity, a phenomenon characteristic of pregnancy.
Typically, GD is diagnosed at 24-28 weeks of gestation by performing OGTT, according to the diagnostic criteria
established by the International Association of Diabetes and Pregnancy Study Groups (IADPSG). Apparently, GD
can develop very early in pregnancy, and can negatively impact on both fetus and mother. Recent studies have
evaluated the role of several adipokines in GD, especially that of leptin, adiponectin, TNF-á and resistin. Adipokines
are a group of proteins secreted by adipocytes, whose secretion is altered in obesity, contributing to metabolic and
vascular changes. At present, there is growing concern for early detection of GD using various biochemical genetic
markers, or various metabolites involved in the pathophysiology of gestational diabetes. Early detection would
allow rapid initiation of appropriate treatment. Moreover, if a link between the pathophysiological mechanisms of
GD and those of obesity could be proven, this would open up new opportunities for the prevention and treatment of
these conditions.
The aim of this review is to provide an overview of these adipokines, as well as of their regulatory mechanisms
and potential contribution to the onset of GD. The evidence so far shows that adiponectin and leptin are most likely
involved in the pathophysiology of this disease.