Enrique Guzman-Gutierrez, Fernando Abarzua, Cristian Belmar, Jyh K. Nien, Marco A. Ramirez, Pablo Arroyo, Carlos Salomon, Francisco Westermeier, Carlos Puebla, Andrea Leiva, Paola Casanello and Luis Sobrevia Pages 750 - 762 ( 13 )
Gestational diabetes mellitus (GDM) is a syndrome compromising the health of the mother and the fetus. Endothelial damage and reduced metabolism of the vasodilator adenosine occur and fetal hyperinsulinemia associated with deficient insulin response and a metabolic rather than mitogenic phenotype is characteristic of this pathology. These phenomena lead to endothelial dysfunction of the fetoplacental unit. Major databases were searched for the relevant literature in the field. Special attention was placed on publications related with diabetes and hormone/metabolic disorders. We aimed to summarize the information regarding insulin sensitivity changes in GDM and the role of adenosine in this phenomenon. Evidence supporting the possibility that fetal endothelial dysfunction involves a functional link between adenosine and insulin signaling in the fetal endothelium from GDM pregnancies is summarized. Since insulin acts via membrane receptors type A (preferentially associated with mitogenic responses) or type B (preferentially associated with metabolic responses), a differential activation of these receptors in this syndrome is proposed.
Adenosine, endothelium, fetus, gestational diabetes, insulin receptor, placenta, hyperinsulinemia, endothelial dysfunction, oral glucose tolerance test, macrosomia
Cellular and Molecular Physiology Laboratory (CMPL), Division of Obstetrics and Gynaecology, School of Medicine, Faculty of Medicine, Pontificia Universidad Catolica de Chile, P.O. Box 114-D, Santiago, Chile.