The Role of Placenta in the Fetal Programming Associated to Gestational Diabetes

Adenosine A2A receptor regulates expression of vascular endothelial growth factor in feto-placental endothelium from normal and late-onset pre-eclamptic pregnancies

“…Regarding feto-placental endothelial cells used in this study, it has been shown that cells from microcirculation (i.e., hPMEC) are more reactive to pro-angiogenic signals than macrovascular endothelium (i.e., HUVEC) [2,33,34]. Despite that, hPMEC and HUVECs have similar response to CGS-21680 when cell proliferation was analyzed (logEC 50 10 −8.7 M vs logEC 50 10 −9.6 M, respectively).…”

Cinnamaldehyde mitigates placental vascular dysfunction of gestational diabetes and protects from the associated fetal hypoxia by modulating placental angiogenesis, metabolic activity and oxidative stress

“…Thus, VEGF/NO balance maintains the placental vascular homeostasis. In GDM, this balance is perturbed as a result of placental metabolic disturbances and oxidative stress [10,11]. Hyperglycemia turns the normally glycolytic EC metabolism into an oxidative metabolism that elevates the mitochondrial respiration, resulting in excessive production of reactive oxygen species (ROS) [12,13].…”

Periodontitis and Gestational Diabetes Mellitus: A Potential Inflammatory Vicious Cycle

“…Additionally, fetuses from GDM pregnancies are more susceptible to short-term adverse outcomes, such as macrosomia, neonatal hypoglycemia, neonatal cardiac dysfunction, and labor difficulties [29,30]. The hyperglycemic status in the intrauterine environment also influences the future newborn's postnatal health through a phenomenon known as "fetal programming", which involves epigenetic changes, such as histone modifications and DNA methylation [31,32]. Fetal programming allows the fetus to adapt to pregnancy exposures; however, it can also predispose to the development of non-communicable chronic diseases, including cardiovascular disease [33,34], obesity, and T2DM [35].…”