ISSN 1662-4009 (online)

ESPE Yearbook of Paediatric Endocrinology (2018) 15 2.13 | DOI: 10.1530/ey.15.2.13


To read the full abstract: Endocrinology. 2017 Jul 1;158(7):2102-2112

Gestational diabetes mellitus (GDM) produces fetal hyperglycemia with increased lifelong risks for the exposed offspring to cardiovascular and other diseases. In-utero exposure to GDM alters metabolic programming in newborns and their placenta, cord tissues, and cord blood. Human umbilical cord mesenchymal stromal cells (hUC-MSCs) of Wharton’s jelly origin undergo adipogenic, osteogenic, and chondrogenic differentiation in vitro. Exposure of these hUC-MSCs to maternal gestational diabetes seems to have a dramatic impact on the metabolic, angiogenic and proliferative ability of these cells. Exposure of these umbilical cord mesenchymal stromal cells to gestational diabetes induces a low proliferative rate, increases population doubling time, reduces cell viability and increases cell death. In addition umbilical cord mesenchymal stromal cells exposed to gestational diabetes have reduced glucose utilization and anti-cancerous ability while enhanced angiogenic ability. The mechanisms by which the hyperglycemia from the gestational diabetes impacts these changes in the hUC-MSCs is not clear. This study found reduced expression of an antiapoptic protein called BCL-xL in the hUC-MSCs exposed to gestational diabetes. In addition there was there was increased expression of genes related to blood vessel formation in the human umbilical vein endothelial cells exposed to gestational diabetes. A key gene involved in atherosclerosis (CD44) was under expressed in the GDM group. These studies suggest that GDM induces complex adverse effects on growth, angiogenic and anti-cancerous potential of human umbilical cord mesenchymal stromal cells and this may have long-term impact on the fetus.