Published online Mar 15, 2015. doi: 10.4239/wjd.v6.i2.338
Peer-review started: August 14, 2014
First decision: November 3, 2014
Revised: December 15, 2014
Accepted: December 29, 2014
Article in press: December 31, 2014
Published online: March 15, 2015
Processing time: 217 Days and 15.3 Hours
Diabetes mellitus (DM) is a health condition characterized by hyperglycemia over a prolonged period. There are three main types of DM: DM type 1 (DM1), DM2 and gestational DM (GDM). Maternal diabetes, which includes the occurrence of DM1 and DM2 during pregnancy or GDM, increases the occurrence of gesttional complications and adverse fetal outcomes. The hyperglycemic intrauterine environment affects not only the fetus but also the placental development and function in humans and experimental rodents. The underlying mechanisms are still unclear, but some evidence indicates alterations in trophoblast proliferation, apoptosis and cell cycle control in diabetes. A proper coordination of trophoblast proliferation, differentiation and invasion is required for placental development. Initially, increased expression of proliferative markers in junctional and labyrinth zones of rat placentas and villous cytotrophoblast, syncytiotrophoblast, stromal cells and fetal endothelial cells in human placentas is reported among diabetics. Moreover, reduced apoptotic index and expression of some apoptotic genes are described in placentas of GDM women. In addition, cell cycle regulators including cyclins and cyclin-dependent kinase inhibitors seem to be affected by the hyperglycemic environment. More studies are necessary to check the balance between proliferation, apoptosis and differentiation in trophoblast cells during maternal diabetes.
Core tip: This review article focuses on current knowledge about the effects of diabetes on trophoblast function such as proliferation, apoptosis and cell cycle control during placental development in human and rodent animal models. It also briefly discusses some placental pathological findings as a consequence of altered metabolic environment during diabetes.