The placenta: when is it affected in maternal diabetes?

Abstract

Maternal diabetes can lead to placental alterations that affect both maternal and fetal health. Although these alterations are mostly evidenced in the second and third trimesters of pregnancy, due to failures in the hematotrophic nutrition necessary for the development and growth of the fetus, they can originate early in pregnancy. In fact, the placenta is an organ that begins to develop at implantation. Therefore, preconceptional maternal health is relevant, and patients with pregestational diabetes (DM1 and DM2) or early gestational diabetes, and even those with risk factors for developing gestational diabetes, may be at increased risk for alterations in placental development and subsequent function.

During the first trimester of pregnancy, when the placenta is developing, the function of the decidua (endometrium of the pregnancy) is critical in providing the histotrophic nutrition and the microenvironment necessary for the proper development of both the embryo and the placenta. If this environment is pro-oxidant and pro-inflammatory, or if the mother has metabolic alterations that prevent proper histotrophic decidual function, placental development may be compromised, with consequences that will be evident at the fetal level, and may lead to decidual alterations in the next generation, as shown by studies in experimental models of diabetes. Our results show that maternal diets rich in unsaturated fatty acids improve prooxidant, proinflammatory and nutritional function-related parameters in the placenta at term of women with gestational diabetes, and that these diets prevent abnormalities in decidual function, feto-placental development and adverse programming of decidual function in the offspring in experimental models of diabetes.