Placental function in maternal obesity
Year: 2020
Type: review
Abstract: Maternal obesity is associated with pregnancy complications and increases the risk for the infant to develop obesity, diabetes and cardiovascular disease later in life. However, the mechanisms linking the maternal obesogenic environment to adverse short- and long-term outcomes remain poorly understood. As compared with pregnant women with normal BMI, women entering pregnancy obese have more pronounced insulin resistance, higher circulating plasma insulin, leptin, IGF-1, lipids and possibly proinflammatory cytokines and lower plasma adiponectin. Importantly, the changes in maternal levels of nutrients, growth factors and hormones in maternal obesity modulate placental function. For example, high insulin, leptin, IGF-1 and low adiponectin in obese pregnant women activate mTOR signaling in the placenta, promoting protein synthesis, mitochondrial function and nutrient transport. These changes are believed to increase fetal nutrient supply and contribute to fetal overgrowth and/or adiposity in offspring, which increases the risk to develop disease later in life. However, the majority of obese women give birth to normal weight infants and these pregnancies are also associated with activation of inflammatory signaling pathways, oxidative stress, decreased oxidative phosphorylation and lipid accumulation in the placenta. Recent bioinformatics approaches have expanded our understanding of how maternal obesity affects the placenta; however, the link between changes in placental function and adverse outcomes in obese women giving birth to normal sized infants is unclear. Interventions that specifically target placental function, such as activation of placental adiponectin receptors, may prevent the transmission of metabolic disease from obese women to the next generation.
Source: Clinical Science
DOI: 10.1042/cs20190266
Authors: Amy C. Kelly, Theresa L. Powell, Thomas Jansson
Institution: University of Colorado Anschutz
Language: English
Field: Medicine
Domain: Health Sciences
Open Access status: green
Awards: mTOR as a trophoblast folate sensor, G2737757659, Regulation of IGFBP-1 Phosphorylation in Fetal Development, Placental adiponectin signaling and fetal programming in maternal obesity, Decidual nutrient sensing and IGFBP-1 phosphorylation in placental insufficiency, Trophoblast mTOR: a critical hub linking maternal nutrient supply to placental function, fetal growth and fetal islet function, Training in Perinatal Medicine
OpenAlex ID: W3017172592