Placental function in maternal obesity.
Placental function in maternal obesity.
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DOI:
10.1042/cs20190266
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发表时间:
2020-04-30
期刊:
影响因子:
--
通讯作者:
Jansson T
中科院分区:
文献类型:
--
作者:
Kelly AC;Powell TL;Jansson T
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 are expected to activate mTOR signalling 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. Interventions that specifically target placental function, such as activation of placental adiponectin receptors, may prevent the transmission of metabolic disease from obese women giving birth to large babies to the next generation. The majority of obese women give birth to normal sized infants and these pregnancies are associated with activation of inflammatory signalling pathways, oxidative stress, decreased oxidative phosphorylation and lipid accumulation in the placenta. Recent bioinformatics approaches expand these alterations to include novel targets, however how placental changes in obese women giving birth to normal sized babies are linked to poor short and long-term infant outcomes is unclear.