Maternal obesity and placental function: impaired maternal-fetal axis.
Frank LouwenNina-Naomi KreisAndreas RitterJuping YuanPublished in: Archives of gynecology and obstetrics (2024)
The prevalence of maternal obesity rapidly increases, which represents a major public health concern worldwide. Maternal obesity is characteristic by metabolic dysfunction and chronic inflammation. It is associated with health problems in both mother and offspring. Increasing evidence indicates that the placenta is an axis connecting maternal obesity with poor outcomes in the offspring. In this brief review, we have summarized the current data regarding deregulated placental function in maternal obesity. The data show that maternal obesity induces numerous placental defects, including lipid and glucose metabolism, stress response, inflammation, immune regulation and epigenetics. These placental defects affect each other and result in a stressful intrauterine environment, which transduces and mediates the adverse effects of maternal obesity to the fetus. Further investigations are required to explore the exact molecular alterations in the placenta in maternal obesity, which may pave the way to develop specific interventions for preventing epigenetic and metabolic programming in the fetus.
Keyphrases
- birth weight
- weight gain
- insulin resistance
- metabolic syndrome
- weight loss
- high fat diet induced
- type diabetes
- public health
- pregnancy outcomes
- oxidative stress
- high fat diet
- body mass index
- healthcare
- gene expression
- gestational age
- skeletal muscle
- emergency department
- electronic health record
- dna methylation
- machine learning
- physical activity
- deep learning
- molecular dynamics
- artificial intelligence
- glycemic control
- preterm birth