An Overview of Obesity, Cholesterol, and Systemic Inflammation in Preeclampsia

Abstract

Preeclampsia (PE), an inflammatory state during pregnancy, is a significant cause of maternal and fetal morbidity and mortality. Adverse outcomes associated with PE include hypertension, proteinuria, uterine/placental abnormalities, fetal growth restriction, and pre-term birth. Women with obesity have an increased risk of developing PE likely due to impaired placental development from altered metabolic homeostasis. Inflammatory cytokines from maternal adipose tissue and circulating cholesterol have been linked to systemic inflammation, hypertension, and other adverse outcomes associated with PE. This review will summarize the current knowledge on the role of nutrients, obesity, and cholesterol signaling in PE with an emphasis on findings from preclinical models.

Keywords: cholesterol; cytokines; hypertension; inflammation; leptin; metabolic abnormalities; obesity; preeclampsia.

Figure 1

Maternal obesity and dyslipidemia promotes preeclampsia through abnormal placental development. The liver oxidizes lipids and excess lipids are shunted to adipose tissue for storage. As adipocytes become hypertrophic in obesity, there is an increase in leptin, total cholesterol, as well as low-density lipoproteins (LDL) in the maternal circulation. This increase in lipid accumulation and dyslipidemia results in endothelial dysfunction and an overall increase in inflammation with increased weight gain during pregnancy, which may contribute to improper vascularization of the placenta and adverse outcomes associated with preeclampsia: elevated maternal blood pressure and fetal growth restriction. Made with BioRender.com (accessed on 11 May 2022).