Permanent implications of intrauterine growth restriction on cholesterol homeostasis

Abstract

Susceptibility to disease begins during fetal life, and adverse events in utero are a critical factor in determining quality of life and overall health. In fact, up to 50% of metabolic syndrome diseases can be attributed to an adverse in utero environment. However, the mechanisms linking impaired fetal development to augmented cholesterol, an important clinical risk factor characterizing the metabolic syndrome and cardiovascular disease, remain elusive. This review discusses the latest research in the fetal programming of cholesterol homeostasis from both clinical studies and animal models. It also underscores the role of the placenta as an important mediator in cholesterol homeostasis during pregnancy and uncovers some of the molecular mechanisms underlying how the homeostatic mechanisms in liver may be impaired in fetal and postnatal life due to undernutrition and/or hypoxia.