Clinically, we apply synthetic glucocorticoids to treat fetal and maternal diseases, such as premature labor and autoimmune diseases. Although its clinical efficacy is positive, the fetus will be exposed to exogenous synthetic glucocorticoids. Prenatal adverse environments (such as xenobiotics exposure, malnutrition, infection, hypoxia and stress) can cause fetuses overexposure to excessive endogenous maternal glucocorticoids. The level of glucocorticoids is the key to fetal tissue maturation and postnatal fate. A large number of studies have found that prenatal glucocorticoids exposure can lead to fetal adrenal dysplasia and dysfunction, continuing after birth and even into adulthood. As the core organ of fetal-originated adult diseases, fetal adrenal dysplasia is closely related to the susceptibility and occurrence of multiple chronic diseases, and there are also obvious gender differences. However, its intrauterine programming mechanisms have not been fully elucidated. This review summarizes recent advances in prenatal glucocorticoids exposure and fetal adrenal developmental programming alterations, which is of great significance for explaining adrenal developmental toxicity and the intrauterine origin of fetal-originated adult diseases.
Keywords: Adrenal; Epigenetic mechanism; Gender differences; Glucocorticoid - insulin like growth 1 axis; Glucocorticoids; Intrauterine programming.
Copyright © 2019 Elsevier B.V. All rights reserved.