PMC:3852299 / 41324-42896 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/3852299","sourcedb":"PMC","sourceid":"3852299","source_url":"http://www.ncbi.nlm.nih.gov/pmc/3852299","text":"Cortisol and the placenta\nIn mammals glucocorticoids are central to fetal growth, tissue development and maturation of various organs [230]. Supraphysiological levels of glucocorticoids cause fetal growth retardation in mammalian models and humans, and reduced intrauterine growth is associated with high maternal and fetal concentrations of glucocorticoids [231,232]. Glucocorticoids are lipophilic and readily cross the placenta, and in rat studies prenatal exposure to the synthetic glucocorticoids dexamethasone or betamethasone reduces birth weight [233]. Normally, fetal physiological glucocorticoid levels are lower than the maternal levels [234]. This gradient is achieved by fetoplacental 11β-HSD2, which metabolises cortisol [235]. This barrier is not impervious and as such a minor percentage of maternal cortisol crosses to the fetus [236]. The efficiency of placental 11β-HSD2 varies considerably [233,237] where the lowest placental 11β-HSD2 activity and presumably, highest fetal exposure to glucocorticoids, results in lower birth weights [223,237].\nSome children diagnosed with ASD or who have higher scores on ASD spectrum screening have low birth weights [20,238,239], which could be an outcome of elevated cortisol levels that occur during the prenatal period. Furthermore, the placenta of female fetuses have increased glucocorticoid inactivation and lower corticoid receptor density than the placentas of males [240], which may render males more vulnerable to elevated maternal cortisol levels and explain gender differences in the prevalence of 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