Endocrine Abstracts

Prenatal exposure to excess glucocorticoids may be causal in programming mood disorders in later life. In support of this hypothesis, maternal stress, treatment during pregnancy with dexamethasone (which crosses the placenta) or inhibitors of feto-placental 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), the physiological ‘barrier’ to maternal glucocorticoids, reduces birth weight and programmes offspring cardio-metabolic and affective behaviours. The e...

Prenatal glucocorticoid overexposure is a key risk factor for susceptibility to neuropsychiatric disorders in adult life. Fetal exposure to glucocorticoids is regulated by 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) an enzyme which inactivates glucocorticoids and is highly expressed in the placenta and fetus. Previous work has established that 11β-HSD2−/− offspring generated by heterozygous matings exhibit altered placental developm...

Fetal glucocorticoid exposure is a key mechanism involved in adverse programming outcomes in the adult, including hypertension, anxiety and insulin resistance. While glucocorticoids may exert their effects directly on the fetus, they may also affect fetal growth through indirect effects on placental function. Regulation of fetal glucococorticoid exposure is achieved by the placental glucocorticoid barrier, which involves glucocorticoid inactivation within the labyrinth zone of...

Background: The late gestational surge in glucocorticoids is vital for the maturation of fetal organs in preparation for birth and survival during the neonatal period. Metabolic maturation of cardiomyocytes involves a switch in fuel substrate from glucose utilization to fatty acid (FA) oxidation. In fetal cardiomyocytes, glucocorticoids induce expression of Ppargc1a (encoding PGC1a, a master regulator of mitochondrial capacity). We hypothesized that glucocorticoids pr...