Searchable abstracts of presentations at key conferences in endocrinology

ea0028s9.3 | Developmental programming of endocrine disease | SFEBES2012

The fetus or the placenta? Targets of glucocorticoid programming

Holmes Megan , Wyrwoll Caitlin , Seckl Jonathan

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...

ea0025oc5.5 | Reproduction and fetal programming | SFEBES2011

Absence of 11β-HSD2 specifically within the fetal brain alters adult ‘depressive' behaviour

Wyrwoll Caitlin , Seckl Jonathan , Holmes Megan

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...

ea0015oc5 | Young Endocrinologist prize session | SFEBES2008

Placental vascular development and nutrient transport in 11β-HSD2−/− mice

Wyrwoll Caitlin , Seckl Jonathan , Holmes Megan

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...

ea0065op1.2 | Adrenal and Cardiovascular | SFEBES2019

Glucocorticoids promote mitochondrial fatty acid oxidation in the fetal heart

Urquijo Helena , Panting Emma N , Carter Roderick N , Agnew Emma J , Wyrwoll Caitlin S , Morton Nicholas M , Chapman Karen E , Ivy Jessica R

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...