Endocrine Abstracts

Glucocorticoids have profound effects in development, altering cell proliferation, differentiation, migration and network formation. It has been shown that the developing fetus is protected from high maternal glucocorticoid levels by the presence of 11beta-HSD2 in the placenta and if this enzyme is inhibited, programmed changes of adult health are observed (hypertension, hyperglycaemia, insulin resistance). The developing brain is a sensitive target for glucocorticoids and hen...

Adverse events in utero permanently alter the structure and physiology of adult offspring, a phenomenon termed 'foetal programming'. In particular, low birth-weight is associated with an increased risk of adulthood hypertension. Glucocorticoid (GC) administration during pregnancy reduces offspring birth-weight and GCs directly elevate blood pressure (BP) in both humans and rodents. Circulating and local renin-angiotensin-aldosterone (RAAS) system(s) may be involved in programm...

Metabolic Syndrome (visceral obesity, insulin resistance, type2 diabetes) resembles Cushing's syndrome, but lacks elevated circulating cortisol levels. This has engendered the hypothesis that excessive local glucocorticoid regeneration, resulting from elevated adipose 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD-1) underlies the Metabolic Syndrome. We report that 11beta-HSD-1 nullizygosity (11beta-HSD-1-/-) reduced intra-adipose corticosterone levels and i...