Searchable abstracts of presentations at key conferences in endocrinology

ea0034p243 | Obesity, diabetes, metabolism and cardiovascular | SFEBES2014

Decreased brain 11β-HSD1 expression following inflammation; a role in regulating brain energy homeostasis?

Verma Manu , Zhang Zhenguang , Mackellar Annie , Seckl Jonathan , Holmes Megan , Chapman Karen

Chronically elevated glucocorticoid (GC) levels alter cognition and increase cardio-metabolic disease risk. Negative feedback suppression of the hypothalamic–pituitary–adrenal (HPA) axis, including at the hippocampus, maintains low/basal circulating GC levels. Intracellular GC can be increased, without alteration in circulating levels, by the activity of 11β-hydroxysteroid dehydrogenase type1 (11β-HSD1). In some tissues, 11β-HSD1 expression is increase...

ea0031oc1.2 | Young Endocrinologists prize session | SFEBES2013

Macrophage-specific 11β-hydroxysteroid dehydrogenase type 1 deficiency promotes angiogenesis but impairs resolution of K/BxN serum induced arthritis

Zhang Zhenguang , Coutinho Agnes , Hadoke Patrick , Salter Donald , Seckl Jonathan , Chapman Karen

Chronic inflammatory disease is often accompanied by angiogenesis and fibrosis. Glucocorticoids (GCs) exert anti-inflammatory and anti-angiogenic effects, in which macrophages are a major target. Local endogenous GC action is controlled by 11β-hydroxysteroid dehydrogenase (11β-HSD), with the type 1 isozyme, 11β-HSD1 converting inactive GCs into active forms. Mice deficient in 11β-HSD1 have a phenotype consistent with reduced glucocorticoid action, including...