Searchable abstracts of presentations at key conferences in endocrinology

ea0011p745 | Steroids | ECE2006

Tissue specific regulation of insulin signalling: a mechanism of glucocorticoid induced obesity?

Gathercole LL , Bujalska IJ , Stewart PM , Tomlinson JW

The pathological effects of glucocorticoids (GC) are exemplified by patients with Cushing’s syndrome who develop central obesity, insulin resistance and in some cases, type 2 diabetes mellitus. It is generally accepted that GC cause insulin resistance, however, both insulin and GC increase adipocyte differentiation. The question therefore arises as to how GC stimulate adipocyte differentiation whilst apparently making adipocytes insulin resistant. We have hypothesized tha...

ea0019oc5 | Young Endocrinologist prize session | SFEBES2009

Selective inhibition of 11β-hydroxysteroid dehydrogenase type 1 improves insulin sensitivity in skeletal muscle through modulation of IRS1 serine phosphorylation

Morgan SA , Gathercole LL , Lavery GG , Sherlock M , Bujalska IJ , Sethi JK , Hegyi K , Stewart PM , Smith DM , Tomlinson JW

Glucocorticoid (GC) excess is characterized by increased adiposity, skeletal myopathy and insulin resistance. Despite increasing use of GCs as therapeutic agents, the precise molecular mechanisms that underpin GC-induced insulin resistance are unknown. Within skeletal muscle, 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) converts cortisone (11-dehydrocorticosterone in rodents) to the active GC, cortisol (corticosterone in rodents) and thus amplifies local GC act...