Searchable abstracts of presentations at key conferences in endocrinology

ea0099p219 | Adrenal and Cardiovascular Endocrinology | ECE2024

11β-hydroxysteroid dehydrogenase type 1 inhibition unmasks multiple pathways that may mitigate the adverse effects of prescribed prednisolone

Pofi Riccardo , Coll Sergi , Othonos Nantia , Miller Hamish , Potter Tom , Escott Jane , Whittaker Andrew , Monfort Nuria , Ventura Rosa , Tomlinson Jeremy

Background: Prednisolone is the most commonly prescribed exogenous glucocorticoid(GC) and its use is frequently associated with the development of iatrogenic Cushing’s Syndrome. Once administered, prednisolone is rapidly converted to inactive prednisone by renal 11β-hydroxysteroid dehydrogenase type 2(11β-HSD2) and subsequently reactivated by 11β-HSD1. We have shown previously that 11β-HSD1 inhibition(with the selective 11β-HSD1 inhibitor, AZD4017...

ea0070oc3.6 | Diabetes, Obesity, Metabolism and Nutrition | ECE2020

11β-Hydroxysteroid dehydrogenase type 1 inhibition protects against the development of adverse metabolic and bone effects of prednisolone: A randomized, double-blind, placebo-controlled trial

Othonos Nantia , Pofi Riccardo , Arvaniti Anastasia , Whittaker Andrew , Stewart Paul , Coleman Ruth , Agbaje Olorunsola , Milton Joanne , Holman Rury , Tomlinson Jeremy W

Glucocorticoids (GC) are commonly prescribed, but their use is associated with significant adverse metabolic and bone effects. 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) regenerates active GC within tissues, tightly controlling the availability of GC to bind and activate the GC receptor; Our preclinical data have shown that 11β-HSD1 knock out mice resist the adverse effects of exogenous GC excess. We have now conducted a randomized, double-blind, placebo...

ea0094oc5.6 | Adrenal and Cardiovascular | SFEBES2023

11βHSD1 inhibition improves cardiac function compared to standard therapy in a translational pig mode through regulation of extracellular matrix

Al Disi Sara , Ascione Raimondo , Johnson Tom , Sammut Eva , Domenico Bruno Vito , Khan Shazia , Singh Trisha , Baz Lopez Daniel , James Carol-Ann , Walker Brian , Mills Nicholas , Webster Scott , Freeman Adrian , Whittaker Andrew , Andrew Ruth , Gray Gillian

Glucocorticoids (GCs) protect cardiomyocytes immediately after myocardial infarction (MI), but GCs subsequently regenerated within the heart by 11β-hydroxysteroid dehydrogenase 1 (11βHSD1) are detrimental during infarct repair, with functional outcomes post-MI improved in mice lacking 11βHSD1. Pharmacological 11βHSD1 inhibition (AZD8329 50mg/kg, 11βHSD1i) was compared to standard clinical therapy (SCT) in a translational pig model (female, 11βHSD1...