Searchable abstracts of presentations at key conferences in endocrinology

ea0028s5.2 | Sprint or marathon: muscling in on the Olympics | SFEBES2012

Exercise effects on fat metabolism and insulin sensitivity in human muscle

Wagenmakers Anton , Shepherd Sam , van Loon Luc , Shaw Christopher

There is an accumulating amount of evidence that the metabolic adaptations to endurance exercise that result in increased intramuscular triglyceride (IMTG) stores and IMTG oxidation during exercise, also exert a protective effect on muscle insulin sensitivity. This seems to be a contradiction (known as the athlete's paradox) as large IMTG stores in sedentary and obese individuals coexist with high levels of fatty acid (FA) metabolites (specifically long-chain acylCoA, DAG and ...

ea0037gp.04.01 | Steroids | ECE2015

Dual 5α-reductase inhibition causes hepatic lipid accumulation in man

Hazlehurst Jonathan , Oprescu Andrei , Nikolaou Nikolaos , Grinbergs Annabel , Davies Nigel , Flintham Robert , Hughes Beverley , Taylor Angela , Yu Jinglei , Wagenmakers Anton , Tomlinson Jeremy

5α reductases 1 and 2 (SRD5A1 and SRD5A2) metabolise cortisol into inactive 5α-dihydrocortisol contributing to the regulation of cortisol availability in addition to their established role in the generation of dihydrotestosterone from testosterone. Dutasteride and finasteride are commonly prescribed to patients with benign prostatic hyperplasia but their potential metabolic effects have only recently been identified. Dutasteride inhibits both SRD5A1and SRD5A2 whilst ...

ea0021oc1.8 | Diabetes and metabolism | SFEBES2009

Cortisol metabolism and hepatic expression of 11β-hydroxysteroid dehydrogenase type 1 in patients with non-alcoholic fatty liver disease

Ahmed Adeeba , Brady Theresa , Bailey Claire , Guest Phillip , Wagenmakers Anton , Newsome Phillip , Hubscher Stephan , Elias Elwyn , Adams David , Tomlinson Jeremy , Stewart Paul

Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome. The role of glucocorticoids (GC) in its pathogenesis, is highlighted in patients with GC excess, Cushing’s syndrome, who develop central adiposity, insulin resistance and in 20% of cases, NAFLD. Although circulating cortisol levels are normal in patients with NAFLD, hepatic cortisol availability is controlled by enzymes that regenerate cortisol from inactive cortisone (11&#94...