Searchable abstracts of presentations at key conferences in endocrinology

ea0044p177 | Obesity and Metabolism | SFEBES2016

Glucocorticoid treatment rapidly increases AgRP and food intake with delayed effects on other metabolic systems

Harno Erika , Davies Alison , Allen Tiffany-Jayne , Sefton Charlotte , Wray Jonathan R , Ramamoorthy Thanuja Gali , Coll Anthony P , White Anne

Glucocorticoids are widely prescribed therapeutic agents, however long term treatment can cause increased morbidity from adverse metabolic events, including weight gain and hyperglycaemia. The mechanisms and site of action which underpin these side-effects are not fully understood. The aim of this study was to characterise phenotypic, biochemical and neurohormonal responses in mice administered corticosterone, with a particular focus on changes seen in the early stages of chro...

ea0059oc3.4 | Obesity & diabetes | SFEBES2018

Knockout of glucocorticoid receptor on AgRP/NPY/GABA (ANG) neurons identifies a potential role for this neuronal population in mediating glucocorticoid–induced insulin resistance in female mice

Harno Erika , Davies Alison , Allen Tiffany-Jayne , Sefton Charlotte , Wray Jonathan R , Coll Anthony P , White Anne

Glucocorticoids (Gcs) are used in the treatment of inflammatory disorders including asthma and rheumatoid arthritis. However, long-term use can cause metabolic side-effects including obesity and diabetes. Previous studies have shown that Gcs increase Agrp expression and that AgRP/NPY/GABA (ANG) neurons can regulate appetite and insulin sensitivity. To investigate the effects of chronic Gc treatment directly on ANG neurons, we crossed AgRP-IRES-Cre with GR...

ea0059p171 | Obesity & metabolism | SFEBES2018

Glucocorticoid-induced metabolic syndrome: establishing the role of AgRP

Sefton Charlotte , Harno Erika , Davies Alison , Allen Tiffany-Jayne , Wray Jonathan R , Coll Anthony P , White Anne

Glucocorticoid (Gc) excess, either from endogenous overproduction in disorders of the hypothalamic-pituitary-adrenal axis or exogenous medical therapy, is recognized to cause adverse metabolic side effects including obesity, hyperphagia, and hyperglycemia. The Gc receptor (GR) is widely expressed in the brain including the hypothalamus which is known to regulate energy balance. We have previously established through the administration of corticosterone (Cort) in the drinking w...

ea0038p218 | Obesity, diabetes, metabolism and cardiovascular | SFEBES2015

Glucocorticoid excess increases hypothalamic AgRP and results in obesity and hyperinsulinaemia in mice

Wray Jonathan , Harno Erika , Davies Alison , Sefton Charlotte , Ramamoorthy Thanuja Gali , Allen Tiffany-Jayne , Coll Anthony P , White Anne

Glucocorticoids (Gcs) are widely prescribed to treat a number of conditions, such as arthritis and asthma. However, patients receiving Gcs often develop metabolic complications such as obesity and hyperglycaemia. The aim of this study was to investigate the molecular mechanisms in the hypothalamus which drive these adverse effects. Male C57BL/6J mice were given ad libitum access to either corticosterone (CORT; 75 μg/ml) or vehicle (V; 1% ethanol) in their drinkin...

ea0038p239 | Obesity, diabetes, metabolism and cardiovascular | SFEBES2015

Hypothalamic glucocorticoid levels increase in an in vivo model of glucocorticoid-induced obesity and hyperinsulinaemia

Sefton Charlotte , Harno Erika , Davies Alison , Small Helen , Allen Tiffany-Jayne , Wray Jonathan , Ramamoorthy Thanuja Gali , Coll Anthony P , White Anne

Glucocorticoid (Gc) excess, either endogenously produced (Cushing’s syndrome) or as a result of exogenous steroid treatment, can cause metabolic disorders such as obesity and hyperglycaemia. The contribution of centrally acting corticosterone in the development of these metabolic disorders is unknown. Gcs regulate the anorexigenic and orexigenic neuropeptides (POMC and AgRP) within the arcuate nucleus of the hypothalamus to modulate energy balance. This study investigated...