Searchable abstracts of presentations at key conferences in endocrinology
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Society for Endocrinology BES 2013

Oral Communications

Obesity, metabolism and bone

ea0031oc4.1 | Obesity, metabolism and bone | SFEBES2013

Glucocorticoid receptor deficiency in cardiomyocytes causes pathological cardiac remodelling in mice

Richardson Rachel , Rog-Zielinska Ewa , Thomson Adrian , Moran Carmel , Kenyon Christopher , Gray Gillian , Chapman Karen

Variation in the glucocorticoid receptor (GR) gene associates with relative glucocorticoid resistance, hypertension and increased cardiovascular disease risk in humans. To investigate the contribution of cardiac GR to this phenotype we have characterised adult male mice with cardiomyocyte and vascular smooth muscle deletion of GR (SMGRKO) and have found left ventricular function to be impaired.SMGRKO mice, generated by crossing GR ‘floxed’ mice...

ea0031oc4.2 | Obesity, metabolism and bone | SFEBES2013

11β-HSD1 knockout mice are protected from the adverse metabolic effects of exogenous glucocorticoid excess

Morgan Stuart , Bujalska Iwona , Gathercole Laura , Hassan-Smith Zaki , Guest Phil , Abrahams Lianne , Stewart Paul , Lavery Gareth , Tomlinson Jeremy

Glucocorticoids (GC), such as prednisolone, are widely prescribed for their anti-inflammatory and immunosuppressive properties. However, they have significant side-effects including insulin resistance and hepatic steatosis. 11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) converts 11-dehydrocorticosterone (11DHC) to active corticosterone (CORT) and thus amplifies local GC action. We hypothesise that enhanced local GC regeneration of exogenously administered GCs by ...

ea0031oc4.3 | Obesity, metabolism and bone | SFEBES2013

Adult offspring of undernourished sheep exhibit epigenetic alterations in HPA axis glucocorticoid receptor

Begum Ghazala , Stevens Adam , Oliver Mark , Jaquiery Anne , Harding Jane , Challis John , Bloomfield Frank , White Anne

Maternal programming increases the risk of alterations in the offspring’s HPA axis. Previously we showed that maternal undernutrition in sheep induces epigenetic changes in the glucocorticoid receptors (GR) within hypothalamic energy balance pathways, without affecting HPA axis GR. However, these studies focussed on fetal tissues1. Here, we investigated whether GR is epigenetically altered in the HPA axis of adult offspring to determine the status of the pathwa...

ea0031oc4.4 | Obesity, metabolism and bone | SFEBES2013

Cholestatic pregnancy programmes metabolic disease in the offspring

Papacleovoulou Georgia , Abu-Hayyeh Shadi , Nikolopoulou Evanthia , Ovadia Caroline , Nikolova Vanya , Jarvelin Marjo-Riitta , Jansen Eugene , Albrecht Christiane , Marin Jose J G , Knisely Alex S , Williasmon Catherine

Epidemiological studies have identified the intrauterine environment as a major contributor to increased rates of metabolic disease in adults, but the underlying mechanisms are poorly understood. Intrahepatic cholestasis of pregnancy (ICP) is a common liver disease of pregnancy that affects 0.5–2% pregnant women and is characterised by increased bile acid (BA) levels in the maternal serum. The influence of ICP on the metabolic health of offspring is unknown.<p class="...

ea0031oc4.5 | Obesity, metabolism and bone | SFEBES2013

Energy intake following infusion of glucagon and GLP-1: a double-blind crossover study

Cegla Jaimini , Troke Rachel , Jones Ben , Tharakan George , McCullough Katherine , Wilde Julia , Lim Chung Thong , Parvizi Naseem , Hussein Mohamed , Minnion James , Cuenco Joyceline , Chambers Edward , Ghatei Mohammad , Tan Tricia , Bloom Stephen

Obesity is a growing global epidemic and current medical therapies have proven inadequate. Endogenous satiety hormones provide an attractive target for the development of drugs which aim to cause effective weight loss with minimal side effects. Two related peptide hormones, glucagon and glucagon-like peptide 1 (GLP-1), are the subject of this investigation. Both have been found to reduce appetite and cause weight loss. Additionally, glucagon increases energy expenditure. It is...

ea0031oc4.6 | Obesity, metabolism and bone | SFEBES2013

Transgenic disruption of 5α-reductase 1 increases susceptibility to liver fibrosis

Livingstone Dawn , Rees Georgina , Weldin Benjamin , MacFarlane David , Walker Brian , Andrew Ruth

5α-Reductase 1 (5aR1) catalyses A-ring reduction of glucocorticoids and androgens, predominantly in liver and modulates steroid hormone action. We previously demonstrated transgenic disruption of 5aR1 predisposes mice to developing fatty liver. Here we tested whether 5aR1 disruption increases susceptibility to the development of liver injury, using the carbon tetrachloride induced liver fibrosis model.Male 5aR1−/− (KO) mice and wild-type...

ea0031oc4.7 | Obesity, metabolism and bone | SFEBES2013

Familial hypocalciuric hypercalcaemia type 3 is caused by mutations in adaptor protein 2 sigma 1

Nesbit M Andrew , Hannan Fadil M , Howles Sarah A , Reed Anita A C , Cranston Treena , Thakker Clare E , Gregory Lorna , Rimmer Andrew J. , Rust Nigel , Graham Una , Morrison Patrick J , Hunter Steven J , Whyte Michael P , Thakker Rajesh V

Familial hypocalciuric hypercalcaemia (FHH) is an autosomal dominant disorder characterized by lifelong elevation of serum calcium concentrations with inappropriately low urinary calcium excretion. Three types referred to as FHH1, FHH2 and FHH3 and located on chromosomes 3q21.1, 19p and 19q13.3, respectively, have been reported. FHH1, caused by loss-of-function mutations of the calcium-sensing receptor (CaSR), accounts for >65% of FHH patients. To identify the gen...

ea0031oc4.8 | Obesity, metabolism and bone | SFEBES2013

Peptide YY regulates bone mineral content and strength

Brassill M J , Rahman S A , Boyde A , Batterham R L , Williams G R , Assett J H D B

Bone loss in anorexia nervosa and following bariatric surgery is associated with an elevated circulating concentration of the gastrointestinal anorexigenic hormone peptide YY (PYY), which acts principally via the Y1R and Y2R receptors. Selective deletion of Y1R in osteoblasts or Y2R in the hypothalamus results in high bone mass, but deletion of PYY has resulted in conflicting skeletal phenotypes leading to uncertainty regarding its role in the regulation of bone mass. We hypot...