Searchable abstracts of presentations at key conferences in endocrinology

ea0038p383 | Steroids | SFEBES2015

Adrenocortical function in glucocorticoid receptor deficient mice

Mohammadi-Zaniani Ghazaleh , Richardson Rachel , Morley Steve , Chapman Karen , Kenyon Chris

Introduction: Humans with glucocorticoid receptor (GR) deficiency and global heterozygous GR knockout (GR+/−) show compensatory activation of the hypothalamic-pituitary-adrenal axis, resulting in salt-sensitive hypertension due to increased mineralocorticoid activity. Previous studies suggest renal mechanisms, including changes in cell proliferation, gene expression and electrolyte transport, may contribute to this phenotype but underlying adaptive adrenal responses have...

ea0037ep74 | Adrenal cortex | ECE2015

An audit of the investigation and follow up of adrenal incidentalomas

McElwaine Fred , Ellis Peter , McCance David , Bell Patrick , Hunter Steven , Courtney Hamish , Mullan Karen

An adrenal incidentaloma is defined as an adrenal mass >1 cm diameter, discovered serendipitously on radiological imaging done for another reason. They are important because a percentage will turn out to be malignant or secrete excess hormones. The aim of the current study was to ascertain if these lesions were being investigated and followed appropriately compared to American Association of Clinical Endocrinologists guidelines. All imaging reports for the calendar year 20...

ea0037ep812 | Pituitary: clinical | ECE2015

Is there a role for the 24 h GH profile in the assessment of acromegaly?

D'arcy Robert , Bell Patrick , Courtney Hamish , McCance David , Hunter Steven , Mullan Karen

Recent Endocrine Society guidelines advocate IGF-1, random GH and nadir GH after oral glucose tolerance test (OGTT) for assessment in acromegaly. In our regional centre the 24 h GH profile has also been used partly because of changing IGF-1 assay methodology but also because of concerns that IGF-1 may not adequately reflect partial therapeutic success. We evaluated 58 GH profiles in 35 patients from April 2008 to November 2012 when both GH and IGF-1 assays remained unchanged. ...

ea0037ep1051 | Thyroid (non-cancer) | ECE2015

Seaweed derived gaseous iodine: a source of iodine intake in coastal communities?

Smyth Peter , Burns Robert , Casey Michael , Andersson Maria , Mullan Karen , O'Dowd Colin

This communication tests the hypothesis that iodine (I2) gas or iodine oxides released from seaweeds previously shown to enhance atmospheric iodine adjacent to seaweed hotspots, may through being inspired by respiration, supply a significant fraction of daily iodine requirements. This could assume importance in a country such as Ireland where iodised salt availability is <5%. Iodine intake was assessed by measuring urinary iodine (UI) excretion using a dry ashing technique...

ea0036P64 | (1) | BSPED2014

Cellular proliferation is increased in both the lesion and non-lesion pancreas in focal congenital hyperinsulinism

Mohamed Zainaba , Han Bing , Newbould Melanie , Cosgrove Karen , Padidela Raja , Banerjee Indraneel , Dunne Mark J

Introduction: Focal congenital hyperinsulinism (F-CHI) is caused by dual-hit pathology, comprising a paternally-inherited ABCC8/KCNJ11 mutation and somatic loss of the maternal allele at chromosome 11p15. This leads to dysregulation of insulin secretion and β-cell overgrowth with a focal domain.Objectives: To compare the proliferative index (PI) of the F-CHI lesion and non-lesion pancreatic tissues to age-matched control pancreata and insul...

ea0036P66 | (1) | BSPED2014

Growth characteristics in children with Temple syndrome: an under-diagnosed imprinting disorder

Lokulo-Sodipe Kemi , Ioannides Yiannis , Davies Justin H , Karen Temple I

Background: Temple syndrome (TS) is a disorder caused by dysregulation of imprinted genes at chromosome 14q32. It is important to distinguish the growth pattern from other imprinting disorders such as Russell–Silver and Prader–Willi syndromes.Aims: To describe the growth pattern in TS.Methods: 51 cases were identified from 11 countries. Height, weight, birth weight and head circumference were converted to SDS using countr...

ea0035p771 | Obesity | ECE2014

Adipocyte fatty acid binding protein (A-FABP) deficiency promotes diet-induced obesity partially via its regulation on adaptive thermogenesis

LingLing Shu , PuiZhi Lee , Mi Zhou , Karen S L Lam , AiMin Xu , Ruby L C Hoo

Introduction: Adipocyte fatty acid binding protein (A-FABP) is a fatty acid chaperone that facilitates the efflux of free fatty acid from cytoplasm into circulation. Previous studies show that A-FABP knockout (KO) mice are more susceptible to diet-induced obesity comparing to wild type (WT) littermates. Here we investigate the underlying mechanism of A-FABP in the regulation of diet-induced obesity.Methods: A-FABP KO mice and their WT littermates were fe...

ea0035p779 | Obesity | ECE2014

The adaptor protein APPL2 acts as a central regulator of energy metabolism

Wang Baile , Cheng Kenneth KY , Li Xiaomu , Lam Karen SL , Xu Aimin

Introduction: We have previously demonstrated that APPL1 maintains glucose homeostasis by promoting both actions and secretion of insulin. Although APPL2 is a close homolog of APPL1, the physiological function of APPL2 is vaguely characterized. Thus, we generated a knockout (KO) mouse model in which APPL2 is deleted in pancreatic β-cells and hypothalamus (which is called APPL2 KO mice) to investigate its role in glucose and energy metabolism.Methods...

ea0034oc2.4 | Endocrine regulation of cell behaviour | SFEBES2014

Influence of glucocorticoid receptor density on development and remodeling of the heart

Richardson Rachel , Rog-Zielinska Eva , Thomson Adrian , Moran Carmel , Gray Gillian , Chapman Karen

Variation in the human glucocorticoid receptor (GR) gene associates with relative glucocorticoid resistance, hypertension and increased cardiovascular disease risk. Mice heterozygous for a null GR mutation (GR+/−) are also glucocorticoid resistant with raised circulating glucocorticoid levels and elevated blood pressure in adulthood. We have characterised the cardiac phenotype of these mice throughout development and investigated their response to cardiovascul...

ea0034p243 | Obesity, diabetes, metabolism and cardiovascular | SFEBES2014

Decreased brain 11β-HSD1 expression following inflammation; a role in regulating brain energy homeostasis?

Verma Manu , Zhang Zhenguang , Mackellar Annie , Seckl Jonathan , Holmes Megan , Chapman Karen

Chronically elevated glucocorticoid (GC) levels alter cognition and increase cardio-metabolic disease risk. Negative feedback suppression of the hypothalamic–pituitary–adrenal (HPA) axis, including at the hippocampus, maintains low/basal circulating GC levels. Intracellular GC can be increased, without alteration in circulating levels, by the activity of 11β-hydroxysteroid dehydrogenase type1 (11β-HSD1). In some tissues, 11β-HSD1 expression is increase...