Endocrine Abstracts

Introduction: Regulation of adiponectin in GH deficiency (GHD), which presents visceral obesity, is still a matter of debate. No studies have evaluated circulating adiponectin isoforms in adult GHD subjects. Aim of this study was to evaluate total adiponectin (TA) and its isoforms (high molecular weight: HMW, medium molecular weight: MMW, low molecular weight: LMW) in hypopituitary adult subjects with and without GHD, in relation to weight, IGF1 and GH levels.<p class="abs...

Introduction: Resistance to thyroid hormone (RTH) is a dominantly inherited syndrome, first identified in 1967 by Refetoff, characterized by reduced organ responsiveness to thyroid hormone. The most typical pattern being an elevated serum free T4 (fT4) concentration in association with non-suppressed TSH, usually accompanied by high serum levels of free T3 (fT3), with a considerable inter-individual variation and heterogeneous phenotype. The most frequent defect which causes R...

Introduction: A rise in serum insulin levels during GH therapy is reported. Insulin resistance is a risk factor for type 2 diabetes, atherosclerosis, dyslipidemia, and hypertension. Few data describe insulin secretion and lipids after the end of GH therapy.Subjects and methods: Aim of our study was to evaluate changes in insulin secretion, sensitivity and lipid profile in children with isolated GHD longitudinally followed during rhGH treatment. We measur...

Introduction: Obesity and connected metabolic alterations are a growing problem in paediatric age, but few data are available in the youngest population. Poor evidences on metabolic syndrome (MS) definition are present in childhood and the most used definitions are those of the modified National Cholesterol Education Program and of the International Diabetes Federation (IDF). Aim of our study was to evaluate the presence of MS in obese children using these two definitions and ...

Physiological role of acylated ghrelin (AG), unacylated ghrelin (UAG) and obestatin is poorly understood especially in childhood. To understand their biological implications in obesity and metabolic syndrome (MS), we measured AG, UAG, obestatin, at fasting and every 60′ during oral glucose tolerance test (OGTT) in 60 prepubertal (PP–OB; 32) and pubertal (P-OB; 28) children. Paediatric IDF 2007 criteria was used to identifying MS. In PP-OB group, 20 (62.5%) children ...

Growth hormone (GH) secretion is regulated by a complex interplay between GH-releasing hormone (GHRH), somatostatin and several other central and peripheral modulatory signals. Ghrelin has been hypothesized as physiological amplifier of GH pulsatility and acts via mechanisms, at least partially, independent of GHRH and somatostatin. The GH response to GHRH is strongly inhibited by previous administration of recombinant human GH (rhGH), likely as a consequence of a somatostatin...

Both hyper- and hypothyroidism show reduced spontaneous and GHRH-stimulated GH secretion. Although impaired GHRH secretion and activity as well as reduced GH pituitary synthesis have been reported in these pathological conditions, a definitive description of the underlying pathophysiological mechanisms have not been provided yet. Ghrelin elicits a potent GH-releasing effect partially mediated by a functional somatostatin antagonism and a synergic interaction with GHRH. Moreove...

Despite the common clinical opinion that thyrotoxicosis is associated with quantitative and qualitative sleep alterations, at present, an objective evaluation of sleep quality and quantity in this clinical condition has never been performed so far. Based on this foregoing, in order to perform a qualitative and quantitative description of sleep in this clinical condition, we enrolled 6 normal-weighted patients suffering from naïve overt hyperthyroidism due to Basedow Disea...

ContextGenetic obesity, including syndromic and non-syndromic forms, represent a minority of cases but gene dysregulations make their management particularly difficult. Among them, Beckwith–Wiedemann syndrome (BWS) is a multisystem human genomic imprinting disorder characterized by overgrowth, macroglossia, abdominal wall defects, hemi hyperplasia, enlarged abdominal organs, and an increased risk of embryonal tumours. The syndrome is caused by genet...

Background: Multiple endocrine neoplasia type 1 (MEN1) is a rare hereditary autosomal dominant tumor syndrome caused by inactivating mutations of the tumor suppressor gene MEN1 which encodes the protein menin. It is characterized by the occurrence of tumors involving two or more endocrine glands, primarily parathyroid, entero-pancreatic, and anterior pituitary, as well as non-endocrine neoplasms. Glucagonomas occur in fewer than 3% of patients with MEN1, causing hyper...