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adrenocortical hyperfunction/obesità
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Pagina 1 a partire dal 375 risultati
Involvement of glucagon-like peptide 1 in the glucose homeostasis regulation in obese and pituitary-dependent hyperadrenocorticism affected dogs.
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The incretin glucagon-like peptide 1 (GLP-1) enhances insulin secretion. The aim of this study was to assess GLP-1, glucose and insulin concentrations, Homeostatic Model Assessment (HOMA insulin sensitivity and HOMA β-cell function) in dogs with pituitary-dependent hyperadrenocorticism (PDH), and
Is there visceral adipose tissue (VAT) intracellular hypercortisolism in human obesity?
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The fact that obesity is a prominent feature of Cushing's syndrome (systemic hypercortisolism of adrenocortical origin) stimulated a 40-year search for evidence of systemic hypercortisolism in human obesity. That search has failed to find such evidence. For the past 15 years, however, studies have
Hypercortisolism and obesity.
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Obesity is a multifactorial heterogenous condition. The location of excess fat on the body determines the risk of morbidity and mortality for significant disease. Visceral, or intraabdominal, fat is the fat depot most highly associated with illness and death from cardiocerebrovascular disease and
Hypercorticism and manganese metabolism in brown adipose tissue of the obese mouse.
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In ob/ob mice, we showed previously that brown adipose tissue (BAT) has an abnormally low manganese (Mn) content associated with low Mn-superoxide dismutase (MnSOD) and succinate dehydrogenase (SDH) activities. These anomalies can be corrected partially by supplementing the diet with Mn. The present
Ablation of TrkB signalling in CCK neurons results in hypercortisolism and obesity.
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Dysregulation of hypothalamic-pituitary-adrenal (HPA) axis activity leads to debilitating neuroendocrine or metabolic disorders such as Cushing's syndrome (CS). Glucocorticoids control HPA axis activity through negative feedback to the pituitary gland and the central nervous system (CNS). However,
Hypercortisolism in obesity-associated hypertension.
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Obesity is prevalent worldwide and associated with co-morbidities that result in increased cardiovascular risk. Hypertension is the most prevalent obesity comorbidity associated with increased cardiovascular risk. Obesity hypertension is a distinct subtype of essential hypertension. While endogenous
Chromatographic analysis of lipid fractions in healthy dogs and dogs with obesity or hyperadrenocorticism.
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Obesity and endogenous hyperadrenocorticism (HAC) are common clinical conditions in veterinary practice, and both conditions have clinical and laboratory similarities, such as weight gain and dyslipidemia. The objective of the present study was to characterize and compare the lipid profiles and
Hypercortisolism and altered glucose homeostasis in obese patients in the pre-bariatric surgery assessment
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Aims: Hypothalamus-pituitary-adrenal axis hyperactivity was suggested to be associated with the metabolic syndrome (MS), obesity and diabetes. The aim of this study was to test whether hypercortisolism was associated with altered glucose
Long-term hypercortisolism induces lipogenesis promoting palmitic acid accumulation and inflammation in visceral adipose tissue compared to HFD-induced obesity.
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Glucocorticoids (GCs) play critical roles in adipose tissue metabolism. Here, we compare in a mouse model the effects of chronic glucocorticoid excess and diet-induced obesity in the white adipose tissue mass and distribution, by focusing on the visceral adipose tissue fatty acid composition
Persistent GHRH-induced PRL secretion in Cushing's syndrome, obesity and exogenous hypercortisolism.
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Endogenous Cushing's syndrome, obesity and chronic glucocorticod treatment are characterized by blunted GH secretion. The administration of GHRH is capable of stimulating a small but significant PRL increase in normal subjects. The current study was designed to determine plasma PRL levels in
Chronic hypercortisolism causes more persistent visceral adiposity than HFD-induced obesity.
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Excessive and prolonged glucocorticoid (GC) exposure, resulting from either prescribed or endogenous hypercortisolism, is associated with a high cardiovascular and metabolic burden (Cushing's syndrome). Although previous studies in humans and mice have reported heterogeneous data about the
The diagnosis of hypercortisolism. Biochemical criteria differentiating patients from lean and obese normal subjects and from females on oral contraceptives.
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Impulsive and basal ACTH secretion phases in normal subjects, in obese subjects with signs of adrenocortical hyperfunction and in hyperthyroid patients.
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[Contribution to the differential diagnosis of obesity and hypercortisolism].
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FUNCTIONAL HYPERCORTISOLISM, VISCERAL OBESITY, AND METABOLIC SYNDROME.
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