Cushing's syndrome

Shibli-Rahhal, Amal; VanBeek, Marta; Schlechte, Janet A.

doi:10.1016/j.clindermatol.2006.04.012

Cited by 108 publications

(70 citation statements)

References 43 publications

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“…In contrast, Cushing's patients with sustained and pronounced hypersecretion of GCs due to pituitary adenomas or ectopic, ACTH-producing tumors and a subsequent elevation of circulating GC levels display central obesity, increased breakdown of skeletal muscle mass, hyperglycemia, fatty liver development, hypertension, elevated cholesterol, immunodeficiency, and insulin resistance [27]. Similar features represent typical side-effects of long-term systemic GC treatment during anti-inflammatory and immunosuppressive therapy [28][29][30].…”

Section: Conditions Of Elevated Gc Levelsmentioning

confidence: 86%

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Glucocorticoids, metabolism and metabolic diseases

Vegiopoulos

Herzig

2007

Molecular and Cellular Endocrinology

448

370

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Since the discovery of the beneficial effects of adrenocortical extracts for treating adrenal insufficiency more than 80 years ago, glucocorticoids (GC) and their cognate, intracellular receptor, the glucocorticoid receptor (GR) have been characterized as critical components of the delicate hormonal control system that determines energy homeostasis in mammals.Whereas physiological levels of GCs are required for proper metabolic control, excessive GC action has been tied to a variety of pandemic metabolic diseases, such as type II diabetes and obesity. Highlighted by its importance for human health, the investigation of molecular mechanisms of GC/GR action has become a major focus in biomedical research. In particular, the understanding of tissue-specific functions of the GC-GR pathway has been proven to be of substantial value for the identification of novel therapeutic options in the treatment of severe metabolic disorders. Therefore, this review focuses on the role of the GC-GR axis for metabolic homeostasis and dysregulation, emphasizing tissue-specific functions of GCs in the control of energy metabolism.

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Section: Conditions Of Elevated Gc Levelsmentioning

confidence: 86%

“…Consistent with an involvement of the GC-GR axis in this phenotype, also Cushing's patients are characterized by a re-distribution of body fat from the periphery to central/abdominal depots [27,167], which seem to represent GR dense fatty tissue compartments that are in particular sensitive to GCs in obese patients [168][169][170].…”

Section: Adipose Tissuementioning

confidence: 97%

Glucocorticoids, metabolism and metabolic diseases

Vegiopoulos

Herzig

2007

Molecular and Cellular Endocrinology

448

370

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“…Jayo, Shively, Kaplan, and Manuck (1993) manipulated stress in male cynomolgus monkeys and found that monkeys randomly assigned to the stress condition had significantly higher amounts of abdominal fat than non-stressed controls. Cushing's syndrome, in which body tissues are chronically exposed to excessive levels of cortisol, provides the strongest evidence in humans that elevated cortisol causes weight gain (Shibli-Rahhal, Van Beek, & Schlechte, 2006). Indeed, a hallmark symptom of Cushing's syndrome is abdominal fat accumulation (Bjorntorp, 2001;Shibli-Rahhal et al, 2006), which is reversed by correcting cortisol levels (Bjorntorp, 2001).…”

Section: Physiological Mechanismsmentioning

confidence: 99%

“…Cushing's syndrome, in which body tissues are chronically exposed to excessive levels of cortisol, provides the strongest evidence in humans that elevated cortisol causes weight gain (Shibli-Rahhal, Van Beek, & Schlechte, 2006). Indeed, a hallmark symptom of Cushing's syndrome is abdominal fat accumulation (Bjorntorp, 2001;Shibli-Rahhal et al, 2006), which is reversed by correcting cortisol levels (Bjorntorp, 2001). The relationship between cortisol and abdominal obesity in the general population is so consistent that researchers have suggested that abdominal obesity be used as an index of long-term increased cortisol (Bjorntorp & Rosmond, 2000).…”

Section: Physiological Mechanismsmentioning

confidence: 99%

Weight stigma is stressful. A review of evidence for the Cyclic Obesity/Weight-Based Stigma model

2014

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A B S T R A C TWeight stigma is highly pervasive, but its consequences are understudied. This review draws from theory in social psychology, health psychology, and neuroendocrinology to construct an original, generative model called the cyclic obesity/weight-based stigma (COBWEBS) model. This model characterizes weight stigma as a "vicious cycle" -a positive feedback loop wherein weight stigma begets weight gain. This happens through increased eating behavior and increased cortisol secretion governed by behavioral, emotional, and physiological mechanisms, which are theorized to ultimately result in weight gain and difficulty of weight loss. The purpose of this review is to evaluate the existing literature for evidence supporting such a model, propose ways in which individuals enter, fight against, and exit the cycle, and conclude by outlining fruitful future directions in this nascent yet important area of research.

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“…Endogenous glucocorticoid excess may arise from ACTH-secreting pituitary tumors, ectopic (nonpituitary) ACTH production, or adrenal tumors. Hypercortisolaemia is associated with increased glucose production, decreased glucose transport and utilization, decreased protein synthesis, increased protein degradation in muscle and body weight gain (Nieuwenhuizen & Rutters, 2008;Shibli-Rahhal et al, 2006); (2) Addison's disease or primary adrenal insufficiency, first described by Addison in 1855, is characterized by an inability of the adrenal cortex to synthesize and secrete glucocorticoids and mineralocorticoids. Chronically, the main clinical findings observed in patients with Addison's disease include malaise, fatigue, anorexia, weight loss, darkening of the skin, hyponatraemia, hypoglycaemia and hyperkalaemia (Nieman and Chanco Turner, 2006).…”

Section: Neuropeptidesmentioning

confidence: 99%