Aberrant Receptor-Mediated Cushing’s Syndrome

Bertagna, Xavier; Groussin, Lionel; Luton, J. P.; Bertherat, Jérôme

doi:10.1159/000067832

Cited by 18 publications

(15 citation statements)

References 18 publications

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“…The ectopic expression of hormone receptors (including receptors for gastric inhibitory polypeptide, catecholamines, serotonin, and vasopressin type 1A) has already been implicated in cortisol production by adrenal tumors and the macronodular adrenal hyperplasia responsible for CS. Such expression is responsible for food-dependent cortisol secretion and unexpected responses to posture or pharmacological agents (Groussin et al 2002b, Bertagna et al 2003. Luteinizing hormone (LH) receptor is present in normal adrenal glands, but is found mostly in the zona reticularis (Pabon et al 1996).…”

Section: Introductionmentioning

confidence: 99%

Expression of progesterone and estradiol receptors in normal adrenal cortex, adrenocortical tumors, and primary pigmented nodular adrenocortical disease

Crémoux

Rosenberg²,

Goussard³

et al. 2008

Endocrine Related Cancer

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Adrenal tumors occur more frequently in women and are the leading cause of Cushing's syndrome during pregnancy. We aimed to evaluate the potential role of sex steroids in the susceptibility of women to adrenocortical tumors. We evaluated the presence of the progesterone receptor (PR), estradiol receptors (ERs), and aromatase in 5 patients with primary pigmented nodular adrenal disease (PPNAD), 15 adrenocortical adenomas (ACAs) and adjacent normal tissues, 12 adrenocortical carcinomas (ACCs), and 3 normal adrenal glands (NA). The expression of PR and ERa was evaluated by enzyme immunoassays, real-time RT-PCR, immunohistochemistry, and cytosol-based ligand-binding assays. ERb and aromatase levels were evaluated by real-time RT-PCR. ERa concentrations were low in NA, in adrenal tissues adjacent to ACA (51G33), in ACC (53G78), and lower in ACA (11G11 fmol/mg DNA). Conversely, PR concentrations were high in NA and adrenal tissues adjacent to ACA, at 307G216 fmol/mg DNA, and were even higher in tumors -726G706 fmol/mg DNA in ACA and 1154G1586 fmol/mg DNA in ACC -and in isolated PPNAD nodules. Binding study results in four tumors were compatible with binding to a steroid receptor. In patients with PPNAD, a strong positive immunohistochemical signal was associated with the sole isolated nodular regions. ERb transcript levels were very high in all samples except those for two ACCs, whereas aromatase levels were low. PR and ERb are clearly present in normal adrenal glands and adrenal tumors. Further studies may shed light on the possible pathogenic role of these receptors in adrenal proliferation.

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Section: Introductionmentioning

confidence: 99%

Expression of progesterone and estradiol receptors in normal adrenal cortex, adrenocortical tumors, and primary pigmented nodular adrenocortical disease

Crémoux

Rosenberg²,

Goussard³

et al. 2008

Endocrine Related Cancer

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“…In Japan, it is a rare cause of Cushing's syndrome that occurs most frequently among middle-aged men (7). The precise etiology of AIMAH is unknown, although recent studies have demonstrated that the aberrant adrenal expression and function of one to several peptide hormone receptors, such as receptors for glucosedependent insulinotropic hormone (GIP), vasopressin, luteinzing hormone/human chorionic gonadotropin (LH/hCG), beta adrenergic agonists, and serotonin, can lead to adrenal cell proliferation and abnormal regulation of steroidogenesis in AIMAH (2,(8)(9)(10).…”

Section: Discussionmentioning

confidence: 99%

Long-term Efficacy of Trilostane for Cushing's Syndrome due to Adrenocorticotropin-Independent Bilateral Macronodular Adrenocortical Hyperplasia

et al. 2011

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A 66-year-old man with Cushing's syndrome due to adrenocorticotropin-independent bilateral macronodular adrenocortical hyperplasia (AIMAH) was treated for 7 years with trilostane, a 3β-hydroxysteroid dehydrogenase inhibitor. Administration of trilostane reduced the serum cortisol level to around the upper limit of normal for 7 years, and symptoms of excessive glucocorticoid production (such as moon face and obesity) were gradually improved. On the other hand, the size of both adrenal glands gradually increased despite treatment with trilostane. Though trilostane therapy could not prevent adrenal growth, it did suppress cortisol secretion over the long term, so it might be a reasonable option for AIMAH in addition to adrenalectomy.

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“…A bizarre and totally unexpected property of GIP is its ability, under certain circumstances, to interact with GIP receptors on adrenocortical cells to stimulate cortisol production and produce a condition known as food-induced Cushing's syndromes [64] . Whether this role of GIP is only and purely a pathological phenomenon or has physiological significance has yet to be ascertained.…”

Section: Pharmacophysiological Properties Of Gipmentioning

confidence: 99%

Human Obesity: Its Hormonal Basis and the Role of Gastric Inhibitory Polypeptide

Marks

2006

Med Princ Pract

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Obesity is an abnormal expansion of the adipose organ and is a pathophysiological response to an imbalance between energy intake and energy expenditure. It is the result of a large number of diverse factors involving heritable and environmental characteristics. A simple definition of obesity is difficult and unsatisfactory and its age dependency has largely been ignored. Differentiation between healthy, age-related plumpness and obesity is often blurred and responsible for overdiagnosis of obesity in the developed world. In the past, epidemiological studies have often ignored the different prognostic significance of the two major phenotypes of human obesity making their conclusions of limited value. The role of heritable factors in determining both the propensity to develop obesity under favourable environmental conditions, including inactivity and unlimited access to fat-rich foods, and the phenotype it assumes received an enormous fillip from experiments involving genetically modified animals. The most important of these have demonstrated the key role played by a number of newly discovered or recently resurrected polypeptide hormones that are released from the intestine in response to food. Molecular manipulation of these hormones, especially of glucose-dependent insulin-stimulatory polypeptide offers a new therapeutic approach.

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Aberrant Receptor-Mediated Cushing’s Syndrome

Cited by 18 publications

References 18 publications

Expression of progesterone and estradiol receptors in normal adrenal cortex, adrenocortical tumors, and primary pigmented nodular adrenocortical disease

Expression of progesterone and estradiol receptors in normal adrenal cortex, adrenocortical tumors, and primary pigmented nodular adrenocortical disease

Long-term Efficacy of Trilostane for Cushing's Syndrome due to Adrenocorticotropin-Independent Bilateral Macronodular Adrenocortical Hyperplasia

Human Obesity: Its Hormonal Basis and the Role of Gastric Inhibitory Polypeptide

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