Abstract
The secretion of cortisol and other steroids from adrenal tumors can be regulated by hormones other than corticotropin following the aberrant expression of several G-protein-coupled receptors (GPCRs). To date, ectopic receptors for gastric inhibitory polypeptide, β-adrenergic receptor agonists, vasopressin (V2 and V3 receptors), 5-hydroxytryptamine (5-HT7 receptor) and, probably, angiotensin II (AT1 receptor) have been identified. Either increased expression or altered activity of eutopic receptors for vasopressin (V1), luteinizing hormone/human chorionic gonadotropin, 5-HT (5-HT4 receptor) and leptin might also be involved. One or more aberrant receptors can be present in unilateral tumors and bilateral macronodular adrenal hyperplasia, at either the early subclinical or overt stages of hormone secretion. The identification of aberrant adrenal GPCRs offers the potential for novel pharmacological therapies that either suppress the endogenous ligands or block the receptor with specific antagonists. The secretion of cortisol and other steroids from adrenal tumors can be regulated by hormones other than corticotropin following the aberrant expression of several G-protein-coupled receptors (GPCRs). To date, ectopic receptors for gastric inhibitory polypeptide, β-adrenergic receptor agonists, vasopressin (V2 and V3 receptors), 5-hydroxytryptamine (5-HT7 receptor) and, probably, angiotensin II (AT1 receptor) have been identified. Either increased expression or altered activity of eutopic receptors for vasopressin (V1), luteinizing hormone/human chorionic gonadotropin, 5-HT (5-HT4 receptor) and leptin might also be involved. One or more aberrant receptors can be present in unilateral tumors and bilateral macronodular adrenal hyperplasia, at either the early subclinical or overt stages of hormone secretion. The identification of aberrant adrenal GPCRs offers the potential for novel pharmacological therapies that either suppress the endogenous ligands or block the receptor with specific antagonists. Erratum: Cushing's syndrome variants secondary to aberrant hormone receptors: Trends in Endocrinology & Metabolism 15 (2004) 8, 375–382 et al.Trends in Endocrinology & MetabolismJanuary, 2005In BriefIn the October 2004 issue of Trends in Endocrinology & Metabolism, the article by André Lacroix, Valérie Baldacchino, Isabelle Bourdeau, Pavel Hamet and Johanne Tremblay contained an error in the Figure layout. The legend for Figure 1 ‘Regulation of steroidogenesis by aberrant hormone receptors in fasciculate cells of adrenal Cushing's syndrome’ relates to the Figure on page 378 and the Figure on page 377 should be with the Figure 2 legend ‘Phenotypic adrenocortical expression of an ectopic GIP receptor’. Full-Text PDF
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