کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2811119 | 1158535 | 2008 | 8 صفحه PDF | دانلود رایگان |

The human adrenal cortex expresses low levels of luteinizing hormone/chorionic gonadotropin receptors (LHCGR), a characteristic gonad-specific G-protein coupled receptor (GPCR). LHCGR levels increase in the adrenal cortex after exposure to chronically elevated gonadotropins (e.g. after gonadectomy). In fact, heightened ectopic LHCGR levels are observed in a subclass of human adrenocortical tumors, and gonadotropin-responsive adrenocortical hyperplasia and tumors occur in several animal species. These findings suggest that adrenocortical responsiveness to LH/CG might be a physiological phenomenon that is amplified in the presence of elevated gonadotropin levels. Such increased gonadotropin action can induce pathologies ranging from adrenocorticotropic hormone (ACTH)-independent Cushing syndrome to malignant adrenal tumors. The authors review the current information on adrenocortical responses to gonadotropins in experimental animals and humans.
Journal: - Volume 19, Issue 7, September 2008, Pages 231–238