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SAYOMI IIDA, KANAME MORIWAKI, HIROSHI FUJII, MASAHIRO GOMI, MAMIKO TSUGAWA, YOSHIHISA NAKAMURA, TERUO KITANI, SEIICHIRO TARUI, Quantitative Comparison of Aromatase Induction by Dexamethasone in Fibroblasts from a Patient with Familial Cortisol Resistance and a Patient with Cortisol Hyperreactive Syndrome, The Journal of Clinical Endocrinology & Metabolism, Volume 73, Issue 1, 1 July 1991, Pages 192–196, https://doi.org/10.1210/jcem-73-1-192
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Abstract
The ability of dexamethasone to induce aromatase activity was tested in fibroblasts from a patient with familial cortisol resistance, a patient with cortisol hyperreactive syndrome, and five normal subjects. Dexamethasone increased enzyme activity in all cases in a concentration-dependent manner (over a range of 1–1000 nmol/L). In fibroblasts from a patient with familial cortisol resistance, the response curve of dexamethasone-induced aromatase activity was shifted to the right compared to that of normal cells. However, the maximal induction of the enzyme at 1 μmol/L dexamethasone was unchanged in cortisol-resistant fibroblasts. On the other hand, in fibroblasts from the patient with the cortisol hyperreactive syndrome, the half-maximal effect of dexamethasone was similar to that in normal cells, but maximum induction of aromatase activity was 2 times greater than that in normal cells. The glucocorticoid antagonist RU 486 inhibited dexamethasone-induced aromatase activity in these patients’ cells and in normal cells in a concentration- dependent manner, indicating that the altered effects of dexamethasone on aromatase induction observed in each cell type were mediated through glucocorticoid receptors.