Endocrine Abstracts

Cushing’s syndrome is a disease caused by excessive glucocorticoids from adrenocortical tumors. In most cases, impaired adrenocortical function is likely caused by atrophy of the normal adrenal tissue as a result of chronic suppression by the low ACTH levels in the hypercortisolism state. Secondary adrenal insufficiency causes with surgical resection of cortisol-secreting tumors. Therefore, we thought that it was necessary to prepare Cushing’s syndrome model rats for establishment of a new treatment method to promote improvement of the function of the remaining adrenal glands after adrenalectomy. Cushing’s syndrome model rats have already been published and they describe changes in blood pressure and body weight. Regarding atrophy of tissues, it is considered that the atrophy of cells and the appearance of apoptosis are observed in such tissues. However, the weight and histological changes of the adrenal glands are not described. In this study, we investigate ACTH, the ratio of adrenal cortex to medulla and number of apoptotic cells as evaluation of atrophic adrenal glands in dexamethasone-treated rats (n=5) compared to control rats (n=5). In the group treated with dexamethasone, an increase in blood pressure (135±24 mmHg), suppression of plasma ACTH (20±12 pg/ml) and the low serum corticosterone levels (7.5±1.1 ng/ml) were observed as compared with the control group. In addition, adrenal gland weight decreased (13.6±1.2 mg), and the low ratio of adrenal cortex to medulla and an increase of apoptotic cells were observed. Compared with control rats, dexamethasone-treated rats showed a significant decrease in hormonal secretory ability both endocrinologically and histologically. Our group is currently conducting experiments to investigate the levels of mRNAs for c-fos in adrenal glands as assessment of the recovery of adrenal atrophy.