Endocrine Abstracts

Cushing’s syndrome is caused by cortisol-secreting adrenocortical adenoma. Surgical resection of cortisol-secreting adenoma results in secondary adrenal insufficiency in most cases. The main mechanism of adrenal insufficiency is that the residual adrenocortical tissue becomes atrophied as a result of chronic suppression of the hypothalamic-pituitary-adrenal (HPA) axis by excessive cortisol levels. Therefore, we have analyzed Cushing syndrome model rats following the previous year’s report in order to develop a new treatment that promotes early functional improvement in postoperative remaining adrenal glands. Increase in blood pressure (117±16 mmHg), decrease in body weight (380±25 g), suppression of ACTH (43±18 pg/ml) and reduction of adrenal weight (14.4±1.7 mg) were significantly confirmed in dexamethasone-treated rats (n=8) compared to the control group (n=8), and a decrease in ratio of adrenal cortex to medulla was also confirmed. These results were similar findings in the previous year. In this experiment, adrenal function was evaluated by reverse transcription PCR (RT-PCR) of adrenal gland tissue and measurement of mRNA. The expression level of CYP11B1 mRNA was calculated as cortisol productivity, and the expression level was significantly decreased in the dexamethasone administration group (0.09) compared to the control (1.00). It was confirmed that the hormone secretion ability of the adrenal cortex was significantly decreased endocrinologically in the model rat as compared with control rats. Our group is now conducting experiments to evaluate the improvement of remaining adrenal function by administering synthetic ACTH formulation.