Abstract
Iodine is an important element in thyroid hormone biosynthesis. Thyroid function is regulated by the hypothalamic-pituitary-thyroid axis (HPT). Excessive iodine leads to elevated thyroid stimulating hormone (TSH) levels, but the mechanism is not yet clear. Type 2 deiodinase (Dio2) is a selenium-containing protease that plays a vital role in thyroid function. The purpose of this study was to explore the role of hypothalamus Dio2 in regulating TSH increase caused by excessive iodine and to determine the effects of iodine excess on thyrotropin-releasing hormone (TRH) levels. Male Wistar rats were randomized into five groups and administered different iodine dosages (folds of physiological dose): normal iodine (NI), 3-fold iodine (3HI), 6-fold iodine (6HI), 10-fold iodine (10HI), and 50-fold iodine (50HI). Rats were euthanized at 4, 8, 12, or 24 weeks after iodine administration. Serum TRH, TSH, total thyroxine (TT4), and total triiodothyronine (TT3) were determined. Hypothalamus tissues were frozen and sectioned to evaluate expression of Dio2, Dio2 activity, and monocarboxylate transporter 8 (MCT8). Prolonged high iodine intake significantly increased TSH expression (p < 0.05), but did not affect TT3 and TT4 levels. Prolonged high iodine intake decreased serum TRH levels in the hypothalamus (p < 0.05). Dio2 expression and activity in the hypothalamus exhibited an increasing trend compared at each time point with increasing iodine intake (p < 0.05). Hypothalamic MCT8 expression was increased in rats with prolonged high iodine intake(p < 0.05). These results indicate that iodine excess affects the levels of Dio2, TRH, and MCT8 in the hypothalamus.
Role of brainstem thyrotropin-releasing hormone-triggered sympathetic overactivation in cardiovascular mortality in type 2 diabetic Goto–Kakizaki rats