scholarly journals Effects of forced swimming stress on thyroid function, pituitary thyroid-stimulating hormone and hypothalamus thyrotropin releasing hormone expression in adrenalectomy Wistar rats

2016 ◽  
Vol 12 (5) ◽  
pp. 3167-3174
Author(s):  
Qiuyan Sun ◽  
Aihua Liu ◽  
Yanan Ma ◽  
Anyi Wang ◽  
Xinhong Guo ◽  
...  
Keyword(s):  
Thyroid Function ◽  
Wistar Rats ◽  
Thyroid Stimulating Hormone ◽  
Thyrotropin Releasing Hormone ◽  
Forced Swimming ◽  
Releasing Hormone ◽  
Swimming Stress ◽  
Forced Swimming Stress ◽  
Stimulating Hormone

Effects of iodine excess on serum thyrotropin-releasing hormone levels and type 2 deiodinase in the hypothalamus of Wistar rats

2021 ◽  
pp. 1-30
Author(s):  
Ying Sun ◽  
Xin Du ◽  
Zhongyan Shan ◽  
Weiping Teng ◽  
Yaqiu Jiang
Keyword(s):  
Thyroid Function ◽  
Wistar Rats ◽  
Iodine Intake ◽  
Thyrotropin Releasing Hormone ◽  
High Iodine ◽  
Releasing Hormone ◽  
Iodine Excess ◽  
Excessive Iodine ◽  
Thyroid Hormone Biosynthesis

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.

scholarly journals The Physiological Role of Thyrotropin-Releasing Hormone in the Regulation of Thyroid-Stimulating Hormone and Prolactin Secretion in the Rat

1978 ◽  
Vol 61 (2) ◽  
pp. 441-448 ◽  
Author(s):  
Arthur R. C. Harris ◽  
Dana Christianson ◽  
M. Susan Smith ◽  
Shih-Lieh Fang ◽  
Lewis E. Braverman ◽  
...  
Keyword(s):  
Physiological Role ◽  
Thyroid Stimulating Hormone ◽  
Prolactin Secretion ◽  
Thyrotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Stimulating Hormone

Thyroid-Stimulating Hormone and Prolactin Responses to Thyrotropin-Releasing Hormone in Common Migraine

Cephalalgia ◽  
1987 ◽  
Vol 7 (4) ◽  
pp. 267-272 ◽  
Author(s):  
Giovanni Murialdo ◽  
Paola Masturzo ◽  
Ugo Filippi ◽  
Diego De Palma ◽  
Daniela Balbi ◽  
...  
Keyword(s):  
Intravenous Administration ◽  
Dose Response ◽  
Thyroid Stimulating Hormone ◽  
Thyrotropin Releasing Hormone ◽  
Healthy Controls ◽  
Response Relationship ◽  
Dose Response Relationship ◽  
Releasing Hormone ◽  
The One ◽  
Stimulating Hormone

Intravenous administration of 50 μg or 200 μg thyrotropin-releasing hormone (TRH) to men with common migraine elicited blunted prolactin (PRL) responses, when compared with healthy controls. The thyroid-stimulating hormone (TSH) response was enhanced after 50 μg TRH in the migraineurs, but not after 200 μg. The physiologic TSH dose-response relationship was abolished in migraine sufferers. The data may be interpreted in the light of dopaminergic and noradrenergic supersensitivity, for PRL and TSH, respectively. The TSH response in migraine differs from the one that occurs in depression.

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