Thyroid-stimulating hormone, response

Morris D D, Garcia M 1983 Thyroid-stimulating hormone response test in healthy horses and effects of phenylbutazone on equine thyroid hormones. American Journal of Veterinary Research 44 503-507 Ralston S L 2002 Insulin and glucose regulation. 

Meij, B. P, J. A. Mol, and A. Rijnberk. 1996. Thyroid stimulating hormone responses after single administration of thyrotrophin-releasing hormone and combined administration of four hypothalamic releasing hormones in beagle dogs. Domestic Animal Endocrinology 13 465-468. 

Shenkman, L., Mitsuma, T., Suphavai, A., and Hollander, C. S., Triiodoth)o o-nine and thyroid-stimulating hormone response to thyrotrophin-releasing hormone. A new test of thyroidal and pituitary reserve. Lancet 1, 111-113 (1972). 

HI. Hall, R., Amos, J., Garry, R., and Buxton, R. L., Thyroid stimulating hormone response to synthetic thyrotrophin-releasing hormone in man. Brit. Med. J. 2, 274-277 (1970). 

Thyroid-stimulating hormone (TSH) should be ordered when thyroid dysfunction is suspected. Hypothyroidism may be responsible for constipation and related symptoms. 

Li+ has been reported to affect virtually every component of the endocrine system to some extent however any resulting clinical manifestations are very rare [169]. Although these influences do not appear to be related to its mechanism of action in manic-depression, some are involved in the side effects experienced by Li+-treated patients. Apart from elevated levels of thyroid stimulating hormone (TSH), Li+ does not appear to affect the basal levels of hormones significantly however some hormone responses are reported to be altered by Li+ treatment of bipolar patients [170]. Neuronal activity stimulates the adrenal medulla to release norepinephrine and epinephrine into the blood and, consequently, the plasma from people with mania and depression shows increased levels of both neurotransmitters [171]. 

Comparative evaluation of anti-human thyroid stimulating hormone (hTSH) antibody, bound to the fifth-generation ammonia core (N5) or the fifth-generation ethylenediamine core (E5) dendrimer (1), did not show any differences in either the effective protein concentrations or the shape of the dose-dependent response curves (calibration curves) as determined from the recovery of standard controls. All the other experiments described here were thus carried out with the fifth-generation (i.e. dia. = 70 A) particles of ethylenediamine core (E5) de-ndrimers. The later particles were selected for their ability to be produced reproducibly on a large scale. 

Demonstration that the effects of thyrotoxicosis or goiter are due to an excess or deficiency in (thyroxine + T3) secretion does not explain how the diseases originate nor why development and metabolic rate are affected. It is thought that some cases of thyrotoxicosis (Graves disease) may be caused by abnormal immune responses mimicking the effects of thyroid-stimulating hormone on the thyroid gland. 

Anterior part produces its own hormones in response to hypothalamic releasing hormones, e.g., adrenocorticotropic hormone ACTH, luteinizing hormone LH, follicle-stimulating hormone FSH, prolactin, growth hormone, thyroid-stimulating hormone TSH Thyroid Regulation of metabolism, development, and maturation... 

Secondary hypothyroidism, or pituitary hypothyroidism, is the consequence of impaired thyroid-stimulating hormone (TSH) secretion and is less common than primary hypothyroidism. It may result from any of the causes of hypopituitarism (e.g., pituitary tumor, postpartum pituitary necrosis, trauma). Patients with secondary hypothyroidism exhibit undetectable or inappropriately low serum TSH concentrations. In secondary hypothyroidism, a normal thyroid gland lacks the normal level of TSH stimulation necessary to synthesize and secrete thyroid hormones. Such patients usually also have impaired secretion of TSH in response to exogenous thyrotropin-releasing hormone (TRH) administration. 

The thyroid-pituitary-hypothalamus axis controls thyroid hormone homeostasis. Thyrotropin-releasing hormone (TRH), released from the hypothalamus, stimulates the synthesis and release of thyroid-stimulating hormone (thyrotropin, TSH) from the anterior pituitary. TSH increases the release of thyroid hormones by several mechanisms, including stimulation of the I pump. While lower than normal levels of T3 and T4 cause an exaggerated response of the pituitary to TRH, released thyroid hormones, in feedback control, blunt the stimulating action of TRH on the pituitary. For further discussion of TSH and TRH biochemistry, see, for example, the review by Kannan48. 

In thyroid cells in culture, ceilcitriol reduces production of cAMP in response to thyr oid stimulating hormone by a nuclear- action on the synthesis of G-protein subunits. However, it also reduces the responsiveness to cAMP, emd attenuates cell growth and iodide uptake in response to thyroid stimulating hormone, with a rapid time course from direct action on protein kinase A (Berg andHaug, 1999). 

Thyrotoxicosis is most commonly caused by Graves disease, which is an autoimmune disorder in which thyroid-stimulating antibody (TSAb) directed against the thyrotropin receptor elicits the same biologic response as thyroid-stimulating hormone (TSH). 

TSH Thyroid-stimulating hormone or thyrotropin a glycoprotein hormone released from the anterior pituitary in response to increased levels of TRH. TSH binds to TSH receptors on the basal membrane of epithelial cells of the thyroid gland to stimulate the release of the thyroid hormones, Tj and T. ... 

We worked out the effective method for obelin conjugation with the other molecules - avidin, antibodies and so on. To analyze the thyroid gland hormones in sera, we synthesized the obelin conjugates with antibodies to the thyroid-stimulating hormone (TSH), antibodies to thyroxin (T4), and T4 itself. The bioluminescent labels obtained were applied for different format solid-phase immunoassay. Fig. 2 illustrates the TSH sandwich-type immunoassay, and the calibration curve built as a dependence of bioluminescent response on hormone concentration in standard sera. This curve was used to determine TSH in 34 patients sera. The results obtained closely corresponded to those provided by the RIA data (r = 0.99). 

Al. Adams, D. D., The presence of an abnormal thyroid stimulating hormone in the serum of some thyrotoxic patients. J. Clin. Endocrinol. Melab. 18, 699-712 (1958). Adams, D. D., and Purves, H. D., Abnormal response in the assay of thyrotropin. Proc. XJniv. Otago Med. School 34, 11 (1956). 

Ml. Macchia, V., and Pastan, I., Action of phospholipase C on the thyroid. Abolition of the response to thyroid-stimulating hormone. J. Biol. Chem. 242, 1864-1869... 

---