Thyrotropin-stimulating hormone

FSH Follicle-stimulating hormone TSH Thyrotropin-stimulating hormone... 

Huseman CA, Moriarty CM, Angle CR. 1987. Childhood lead toxicity and impaired release of thyrotropin-stimulating hormone. Environ Res 42 524-533. 

High doses of caffeine produce a stresslike neuroendocrine response (Spindel 1984 Spindel et al. 1984). This includes increased levels of corticosterone, jS-endorphin, and decreased serum growth hormone and thyrotropin-stimulating hormone in the rat. However, similar effects are not observed in humans until approximately 500 mg is consumed, the equivalent of 5 cups of coffee. At this dose in humans, elevations are seen in adrenocorticotrophic hormone, jS-endorphin, and cortisol. 

Thyrotropin stimulating hormone (TSH) Bovine pituitary Identification of thyroid cancer metastases in patients previously treated for thyroid cancer... 

Cortisol hypersecretion, blunted growth hormone and prolactin responses, blunted thyrotropin-stimulating hormone (TSH) response to TRH, reduced luteinizing hormone secretion, and disturbances in b-endorphin, vasopressin, and calcitonin have all been associated with depression. 

Thyrotropin-releasing hormone (TRH) is a hypothalamic tripeptide (pGlu-His-Pro-NH2) that increases thyrotropin-stimulating hormone, leading... 

Prolactin is an essential hormone for normal production of breast milk following childbirth. It also plays a pivotal role in a variety of reproductive functions. Prolactin is regulated primarily by the hypothalamus-pituitary axis and secreted solely by the lactotroph cells of the anterior pituitary gland. Under normal conditions, secretion of prolactin is predominantly under inhibitory control by dopamine and acts on the D2 receptors located on the lactotroph cells. Increase of hypothalamic thyrotropin-releasing hormone (TRH) in primary hypothyroidism can stimulate the release of prolactin. 

On the other hand, some receptors are truly promiscuous in that they can activate two or more G-proteins from quite different classes, even in their normal cellular environment. For example, similar concentrations of thyroid-stimulating hormone (TSH 0.1-100 U/ml) can stimulate the incorporation of 32P-GTP into a, aQ, a12, a13, as, and aq/11 through activation of the thyrotropin receptor in membranes from human thyroid gland. TRH activation of Ca2+ currents in GH3 cells is obtunded equally by antisense-depletion of l2, aa, and aq/11, but not of aQ. Some individual genotypic P2y nucleotide receptors can also couple with equal affinity to PTx-sensitive and PTx-insensitive G-proteins in sympathetic neurons. The degree, or otherwise, of such promiscuity is presumably determined by the structure of the receptor protein itself. 

A trophic hormone acts on another endocrine gland to stimulate secretion of its hormone. For example, thyrotropin, or thyroid-stimulating hormone (TSH), stimulates the secretion of thyroid hormones. Adrenocorticotropin, or adrenocorticotropic hormone (ACTH), stimulates the adrenal cortex to secrete the hormone cortisol. Both trophic hormones are produced by the pituitary gland in fact, many trophic hormones are secreted by the pituitary. The pituitary gland is sometimes referred to as the "master gland" because its hormones regulate the activity of other endocrine glands. 

Located in close proximity to the primary capillary plexus in the hypothalamus are specialized neurosecretory cells. In fact, the axons of these cells terminate on the capillaries. The neurosecretory cells synthesize two types of hormones releasing hormones and inhibiting hormones (see Table 10.2). Each of these hormones helps to regulate the release of a particular hormone from the adenohypophysis. For example, thyrotropin-releasing hormone produced by the neurosecretory cells of the hypothalamus stimulates secretion of thyrotropin from the thyrotrope cells of the adenohypophysis. The hypo-thalamic-releasing hormone is picked up by the primary capillary plexus travels through the hypothalamic-hypophyseal portal veins to the anterior pituitary leaves the blood by way of the secondary capillary plexus and exerts its effect on the appropriate cells of the adenohypophysis. The hypophyseal hormone, in this case, thyrotropin, is then picked up by the secondary capillary plexus, removed from the pituitary by the venous blood, and delivered to its target tissue. 

TSH-secreting pituitary adenomas are diagnosed by demonstrating lack of TSH response to thyrotropin-releasing hormone stimulation, inappropriate TSH levels, elevated TSH a-subunit levels, and radiologic imaging. 

Zhu, C. C., Cook, L. B., and Hinkle, P. M. (2002) Dimerization and phosphorylation of thyrotropin-releasing hormone receptors are modulated by agonist stimulation. J. Biol. Chem. 277,28228-28237. 

Neuropeptides are often grouped by their structural similarity or tissue source. Among these are the hypothalamic releasing factors (e.g., corticotrophin-releasing factor [CRF], thyrotropin-releasing hormone), anteior pituitary hormones (e.g., adrenocorticotrophic hormone [ACTFI], follicle-stimulating hormone [FSFI]), and posterior pituitary hormones... 

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