Thyroid stimulating hormone release

Hypothyroidism (thyroid hormone deficiency) may result from autoimmune disease (Hashimoto s disease) or from deficient synthesis of TSH or TRH (thyroid-stimulating hormone-releasing factor). Because adequate ingestion of iodine is a prerequisite for thyroid hormone synthesis, iodine deficiency also causes hypothyroidism. In children, thyroid hormone deficiency (called cretinism) causes depressed growth and mental retardation. Severe hypothyroidism in adults (myxedema) results in symptoms such as edema (abnormal fluid accumulation) and goiter. Hypothyroidism is usually treated with hormone replacement therapy. 

Thyroid stimulating hormone releasing factor (TSH-RF), sometimes known as thyrotrophin-releasing factor (TRF). 

Figure 1 A schematic diagram of the endocrine system of fish. TRH = thyrotrophin releasing hormone GnRH = gonadotrophin releasing hormone CRH = corticotrophin releasing hormone TSH = thyroid stimulating hormone GtH = gonadotrophins I and II ...

Otfier fiormones accelerate tfie release of free fatty acids from adipose tissue and raise tfie plasma free fatty acid concentration by increasing the rate of lipolysis of the triacylglycerol stores (Figure 25—8). These include epinephrine, norepinephrine, glucagon, adrenocorticotropic hormone (ACTH), a- and P-melanocyte-stimulat-ing hormones (MSH), thyroid-stimulating hormone (TSH), growth hormone (GH), and vasopressin. Many of these activate the hormone-sensitive hpase. For an optimal effect, most of these lipolytic processes require the presence of glucocorticoids and thyroid hormones. These hormones act in a facilitatory or permissive capacity with respect to other lipolytic endocrine factors. 

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]. 

TRH thyrotropin-RH (protirelin) stimulates the release of TSH (thyroid stimulating hormone = thyrotropin). 

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... 

Thyroid-Releasing Hormone Toxic Substances Control Act Thyroid Stimulating Hormone Treatment Technique Threshold of Toxicological Concern Target-organ Toxicity dose Unscheduled DNA Synthesis Uncertainty Factor United Nations... 

Somatostatin inhibits secretion of growth hormone and other hormones such as prolactin from the anterior pituitary and is widely distributed in the brain in interneurons and projection pathways. All parts of the cortex contain local circuit somatostatin positive neurons, concentrated in layers V and VI, as does the amygdala and striatum. The nucleus accumbens and adjacent ventral putamen and caudate—designated limbic striatum—have particularly high concentrations of fibres. By contrast, TRH which regulates release of thyroid stimulating hormone and prolactin by the pituitary is generally confined to nuclei in and around the hypothalamus. 

The secretion of anterior pituitary hormones is controlled in part by hypothalamic regulatory factors that are stored in the hypothalamus and are released into the adenohypophyseal portal vasculature. Hypothalamic regulatory factors so far identified are peptides with the exception of dopamine. Secretion of anterior pituitary hormones is also controlled by factors produced more distally that circulate in the blood. Predominant control of hormone production may be relatively simple, as with thyroid-stimulating hormone (TSH), the production of which is primarily stimulated by thyrotropin-releasing hormone (TRH) and inhibited by thyroid hormones, or it may be complex, as with prolactin, the production of which is affected by many neurotransmitters and hormones. 

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. 

---