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The TSH, in turn, stimulates the thyroid to produce thyroid hormone until levels in the blood return to normal. Thyroid hormone exerts negative feedback control over the hypothalamus as well as anterior pituitary, thus controlling the release of both TRH from hypothalamus and TSH from anterior pituitary gland. [2]
The concentration of thyroid hormones (T 3 and T 4) in the blood regulates the pituitary release of TSH; when T 3 and T 4 concentrations are low, the production of TSH is increased, and, conversely, when T 3 and T 4 concentrations are high, TSH production is decreased. This is an example of a negative feedback loop. [5]
According to newer theories, [2] elevated concentrations of TSH and thyroid hormones in type 2 allostasis result from an up-regulated set point of the feedback loop, which ensues from increased TRH expression in the basolateral amygdala and the paraventricular nucleus of the hypothalamus in response to stress. [13] [14]
Negative correlation of Jostel's TSH index to the urinary excretion of certain phthalates suggests that endocrine disruptors may affect the central set point of thyroid homeostasis. [28] Drugs that reduce the TSH index, probably via effects on the central set point of the feedback loop, include mirtazapine [29] and oxcarbazepine. [30]
Estrogen forms a negative feedback loop by inhibiting the production of GnRH in the hypothalamus. Inhibin acts to inhibit activin, which is a peripherally produced hormone that positively stimulates GnRH-producing cells. Follistatin, which is also produced in all body tissue, inhibits activin and gives the rest of the body more control over the ...
The lack of thyroid hormones will lead to decreased negative feedback on the pituitary, leading to increased production of thyroid-stimulating hormone, which causes the thyroid to enlarge (the resulting medical condition is called endemic colloid goitre; see goitre). [59]