References.<unk>  homeostasis results from a multi-loop feedback system that is found in virtually all higher vertebrates. Proper function of thyrotropic feedback control is indispensable for growth, differentiation, reproduction and intelligence. Very few animals (e.g. axolotls and sloths) have impaired<unk>  homeostasis that exhibits a very low set-point that is assumed to underlie the metabolic and ontogenetic anomalies of these animals. The<unk>  gland secretes thyrotropin (TSH;<unk>  Stimulating Hormone) that stimulates the<unk>  to secrete thyroxine (T4) and, to a lesser degree, triiodothyronine (T3). The major portion of T3, however, is produced in peripheral organs, e.g. liver, adipose tissue, glia and skeletal muscle by deiodination from circulating T4. Deiodination is controlled by numerous hormones and nerval signals including TSH, vasopressin and catecholamines. Both peripheral<unk>  hormones (iodothyronines) inhibit thyrotropin secretion from the<unk>  (negative feedback). Consequently, equilibrium concentrations for all hormones are attained. TSH secretion is also controlled by thyrotropin releasing hormone (thyroliberin, TRH), whose secretion itself is again suppressed by plasma T4 and T3 in CSF (long feedback, Fekete–Lechan loop). Additional feedback loops are ultrashort feedback control of TSH secretion (Brokken-Wiersinga-Prummel loop) and linear feedback loops controlling plasma protein binding. Recent research suggested the existence of an additional feedforward motif linking TSH release to deiodinase activity in humans. The existence of this TSH-T3 shunt could explain why deiodinase activity is higher in hypothyroid patients and why a minor fraction of affected individuals may benefit from substitution therapy with T3. Convergence of multiple afferent signals in the control of TSH release including but not limited to T3, cytokines and TSH receptor antibodies may be the reason for the observation that the relation between free T4 concentration and TSH levels deviates from a pure loglinear relation that has previously been proposed. Recent research suggests that ghrelin also plays a role in the stimulation of T4 production and the subsequent suppression of TSH directly and by negative feedback.
Hypothalamic–pituitary–thyroid axis
Hypothalamic–pituitary–somatotropic axis
Hypothalamic–pituitary–prolactin axis
Hypothalamic–pituitary–gonadal axis
Hypothalamic–pituitary–adrenal axis
Sympathoadrenal system
Thyroid's secretory capacity
Endocrine system