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function of the hypothalamus–pituitary–thyroid axis (HPT) is no exception ( Figs 1 and 2 ). Since the end of the 19th century, European physicians and surgeons associated neck swelling (thyroid enlargement, goiter), with iodine deficiency, cretinism, and

( Walpita et al . 2007 ). Stimulatory effects of cortisol on the HPT axis have also been suggested in teleost fish. In brook charr ( Salvelinus fontinalis ) long-term exposure to cortisol increased the hepatic conversion of T 4 to T 3 ( Vijayan et al

mRNA expression from non-hypophysiotropic aPVN neurons showed no significant differences in animals either fed in light or in darkness phase ( Fig. 2A , B , C , J ). Hypophysiotropic TRHergic neurons of medial and caudal PVN direct HPT axis function

( Decuypere et al . 1990 ). THs are known to play an important role in controlling their own secretion through feedback effects acting on the different levels of the hypothalamo–pituitary–thyroidal (HPT) axis. In birds, information on TH feedback is scarce

alterations in the central part of the hypothalamus–pituitary–thyroid (HPT) axis are combined with reduced production of T 3 and impaired clearance of rT 3 by the liver, and with specific changes in peripheral TH metabolism in major T 3 target organs

exercise ( Kujala et al . 1990 ). Qualitatively and quantitatively normal spermatogenesis is critically dependent on an intact hypothalamus–pituitary–testis (HPT) axis. Androgens are essential for the maintenance of normal spermatogenesis. Reactive oxygen

thyroxine (T 4 ) – as well as their degrading effects on fuel reservoirs. TRH is the hypophysiotropic factor that controls HPT axis function. This peptide is synthesized in the medial PVN (mPVN) of the hypothalamus and released into the portal blood to

the brainstem play a key role in regulation of the HPT axis in response to cold. Both noradrenergic (LC and NTS, orange arrows) and adrenergic (C1–3 regions, brown arrow) axons establish contacts with TRH neurons in the PVN ( Fekete & Lechan 2014 ). AH

Introduction During fasting, profound changes occur in the hypothalamic part of the hypothalamic–pituitary–thyroid axis (HPT axis), i.e. increased type 2 deiodinase (D2) activity in the arcuate nucleus (ARC) ( Diano et al. 1998

–pituitary–thyroid (HPT) axis function has not previously been performed. Recent evidence arising from analysis of lymphocyte development and function in mice with genetic defects in the expression of thyroid hormones or their receptors suggested that these