Mild elevation of prolactin is seen in hypothyroidism due to the stimulatory effect of thyrotropin-releasing hormone
on prolactin release.
The elevated concentration of PRL may be resulted from a compensatory increase of thyrotropin-releasing hormone
(TRH) in response to thyroid function failure in SCH.23 It is well-known that PRL has important roles in modulating hypothalamic-pituitary-gonad axis function, and GnRH pulsatility.8,24 The remarkable PRL elevation has been demonstrated to adversely affect sexual activity and leads to impaired libido, and erectile dysfunction.25 Hence the relative PRL increase accompanied with TSH elevation in SCH patients may be another factor to affect erectile function, however this observation need to be studied further to confirm this observation.
Various etiological mechanisms such as autoimmune vasculitis, auto anti bodies directed against brainthyroid antigens, encephalomyelitis-associated demyelination, global cerebral hypo perfusion, a direct toxic effect of thyrotropin-releasing hormone
, and neuronal dysfunction due to brain edema have been presented as the underlying pathogenesis of HE6.
In chickens, the somatotropic axis is regulated by GHRH, thyrotropin-releasing hormone
(TRH), and somatostatin by the secretion of the growth hormone (GH) .
TSH is again regulated by the thyrotropin-releasing hormone
(TRH), which is produced from the hypothalamus .
Primary hypothyroidism leads to increased thyrotropin-releasing hormone
(TRH) release from hypothalamus, which has a physiologic trophic effect on thyrotrophs and lactotrophs resulting in increased TSH and prolactin levels, respectively (3,5).
Effects of thyrotropin-releasing hormone
on the sleep EEG and nocturnal hormone secretion in male volunteers.
(TRH) and gonadotropin-releasing hormone (GnRH) provocation tests were administered in patients who lived up to day 4, in order to evaluate the HPG axis on the 4th day.
Neurons within the hypothalamus produce and secrete releasing hormones, such as corticotropin-releasing factor (CRF), luteinizing hormone--releasing hormone (LHRH), thyrotropin-releasing hormone
(TRH), and growth hormone--releasing hormone (GRH), as well as inhibiting hormones, such as somatostatin and dopamine, directly into the blood vessel connecting the hypothalamus with the pituitary gland (i.e., the hypothalamic--hypophyseal portal vein).
Secretion of thyrotropin-releasing hormone
(TRH) by the hypothalamus controls the release of thyroid-stimulating hormone (TSH) by the pituitary gland, which controls the release of [T.sub.3] and [T.sub.4] from the thyroid.
The hypothalamic thyrotropin-releasing hormone
(TRH) receptor induces the hypophysis production of the thyroid-stimulating hormone (TSH), which, in turn, stimulates the synthesis and secretion of the THs, as illustrated in Fig.
Effect of feeding thyrotropin-releasing hormone
to lactating sows.