Thyroid glands: novel sites of growth hormone action

Abstract

Thyroid hormones inhibit the synthesis and release of GH in avian species. This may represent a feedback mechanism, since GH enhances the peripheral production of tri-iodothyronine (T3). The possibility that GH may also have direct effects on thyroidal function was therefore investigated. The basal and thyrotrophin-induced release of thyroxine (T4) from incubated chicken thyroid glands was not enhanced, however, in the presence of chicken GH. Contrarily, GH impaired T4 release in a dose-related way. These actions were probably mediated by specific receptors, since binding sites for radiolabelled GH were demonstrated on the plasma membranes of chicken thyroid glands. Expression of the GH receptor gene in these tissues was also demonstrated using a cRNA probe for the rabbit liver GH receptor, which specifically hybridized with RNA moieties of 4.4 kb, 2.7 kb and 1.0 kb. Moreover, reverse transcription of thyroidal RNA and its amplification in the presence of 3'- and 5'-oligonucleotide primers coding for the extracellular or intracellular domains of the GH receptor generated electrophoretically separable fragments of 500 bp and 800 bp respectively, as would be expected from analysis of the hepatic GH receptor cDNA sequence. Digestion of the 500 bp fragment with NcoI or EcoRI also produced moieties of expected size (350 bp and 150 bp or 325 bp and 175 bp respectively), as did BamHI or HaeIII digestion of the 800 bp fragment (yielding fragments of 550 bp and 275 bp or 469 bp and 337 bp respectively). Translation of the GH receptor mRNA was also indicated by the immunocytochemical demonstration of GH receptors in thyroid follicular and parafollicular cells, using a specific polyclonal antibody raised against the chicken GH-binding protein. These results therefore provide evidence, for the first time, of GH receptor gene expression in thyroid tissue and the translation of functional GH receptors in thyroid glands. These results also demonstrate differential effects of GH on the extracellular concentrations of T3 and T4, which may permit subtle regulation within the somatotroph-thyroid axis.

Papillary thyroid carcinoma after recombinant GH therapy for Turner syndrome

“…GH receptor immunoreactivity has also been reported in other tumor types, such as hepatocellular carcinoma (22) and occasionally in tumors appearing after GH therapy in immunocompromised patients (23). In our cases we found intense diffuse immunoreactivity in papillary carcinoma cells, though note that GH receptors have also been detected in normal thyroid cells of chickens (24), humans and rats (25). Other studies have also demonstrated the presence of the IGF-1 receptor in thyroid papillary carcinomas (26).…”

Testing the carotenoid-based sexual signalling mechanism by altering CYP2J19 gene expression and colour in a bird species

“…[29], and large species-related differences have also been reported (see electronic supplementary material). On the other hand, the lack of significant differences in circulating hormone levels among our specific T3 dosages could be interpreted as a result of a negative feedback regulation to avoid excessive hormone circulation at the end of the experiment [41,56,57]. The dosage-related effects detected on bill redness could, however, be a consequence of differences in plasma levels days before blood sampling.…”

The Hypothalamic-Pituitary-Thyroid (HPT) Axis in Birds and Its Role in Bird Development and Reproduction

“…Historically, many studies have shown that both mammalian TSHs and avian pituitary homogenates stimulate thyroid gland activities (radioiodine uptake, thyroid hormone release, and gland growth; see, e.g., work by MacKenzie, 1981), and these activities are mediated via TSH receptors (Hull et al, 1995).…”

“…The effects of GH on deiodinases vary with deiodinase type and tissue; GH decreases hepatic 5D III (effect at the level of transcription) but does not alter 5 D II in the brain ( Van der Geyten et al, 2001). GH receptors are present in the thyroid and in vitro studies indicate that GH decreases T 4 release from the thyroid and may directly stimulate thyroid gland growth (Hull et al, 1995).…”