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PubMed1984

Effects of hysterectomy and in-vivo treatment with uterine extracts on plasma concentrations of growth hormone, thyrotrophin and thyroid hormones in rats: a kinetic study.

Plasma concentrations of GH, TSH, tri-iodothyronine (T3) and thyroxine (T4) were measured in adult rats 2 and 4 weeks after ovariectomy and and ovariohysterectomy. Two weeks after ovariohysterectomy, the concentration of GH was significantly higher, but TSH and T3 concentrations were significantly lower than in rats which had been ovariectomized only. Hysterectomy had no effect on plasma GH and TSH concentrations if it was performed 2 weeks after ovariectomy. Plasma T3 had decreased by 2 weeks after ovariectomy but returned to pretreatment levels by 4 weeks. Recovery of the plasma T3 concentration was not observed if ovariectomy was followed by hysterectomy, since a further decrease of plasma T3 occurred. Plasma T4 was not significantly influenced either by ovariectomy or by ovariohysterectomy. Steroid-free uterine extracts given i.p. to ovariohysterectomized rats reduced plasma GH within 24 h of injection. Increases in plasma TSH, T3 and T4 were achieved in ovariohysterectomized rats with injections of uterine extracts (from intact, oestrogen-treated or castrated rats), but the increases were not consistent for the three hormones either as regards time after injection, nor for which particular extracts were effective. It concluded that the uterus may contain factors which influence the GH storage and secretion and TSH-thyroid regulation in rats.

Animals↗
PubMed1987

The inhibitory effects of calmodulin antagonists on TSH-stimulated thyroid hormone release by mouse thyroid lobes.

Calcium ions have been shown to play a mojor regulatory role in the release of various hormones from a wide variety of endocrine organs. More recently, in vitro evidence suggests that a calcium-binding protein, calmodulin, is also involved in the release of many hormones. So we examined the effects of several types of calmodulin antagonists on TSH-stimulated thyroid hormone release in vitro. Mouse thyroid lobes (one thyro-tracheal unit/tube) were incubated in Krebs-Ringer bicarbonate buffer at 37 degrees C for 4h. Free thyroxine (fT4) released in the incubation medium, thyroidal cAMP and calmodulin content were measured by RIA. TSH (5 mU/ml) and dibutyryl cAMP (DBC) (200 micrograms/ml) caused a 2-4 fold increase in thyroidal release of fT4. The stimulatory effects of TSH on fT4 release were significantly inhibited by trifluoprazine and prenylamine lactate at the concentration of 5 X 10(-5) M. More specific calmodulin antagonists, W-7 and W-13, were also shown to inhibit TSH stimulation of fT4 release at the concentration of 5 X 10(-5) M. In contrast, TSH stimulation of fT4 release was not depressed by non-specific antagonists, W-5 or W-12, at the same concentration as 5 X 10(-5) M. Further, W-13 also markedly inhibited DBC-stimulated fT4 release. Neither TSH nor PGI2 altered the thyroidal calmodulin content, dissociating with a marked increase in the cAMP concentration. These results suggest that calmodulin plays an important role in TSH-stimulated thyroid hormone release and further that this mechanism exists, at least in part, at the site subsequent to the generation of cAMP.

Animals↗
PubMed1988

Characterization of specific thyroid hormone receptors in bone.

Thyroid hormones stimulate bone turnover in vivo and increase Ca release from bone in vitro. To investigate further the effects of thyroid hormones in bone, we have characterized specific nuclear receptors for [125I]tri-iodothyronine (T3) in neonatal mouse calvaria. Maximal specific binding of [125I]T3 to isolated nuclei occurred within 60 min at 22 degrees C. [125I]T3 binding was completely and rapidly displaced by the addition of 10(-6) M unlabeled T3; the dissociation appears to be first order with t1/2 = 36 min. The IC50 for competition by unlabeled T3 was approximately 10(-8) M. The relative affinity of thyroxine (T4) for the receptor was approximately 10 X lower than T3, consistent with its lower biological potency in most target tissues for thyroid hormones. Only weak competition was observed with diiodotyrosine at concentrations up to 10(-4) M. We have previously shown that the cardiotonic agent milrinone stimulates bone resorption in vitro with characteristics similar to those of T4. Structural homology between milrinone and T4 was recently reported. Milrinone, like diiodotyrosine, was only a weak competitor for binding at concentrations up to 10(-4) M. Milrinone inhibited collagen synthesis in the calvaria. The results suggest that the effects of milrinone on bone turnover in calvaria in vitro are probably not mediated through a thyroid hormone receptor.

Animals↗
PubMed1976

Serum thyrotropin response to thyrotropin-releasing hormone and free thyroid hormone indices in patients with familiar thyroxine-binding globulin deficiency.

The response in serum thyrotropin (TSH) to synthetic thyrotropin-releasing hormone (TRH) as well as serum free thyroxine index (FT4I) and free triiodothyronine index (FT3I) was investigated in six patients with familial thyroxine-binding-globulin (TBG) deficiency. The total serum thyroxine (T4) and triiodothyronine (T3) concentrations were significantly decreased, compared with those of normal subjects (3,4 +/- 0.9 microng/dl, mean +/- S.D. vs. 9.0 +/- 1.5 microng/dl, p less than 0.01 and 87 +/- ng/dl vs. 153 +/- 37 ng/dl, p less than 0.01, respectively). FT4I was lower than the normal range in all but one (5.3 +/- 1.5 vs. 8.9 +/- 1.6, p less than 0.01), whereas FT3I was all in the normal range and of no significant difference from the normal control (132 +/- 22 vs 148 +/- 25). Serum TSH concentrations in TBG deficiency were all in the normal range (1.0-4.2 micronM/ml) and the maximum TSH increments following TRH 500 microng iv were 8.9 +/- 2.0 micronU/ml and of no significant difference from the normal control (10.2 +/- 4.5 micronU/ml). These results indicate that the euthyroid state in familial TBG deficiency is more clearly defined by TRH-test and the normal response to TRH in familial TBG deficiency is presumably under the control of the serum free T3 level rather than the serum free T4 level.

Adult↗
PubMed2000

Peripheral metabolism of thyroid hormones: a review.

Peripheral metabolism of thyroid hormones is a critical component of the impact these hormones have on intracellular function. Thyroid hormones can be metabolized in peripheral tissue by deiodination, conjugation, deamination, and decarboxylation enzyme reactions. Therefore, alterations in these metabolic pathways might significantly impact the quantity of specific thyroid hormone metabolites influencing function at the cellular level. Available evidence also suggests that, under some circumstances, the activity of hepatic antioxidant enzyme systems and lipid peroxidation might influence the peripheral metabolism of thyroid hormones. Several syndromes, such as "euthyroid sick syndrome" and "low T3 syndrome," have been classified within the medical literature. The common feature of these disorders is a low level of circulating T3, with generally normal to slightly elevated blood T4 levels and either normal or slightly suppressed TSH levels. This pattern of altered thyroid hormone levels is generally agreed to be a result of impairment in extra-thyroidal peripheral metabolism. Hepatic and renal pathology, as well as catabolic states such as those induced subsequent to severe injury, illness, or trauma result in consistent shifts in the thyroid hormone profile, secondary to their impact on peripheral enzyme pathways. Lifestyle factors, such as stress, caloric restriction, and exercise, influence peripheral metabolism of thyroid hormones. Exposure to toxic metals, chemical poisons, and several drugs can also influence the peripheral fate of thyroid hormones. While the role of vitamins, minerals, and botanical extracts in thyroid hormone metabolism requires further elucidation, current evidence supports a role for selenium in the hepatic 5'-deiodination enzyme.

Energy Intake↗
PubMed2002

Thyroid hormone transporters: recent advances.

Thyroid hormones, being hydrophobic, were thought to enter target cell membranes by passive diffusion. However, recent studies have documented the existence of numerous organic anion transport systems, about half of which also transport thyroid hormones into (and possibly out of) a variety of target cells. Several of the genes encoding thyroid hormone transporters have been characterized by means of molecular approaches. Here, we discuss the classification of thyroid hormone transporters, with emphasis on how they are influenced by their ionic milieu and what their symported organic anions are.

Amino Acid Transport Systems↗
PubMed1977

Serum thyrotropin response to thyrotropin-releasing hormone and free thyroid hormone indices in patients with familial thyroxine-binding globulin deficiency.

The response in serum thyrotropin (TSH) to synthetic thyrotropin-releasing hormone (TRH) as well as serum free thyroxine index (FT4I) and free triiodothyronine index (FT3I) was investigated in six patients with familial thyroxine-binding-globulin (TBG) deficiency. The total serum thyroxine (T4) and triiodothyronine (T3) concentrations were significantly decreased, compared with those of normal subjects (3.4 +/- 0.9 microgram/dl, mean +/- SD. vs. 9.0 +/- 1.5 microgram/dl, p less than 0.01 and 87 +/- 27 ng/dl vs. 153 +/- 37 ng/dl, p less than 0.01, respectively). FT4I was lower than the normal range in all but one (5.3 +/- 1.5 vs. 8.9 +/- 1.6, p less than 0.01), whereas FT3I was all in the normal range and of no significant difference from the normal control (132 +/- 22 vs. 148 +/- 25). Serum TSH concentrations in TBG deficiency were all in the normal range (1.0-4.2 muU/ml) and the maximum TSH increments following TRH 500 microgram iv were 8.9 +/- 2.0 muU/ml and of no significant difference from the normal control (10.2 +/- 4.5 muU/ml). These results indicate that the euthyroid state in familial TBG deficiency is more clearly defined by TRH-test and the normal response to TRH in familial TBG deficiency is presumably under the control of the serum free T3 level rather than the serum free T4 level.

Adult↗
PubMed1975

Thyroid hormone and the kidney.

Thyroid hormones affect both renal morphology and function. They are required for kidney growth and development, and thyroid deficiency results in decreased renal plasma flow and glomerular filtration rate and in impaired urinary concentration and dilution. Thyroid hormones also influence membrane transport and electrolyte metabolism, and alterations in mineral metabolism in hyperthyroidism frequently cause calcium nephropathy which affects renal function adversely. The kidney plays an important role in the peripheral metabolism of iodine and thyroid hormones, and thyroid function is altered in certain kidney diseases, particularly chronic renal failure. The pathogenesis of these alterations is currently under active investigation.

Animals↗
PubMed1980

Endocrine and behavioral changes in depression after thyrotropin-releasing hormone (TRH). Alteration by pretreatment with thyroid hormones.

The effects of pretreatment with a single dose of thyroid hormones (TH) on the subsequent endocrine and behavioral response to TRH was evaluated in unipolar depressed women. TH pretreatment altered neither serum levels of thyroid hormones nor the TRH-induced TSH response. It antagonized, however, the behavioral response to TRH. This was apparent in 2 self-assessment scales but not in an objective rating scale. Taken together the data suggest that (a) there is an impaired pituitary response to TH feedback in depressed patients; (b) TH pretreatment may affect self-assessment of behavioral effects of TRH in depression.

Adult↗
PubMed1989

Trans-activation by thyroid hormone receptors: functional parallels with steroid hormone receptors.

The effects of thyroid hormones are mediated through nuclear receptor proteins that modulate the transcription of specific genes in target cells. We previously isolated cDNAs encoding two different mammalian thyroid hormone receptors, one from human placenta (hTR beta) and the other from rat brain (rTR alpha), and showed that their in vitro translation products bind thyroid hormones with the characteritistic affinities of the native thyroid hormone receptor. We now demonstrate that both of the cloned receptors activate transcription from a thyroid hormone-responsive promoter in a hormone-dependent manner, with rTR alpha eliciting a greater response than hTR beta. The putative functional domains of the thyroid hormone receptors were examined by creating chimeric thyroid hormone/glucocorticoid receptors, producing receptors with hybrid functional properties. These experiments support the proposal that the thyroid hormone receptors are composed of interchangeable functional domains, and indicate that the mechanism of hormone-inducible gene regulation has been conserved in steroid and thyroid hormone receptors.

Animals↗
PubMed1996

Nongenomic actions of thyroid hormone.

Nongenomic actions of thyroid hormone are by definition independent of nuclear receptors for the hormone and have been described at the plasma membrane, various cell organelles, the cytoskeleton, and in cytoplasm. The actions include alterations in solute transport (Ca2+, Na+, glucose), changes in activities of several kinases, including protein kinase C, cAMP-dependent protein kinase and pyruvate kinase M2 (PKM2), effects on efficiency of specific mRNA translation and mRNA t1/2, modulation of mitochondrial respiration, and regulation of actin polymerization (promotion of formation of F-actin). Iodothyronines also can regulate nongenomically the state of contractile elements in vascular smooth muscle cells (VSMC). The physiologic significance at the cellular level of certain of these actions has been demonstrated, for example, in the cases of myocardiocyte Na+ current, red cell Ca2+ content, and the control by hormone-induced alterations in actin solubility of cell surface activity of iodothyronine 5'-monodeiodinase activity and the intracellular distribution of protein disulfide isomerase activity. The physiologic significance of these actions at the organ or system level is less clear, but extranuclear effects of thyroid hormone on myocardial Na+ channel, sarcoplasmic reticulum Ca(2+)-ATPase activity, and contractile state of VSMC may each contribute to acute effects of thyroid hormone on cardiac output that have recently been described clinically. The molecular mechanisms for nongenomic actions are incompletely understood; relevant binding sites and signal transduction pathways have been described for hormone actions on plasma membrane Ca(2+)-ATPase activity, and PKM2 monomer is known to bind T3 and, as a result, prevent activation of the kinase via tetramer formation. Nongenomic actions of thyroid hormone may have different structure-activity relationships of iodothyronines from those effects that depend upon nuclear receptors; they may have different time courses and may invoke complex signal transduction pathways before the action is detected.

Animals↗
PubMed1997

Modification of thyroid hormone and 9-cis retinoic acid signaling by overexpression of their cognate receptors using adenoviral vector.

Tissue responsiveness to a hormone is dependent on the amounts of its receptor expressed under physiological conditions. In the present report, we compared the magnitude of ligand-dependent transactivation mediated by two nuclear hormone receptors, thyroid hormone receptor beta (TR) and retinoid X receptor alpha (RXR), when overexpressed in a variety of cell lines. TR, RXR and reporter (luciferase) genes under the control of artificial hormone response elements were introduced into the cells using recombinant adenovirus (Ad) vectors, to ensure highly efficient gene delivery. Although the amounts of TR expressed were similar in the cell lines infected with Ad-TR, T3 dependent induction of reporter gene expression was significantly greater in HepG2 than in Cos7, GH3, or JEG3 cells, indicating that factors other than TR are limiting the responsiveness to T3. The enhanced response to 9-cis retinoic acid in cells overexpressing RXR was much greater in JEG3 than in HepG2 which had the highest responsiveness to T3 under TR overexpression. These results indicate that the factors affecting T3 responsiveness are not identical to those affecting the 9-cis retinoic acid responsiveness. On the other hand, overexpression of RXR in addition to TR resulted in a decrease in T3-responsiveness in all the cell lines tested, suggesting that some cofactors are common to TR and RXR.

Adenoviridae↗
PubMed2002

Thyroid hormone receptors and type I iodothyronine 5'-deiodinase activity of human thyroid toxic adenomas and benign cold nodules.

The majority of thyroid adenomas are of clonal origin. In a subset of toxic adenomas (TAs) and cold nodules (CNs) activating mutations in the thyrotropin (TSH) receptor or G s -alpha gene may explain the altered functions in these benign tumours. The present study was undertaken to investigate the status of functional thyroid hormone receptors, major thyroid hormone signal mediators, in both the human TAs and CNs in comparison with a normal thyroid tissue from the same patient. Electrophoretic mobility shift assays using a DR4 ("direct repeats" 4), a thyroid hormone responsive element (TRE) of human type I iodothyronine 5'-deiodinase demonstrated the DNA-binding of thyroid hormone receptors (TRs) in thyroid tissue nuclear extracts. A significant increase (p < 0.05) in the functional binding properties of TRs to the DR4 thyroid hormone responsive element was found in TAs when compared to normal thyroid tissue. Contrary, a marked diminution in the TR-TRE complex formation was found in CNs in comparison with normal thyroid tissue. In addition, functional activity of the iodothyronine 5'-deiodinase (5'DI) was analyzed in benign tumours, thyroid TAs and CNs in comparison with that of normal thyroid tissue. A significantly increased (p < 0.01) activity of 5'DI was demonstrated in TAs, and in contrast, decreased values of the enzyme activity were found in CNs when compared to a normal tissue. From the data it is suggested that both the status of TR-TRE complex formation and the activity of the 5'DI may be altered in benign tumours of human thyroid gland.

Adenoma↗