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PubMed1989

Human carboxyl-terminal variant of alpha-type c-erbA inhibits trans-activation by thyroid hormone receptors without binding thyroid hormone.

Multiple thyroid hormone (T3; L-3,3',5-triiodothyronine) receptors related to the viral oncogene v-erbA have been identified in mammalian tissues and have been shown to mediate certain actions of T3. The role of a carboxyl-terminal variant of alpha-type c-erbA (c-erbA alpha-2) is controversial, since the human form has been reported to be a T3 receptor, while the rat form has been shown to not bind T3. In fact, the rat homolog of c-erbA alpha-2 has been reported to be an inhibitor of T3 action. We have compared the properties of human c-erbA alpha-2 with those of its rat homolog and with other forms of c-erbA. Neither form of c-erbA alpha-2 binds T3 with high affinity whether synthesized in reticulocyte lysates or by transient expression in mammalian cells. Also, neither form increases the expression of a T3-responsive gene. However, human c-erbA alpha-2 inhibits T3 action mediated by a T3-receptor form of c-erbA to an extent similar to that of rat c-erbA alpha-2. Our data strongly suggest that human c-erbA alpha-2 has a biological function similar to that of its rat homolog. Thus, the modulation of T3 action by an endogenous inhibitor related to T3 receptors is likely a general regulatory mechanism.

Amino Acid Sequence↗

PubMed1975

A comparison of the effects of the calcitonins, steroid hormones and thyroid hormones on the response of bone to parathyroid hormone in tissue culture.

A bone culture system was used to compare the effects of several hormones on the response of 5-day-old mouse calvaria to parathyroid hormone (PTH). The results showed that salmon calcitonin was almost 10-5 times more active than any other hormone in preventing the PTH-induced release of calcium and caused a dose-related inhibition of calcium release over a range of 0-2-200 milli MRC units/culture. A high dose of calcitonin (200 milli MRC units) caused a net accretion of calcium in the absence of PTH. Progesterone and testosterone were more active than the naturally occurring oestrogens although a synthetic oestrogen (stillboestrol diphosphate) had approximately the same potency. High concentrations of these hormones caused a net accretion of calcium whether or not PTH was present. Cortisol was only effective at high doses, as was the steroid precursor cholesterol. In the present culture system the thyroid hormones (triiodothyronine and thyroxine) inhibited the action of PTH. It was concluded that these agents acted in a similar fashion to the oestrogens. That is, they prevented the accumulation of citric acid induced by PTH by reducing the rate of glycolysis. None of the hormones affected the inhibition of citrate oxidation caused by PTH. The results also showed that, whilst these hormones inhibited PTH-mediated bone resorption, they had an action on bone independent of PTH. Experiments with clomiphene citrate failed to demonstrate an oestrogen receptor in bone.

Animals↗

PubMed1995

Modulation of thyroid hormone action by mutant thyroid hormone receptors, c-erbA alpha 2 and peroxisome proliferator-activated receptor: evidence for different mechanisms of inhibition.

Thyroid hormone action is not only determined by hormone availability, but also by target organ sensitivity. A dominant negative interaction is known to occur between thyroid hormone receptors (TRs) and the non-ligand binding splicing variant c-erbA alpha 2 as well as mutant TR beta 1 from kindreds with resistance to thyroid hormone. We compared the inhibitory effect of naturally occurring mutant hTR beta 1, artificially created hTR alpha 1 mutants, c-erbA alpha 2 and the human peroxisome proliferator-activated receptor (hPPAR) on three prototypic T3-response elements (TREs), TRE-PAL, DR + 4 and TRE-LAP. The inhibitory effect of mutant hTR alpha 1 and beta 1 occurred only on TRE-LAP and to a minor degree on DR + 4 when equimolar ratios of mutant/wildtype receptor were present. In contrast, the c-erbA alpha 2 splicing variant and the hPPAR inhibited TR action on all three TREs. Gel mobility shift experiments in the presence of T3 showed increased binding of mutant hTR alpha 1 and beta 1 only to TRE-LAP compared to the binding of wildtype hTRs, thereby explaining their TRE-selective dominant negative potency. Contrarily, equal amounts of c-erbA alpha 2 or hPPAR protein did not bind to either of the three response elements even in the presence of RXR. Since the TR:RXR heterodimers were only partially displaced from DNA in the presence of excess amounts of c-erbA alpha 2, it is likely that the TRE-unspecific dominant negative action of c-erbA alpha 2 is due in part to competition for DNA-binding and for TR-auxiliary proteins. In contrast, equimolar amounts of hPPAR completely inhibited the DNA-binding of hTR beta 1:RXR heterodimers, but not of TR:TR homodimers, suggesting that hPPAR has a higher RXR-binding affinity and is therefore a potent competitor for intranuclear RXR. Since thyroid hormones and peroxisome proliferators regulate in part a similar subset of target genes involved in fatty acid metabolism, these results suggest the possibility of cross-talk among the thyroid hormone and peroxisome proliferator signalling pathways. In summary, the results suggest that thyroid hormone action can be modulated by at least three different mechanisms: (i) increased binding of mutant hTRs to specific TREs; (ii) efficient competition for limiting amounts of RXR through the preferential formation of hPPAR:RXR, rather than TR:RXR heterodimers; and (iii) competition for binding to DNA and to auxiliary proteins other than RXR in the case of c-erbA alpha 2.

DNA↗

PubMed1999

Effects of oral chlortetracycline and dietary protein level on plasma concentrations of growth hormone and thyroid hormones in beef steers before and after challenge with a combination of thyrotropin-releasing hormone and growth hormone-releasing hormone.

The objective of this study was to determine the effect of a subtherapeutic level of chlortetracycline (CTC) fed to growing beef steers under conditions of limited and adequate dietary protein on plasma concentrations of GH, thyroid-stimulating hormone (TSH), and thyroid hormones before and after an injection of thyrotropin-releasing hormone (TRH) + GHRH. Young beef steers (n = 32; average BW = 285 kg) were assigned to a 2x2 factorial arrangement of treatments of either a 10 or 13% crude protein diet (70% concentrate, 15% wheat straw, and 15% cottonseed hulls) and either a corn meal carrier or carrier + 350 mg of CTC daily top dressed on the diet. Steers were fed ad libitum amounts of diet for 56 d, and a jugular catheter was then placed in each steer in four groups (two steers from each treatment combination per group) during four consecutive days (one group per day). Each steer was injected via the jugular catheter with 1.0 microg/kg BW TRH + .1 microg/kg BW GHRH in 10 mL of saline at 0800. Blood samples were collected at -30, -15, 0, 5, 10, 15, 20, 30, 45, 60, 120, 240, and 360 min after releasing hormone injection. Plasma samples were analyzed for GH, TSH, thyroxine (T4), and triiodothyronine (T3). After 84 d on trial, the steers were slaughtered and the pituitary and samples of liver were collected and analyzed for 5'-deiodinase activity. Feeding CTC attenuated the GH response to releasing hormone challenge by 26% for both area under the response curve (P<.03) and peak response (P<.10). Likewise, CTC attenuated the TSH response to releasing hormone challenge for area under the response curve by 16% (P<.10) and peak response by 33% (P<.02), and attenuated the T4 response for area under the curve by 12% (P<.08) and peak response by 14% (P<.04). Type II deiodinase activity in the pituitary was 36% less (P<.02) in CTC-fed steers than in steers not fed CTC. The results of this study are interpreted to suggest that feeding subtherapeutic levels of CTC to young growing beef cattle attenuates the release of GH and TSH in response to pituitary releasing hormones, suggesting a mechanism by which CTC may influence tissue deposition in cattle.

Animal Nutritional Physiological Phenomena↗

PubMed1993

The effects of corticosteroid hormones and thyroid hormones on lymphocyte viability and proliferation during development and metamorphosis of Xenopus laevis.

Metamorphosis in the South African clawed frog, Xenopus laevis, is characterized by a striking loss of lymphocytes in the thymus, liver, and spleen. Changes in the proliferative responses of splenocytes and thymocytes to T cell mitogens and semi-allogeneic cells are also observed at metamorphosis. Because the levels of circulating thyroid hormones (TH) and corticosteroid hormones (CH) increase dramatically during the climax of metamorphosis, we have investigated the possible role of TH and CH as mediators of the changes in lymphocyte numbers or lymphocyte function. Here we report on the in vitro effects of CH and TH on lymphocyte viability and on phytohemagglutinin-P (PHA)-stimulated lymphocyte proliferation at prometamorphosis and climax of metamorphosis. We have observed consistently significant inhibition of proliferation by corticosterone. In contrast, we have observed inconsistent inhibition of proliferation by both thyroxine (T4) and triiodothyronine (T3). In short-term studies, the viability of thymocytes and splenocytes was reduced in the presence of CH but not TH. These observations are consistent with a hypothesis that loss of larval lymphocytes and changes of lymphocyte function at metamorphosis may be due to elevated concentrations of CH rather than TH. Because CH have been shown to enhance TH-induced effects during metamorphosis, we looked at the combined effects of these agents on PHA-stimulated lymphocyte proliferation. While each agent was inhibitory in several experiments, there was no significantly greater inhibition when splenic lymphocytes were cultured with both.

Adrenal Cortex Hormones↗

PubMed1996

Recessive resistance to thyroid hormone in mice lacking thyroid hormone receptor beta: evidence for tissue-specific modulation of receptor function.

The diverse functions of thyroid hormone (T3) are presumed to be mediated by two genes encoding the related receptors, TRalpha and TRbeta. However, the in vivo functions of TRalpha and TRbeta are undefined. Here, we report that targeted inactivation of the mouse TRbeta gene results in goitre and elevated levels of thyroid hormone. Also, thyroid-stimulating hormone (TSH), which is released by pituitary thyrotropes and which is normally suppressed by increased levels of thyroid hormone, was present at elevated levels in homozygous mutant (Thrb-/-) mice. These findings suggest a unique role for TRbeta that cannot be substituted by TRalpha in the T3-dependent feedback regulation of TSH transcription. Thrb-/- mice provide a recessive model for the human syndrome of resistance to thyroid hormone (RTH) that exhibits a similar endocrine disorder but which is typically caused by dominant TRbeta mutants that are transcriptional inhibitors. It is unknown whether TRalpha, TRbeta or other receptors are targets for inhibition in dominant RTH; however, the analysis of Thrb-/- mice suggests that antagonism of TRbeta-mediated pathways underlies the disorder of the pituitary-thyroid axis. Interestingly, in the brain, the absence of TRbeta may not mimic the defects often associated with dominant RTH, since no overt behavioural or neuroanatomical abnormalities were detected in Thrb-/- mice. These data define in vivo functions for TRbeta and indicate that specificity in T3 signalling is conferred by distinct receptor genes.

Amino Acid Sequence↗

PubMed2000

Search for abnormalities of nuclear corepressors, coactivators, and a coregulator in families with resistance to thyroid hormone without mutations in thyroid hormone receptor beta or alpha genes.

The syndrome of resistance to thyroid hormone (RTH) is characterized by decreased tissue responsiveness to thyroid hormones. Inheritance is usually autosomal dominant due to mutations in the ligand-binding domain or adjacent hinge region of the thyroid hormone receptor beta (TRbeta) gene. Six of 65 families with the RTH phenotype studied in our laboratory had normal TRbeta1 and TRbeta2 gene sequences. Their clinical characteristics were not different from those of subjects with TRbeta gene mutations. Four of the 6 families were amenable to linkage analysis, and TRalpha involvement was excluded. Candidate genes were then evaluated for their possible involvement in the RTH phenotype in these 4 families: 2 coactivators [NCoA-1 (SRC-1) and NCoA-3 (AIB-1)], 2 corepressors (NCoR and SMRT), and a coregulator (RXRgamma). DNA was obtained from 8 affected subjects and 41 of 45 living first degree relatives. In 2 of the 4 families, the mode of inheritance could be determined by pedigree analysis and was found to be autosomal dominant. Linkage analyses were performed using polymorphic markers near or within the 5 candidate genes. When analyses were not informative or linkage could not be excluded, direct sequencing of the genes in question was performed. Involvement of NCoA-1 was excluded in all four families assuming autosomal dominant inheritance. Roles for NCoR, SMRT, and NCoA-3 were excluded in three and a role for RXRgamma was excluded in two of the four families. However, if the two families without proven dominant mode of inheritance were compound heterozygous, only the involvement of NCoA-1 could be excluded in both. Roles for NCoR, SMRT, and RXRgamma were excluded in one of these two families. Thus, NCoA-1 and RXRgamma genes were not found to be the cause of RTH in subjects without TR gene mutations even though the absence of NCoA-1 and RXRgamma is the cause of RTH in mice. Involvement of other candidate genes in the mediation of thyroid hormone action as well as intracellular hormone transport needs to be explored in these families with non-TRbeta, TRalpha RTH.

Animals↗

PubMed1999

Differential expression of thyroid hormone receptor isoforms by thyroid hormone and lithium in rat GH3 and B103 cells.

BACKGROUND: The interaction between lithium, a mood stabilizer, and the thyroid axis has been extensively studied; however, the regulation of thyroid hormone receptors by lithium is yet to be investigated. METHODS: To test whether lithium affects thyroid hormones at the receptor level, we examined the effects of lithium in combination with triiodothyronine (T3) on gene expression of thyroid hormone receptor isoforms in GH3 and B103 cells. RESULTS: The pattern of expression as well as the magnitude of regulation of the different thyroid hormone receptor isoforms appeared to be cell line specific. Whereas T3 regulated all four isoforms in GH3 cells at both time points, T3 did not alter thyroid hormone receptor TR alpha 1 and TR alpha 2 mRNA in B103 cells. Addition of lithium to thyroid hormone-deficient GH3 cells decreased TR alpha 1, alpha 2, and beta 2 expression without affecting TR beta 1 expression at 2 but not 5 days. Addition of lithium to T3-treated GH3 cells did not further modulate gene expression of TR alpha 1, alpha 2, beta 1, or beta 2 when compared to cells treated with T3 alone. The effects of lithium in B103 cells appeared to be isoform specific as well as time dependent, since TR alpha 1 expression was selectively decreased in B103 cells, when treated with T3 in the presence of lithium. CONCLUSIONS: The present study provides direct evidence that T3 and/or lithium regulate TR gene expression in vitro in a both time-dependent and cell line-specific manner.

Adenoma↗

PubMed1976

Thyrotropin-releasing hormone and thyroid hormone interactions on thyrotropin secretion in the rat: lack of inhibiting effects of small doses of triiodo-L-thyronine in the hypothyroid rat.

Rats were thyroidectomized (T) and injected once daily with thyroxine (T4) or triiodothyronine (T3) ip; circulating thyrotropin (TSH) levels and TSH response to 100 ng of thyrotropin releasing hormone (TRH) iv, were measured in different groups of rats at several intervals after the last dose of T4 or T3. It was found that T rats on 1.8 mug T4 or 0.4 mug T3/100 g BW/day, response to TRH decreased after the injection of the hormone, maximum suppressive effect being found about 7-8 h after T4, or 4 h after T3. The response increased as T4 or T3 levels reached a nadir, in agreement with present views on TRH, T4, and T3 interactions at the pituitary level. The degree of TSH response to TRH appears as a sensitive parameter of T4 or T3 activity in this experimental model. However, in T rats on 0.2 mug T3/100 g BW/day, TSH response to TRH did not decrease, but actually increased, after the daily injection of T3. These animals appeared to be in a state of continuous thyroid hormone deficiency. The same 0.2 mug T3 dose effectively suppresses the elevated basal TSH levels of these animals. It is also capable of decreasing TSH response to 100 ng TRH in animals under more "euthyroid" conditions. These results in the T rats on 0.2 mug T3 are not easily fitted into the relatively simple model frequently described to explain TRH-T3 interactions and TSH secretion.

Animals↗

PubMed1991

Thyroid disease in middle-aged and elderly Swedish women: thyroid-related hormones, thyroid dysfunction and goitre in relation to age and smoking.

The prevalence of thyroid disease and the concentration of thyroid hormones and thyrotropin were studied in a random population sample of 1154 women, aged 50-72 years, with special reference to the effect of age and smoking. The prevalence of spontaneous hypothyroidism was 3.3% (previously unknown overt and mild disease 1.3%) and the prevalence of hyperthyroidism was 2.5% (previously unknown disease 0.2%). Clinically suspected hyper- or hypothyroidism (very weak to strong) was recorded in 288 women, but was only verified in three cases. The prevalence of visible and palpable thyroid enlargement was 2.1% and 13-14%, respectively. Total thyroxine concentrations increased and free tri-iodothyronine levels decreased significantly with age (P less than 0.001). The serum thyrotropin concentrations were lower in smoking women than in non-smokers in the 50- and 58-year age groups (P less than 0.05). There was no increase in the prevalence of thyroid disease or goitre in the women who were smokers at the time of the study.

Age Factors↗

PubMed1993

[The effect of thyroid hormone on thyroid cancer growth].

Differentiated thyroid cancer, like breast cancer, prostatic cancer, and endometrial cancer of the uterus, is well known to be hormone sensitive. Experimental investigations have demonstrated that differentiated thyroid cancer cells have TSH (thyroid-stimulating hormone) receptor on the plasma membrane and that the growth regulation of differentiated thyroid cancer depends upon TSH. Therefore, suppression of TSH with thyroid hormone is rational for the treatment of recurrent thyroid cancer. Recurrent differentiated thyroid cancers reportedly cause regression in response to thyroid hormone administration, but the outcome of adjuvant therapy with thyroid hormone after operation for differentiated thyroid carcinoma is controversial. It is very difficult to analyze the difference in survival rate between the postoperative patient with and without thyroid hormone, because of the excellent postoperative survival rate of differentiated thyroid cancer patients. Further clinical studies and laboratory investigations about TSH suppression in adjuvant therapy for differentiated thyroid cancer are necessary to elucidate the impact of thyroid hormone on survival after operation.

Adult↗

PubMed1994

Effects of thyroid hormone and thyroid dysfunction on the cardiovascular system.

Thyroid disease is common in veterinary practice. The heart, especially the myocardium, is sensitive to thyroid hormone, and deficiencies or excesses can alter cardiovascular function. Observed changes result from direct effects upon the myocardium and indirect effects that result from effects upon the vasculature and peripheral tissues. Clinically significant cardiovascular abnormalities related to hypothyroidism are rare. If present, they are primarily manifest as reduced left ventricular pump function, as apparent echocardiographically, or arrhythmias. Hyperthyroidism is common in the cat and infrequently encountered in dogs. Clinically significant cardiovascular manifestations are common and often dramatic. Hyperdynamic systolic function and mild myocardial hypertrophy are common manifestations which may lead to overt congestive and high output heart failure. If signs of congestive heart failure or significant arrhythmias are not evident, specific therapy need only be directed toward restoration of the euthyroid state. In most cases the cardiovascular changes associated with thyroid dysfunction are completely reversible.

Animals↗

PubMed1984

Interrelationships among body mass, thyrotropin, thyroid hormones, and thyroid-hormone binding proteins in healthy 70-year-old men.

In a previous study of a representative population of 460 men of age 70, we found that the free thyroxin (free T4) concentration was negatively correlated to body mass. In the present study we analyzed other indicators of thyroid function in relation to body mass and body mass index in 181 individuals without any disease or medication influencing thyroidal homeostasis or body mass. There was a significant negative relationship between body mass and body mass index and free T4, total T4, and 3,3',5'-triiodothyronine (rT3). Thus, individuals with high body mass normally had lower circulating concentrations of these hormones than lean individuals, whereas there was no such relationship for thyrotropin or 3,5,3'-triiodothyronine (T3). The thyroid-hormone binding proteins (thyroxin-binding globulin, prealbumin, and albumin) did not correlate with body mass or body mass index. As expected, thyroxin-binding globulin correlated with T4, T3, and rT3, but not with free T4 or thyrotropin. Concentrations of serum albumin correlated with T3 and rT3 concentrations but not with free T4, T4, or thyrotropin concentrations. Thyrotropin concentrations correlated negatively with free T4, T4, and rT3, but not with T3, indicating that circulating T4 plays the dominant role in feedback regulation of thyrotropin in healthy individuals.

Aged↗

PubMed1984

Endocrine changes during natural spawning in the white sucker, Catostomus commersoni. I. Gonadotropin, growth hormone, and thyroid hormones.

White suckers (Catostomus commersoni; Cypriniformes, Teleosteii) spawning in a small stream in central Alberta were captured during different stages of their spawning migrations in 1981 and 1982, blood was sampled, and the fish were examined to determine their reproductive condition. Blood samples were analyzed for gonadotropin (GtH), growth hormone (GH), triiodothyronine (T3), and thyroxine (T4) by radioimmunoassay. GtH levels in both sexes were lowest prior to the onset of spawning, increased significantly in spawning males, females in which germinal vesicle migration had begun, and ovulated females and then dropped significantly in spent fish of both sexes. GH was lowest in prespawning females, increased significantly at ovulation, and remained high in spent females. In contrast, GH levels in males were relatively constant throughout spawning. In both sexes, highest T4 levels were found in prespawning fish, and T4 decreased significantly in spent fish. Although a similar decline was seen in T3 in 1981, in 1982 there were no T3 changes associated with changes in reproductive condition. No significant diurnal variations were detected in the levels of GtH or T3; T4 levels appeared to vary on a diurnal basis in prespawning males only. Spawning activity in both sexes therefore appears to be associated with increases in GtH occurring at ovulation in females and at the initiation of spawning in males. GH levels may also be related to reproductive condition in females, but not in males. The relationship of thyroid hormone levels to reproductive condition is less clear, however, and these levels may reflect both endocrine and environmental influences on thyroid function.

Animals↗

PubMed1996

Dominant-negative mutant thyroid hormone receptors prevent transcription from Xenopus thyroid hormone receptor beta gene promoter in response to thyroid hormone in Xenopus tadpoles in vivo.

We describe a dominant-negative approach in vivo to assess the strong, early upregulation of thyroid hormone receptor beta (TR beta) gene in response to thyroid hormone, characteristic of the onset of natural and thyroid hormone-induced amphibian metamorphosis, 3,3',5-Triiodo-thyronine (T3) treatment of organ cultures of premetamorphic Xenopus tadpole tails coinjected in vivo with the wild-type Xenopus TR beta (wt-xTR beta) and three different thyroid responsive element chloramphenicol acetyltransferase (TRE-CAT) reporter constructs, including a direct repeat +4 (DR +4) element in the -200/+87 fragment of the xTR beta promoter, resulted in a 4- to 8-fold enhancement of CAT activity. Two human C-terminal TR beta 1 mutants (delta-hTR beta 1 and Ts-hTR beta 1), an artificial Xenopus C-terminal deletion mutant (mt-xTR beta), and the oncogenic viral homology v-erbA, none of which binds T3, inhibited this T3 response of the endogenous wt-xTR in Xenopus XTC-2 cells cotransfected with the -1600/+87 xTR beta promoter-CAT construct, the potency of the dominant-negative effect of these mutant TRs being a function of the strength of their heterodimerization with Xenopus retinoid X receptor gamma. Coinjection of the dominant-negative Xenopus and human mutant TR beta s into Xenopus tadpole tails totally abolished the T3 responsiveness of the wt-xTR beta with different TREs, including the natural DR +4 TRE of the xTR beta promoter.

Amino Acid Sequence↗

PubMed2004

The novel missense mutation methionine 442 threonine in the thyroid hormone receptor beta causes thyroid hormone resistance: a case report.

We report a family with thyroid hormone resistance caused by a novel mutation M442T in the thyroid hormone receptor beta (TRbeta) gene. The 59-year-old propositus and one of his two daughters had typical clinical signs of reduced responsiveness of tissues to thyroid hormones. Thus, elevated free T (3) and T (4) plasma concentrations in coexistance with a diffuse nodular goiter, nonsuppressed TSH, and atrial fibrillation with tachycardia were present in the propositus. His affected daughter also had increased levels of free T (3) and T (4) with slightly elevated TSH concentrations. Both affected members harboured a heterozygous M442T TRbeta mutation. The unaffected child had no mutation in the TRbeta gene and no clinical manifestations.

Atrial Fibrillation↗

PubMed1996

Effect of thyroid hormone on growth. Lessons from the syndrome of resistance to thyroid hormone.

Thyroid hormone deprivation results in deleterious effects on bone growth. The delayed bone development is mediated by a direct effect of thyroid hormone on bone and an indirect effect of the hormone on GH release and IGF-1 action. Both TR alpha and TR beta are expressed in bone cells. To examine the role of TR beta on bone, we have reviewed the growth abnormalities in the human syndrome of RTH caused by mutations in the TR beta gene. The mutant TR beta reduces the tissue responsiveness to thyroid hormone, producing in some tissues variable degrees of thyroid hormone deprivation. With regard to bone, relative thyroid hormone deficiency caused by the mutant TR beta produces short stature and delayed bone growth but does not attenuate growth to the extent that absolute thyroid hormone deficiency does. These observations indicate that an intact TR beta is required for normal bone development and growth.

Bone and Bones↗

PubMed1982

Catecholamine-thyroid hormone interactions: II. Thyroid hormone and platelet MAO activity in patients with thyroid disorders.

Platelet monoamine oxidase (MAO) activity and serum thyroxine indices were determined in 62 children and adolescents currently undergoing medical treatment for various thyroid disorders. The platelet MAO activity of these patients was similar to that of control and contrast groups previously reported, and there were no differences when patients were grouped according to specific thyroid disorders. Estimated free thyroxine and total thyroxine levels were generally in the upper normal or slightly elevated range and were not significantly related to MAO activity.

Adolescent↗