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PubMed1983

Pituitary and thyroid hormone responses of heifers after ferulic acid administration.

I evaluated effects of ferulic acid on concentrations of endocrine hormones of eight Holstein heifers. Cattle were fitted with indwelling jugular cannulae 24 h before experimentation. After control blood samples were taken, animals were assigned randomly to groups of four and infused with 100 or 500 mg of ferulic acid. Prolactin, growth hormone, luteinizing hormone, and thyroid hormones were measured in sera from blood samples. Blood sampling or ethanol infusion did not affect serum concentrations of prolactin. Serum prolactin was elevated 5 min after infusion of ferulic acid. Peak serum prolactin concentrations were 15 min after 100 mg of ferulic acid and between 10 and 30 min after 500 mg ferulic acid. Prolactin remained high until 120 min post drug administration. Control bleeding and ethanol administration did not alter serum growth hormone concentrations. Serum growth hormone concentrations were elevated slightly by ferulic acid. The increase was 5 min after drug administration. Baseline concentrations were established 60 to 90 min after administration. Ferulic acid did not affect luteinizing hormone or thyroid hormones. Ferulic acid, a constituent of corn and wheat germ, may affect release of pituitary hormones in cattle.

Animals↗
PubMed2005

Analysis of thyroid hormone receptor betaA mRNA expression in Xenopus laevis tadpoles as a means to detect agonism and antagonism of thyroid hormone action.

Amphibian metamorphosis represents a unique biological model to study thyroid hormone (TH) action in vivo. In this study, we examined the utility of thyroid hormone receptors alpha (TRalpha) and betaA (TRbetaA) mRNA expression patterns in Xenopus laevis tadpoles as molecular markers indicating modulation of TH action. During spontaneous metamorphosis, only moderate changes were evident for TRalpha gene expression whereas a marked up-regulation of TRbetaA mRNA occurred in hind limbs (prometamorphosis), head (late prometamorphosis), and tail tissue (metamorphic climax). Treatment of premetamorphic tadpoles with 1 nM 3,5,3'-triiodothyronine (T3) caused a rapid induction of TRbetaA mRNA in head and tail tissue within 6 to 12 h which was maintained for at least 72 h after initiation of T3 treatment. Developmental stage had a strong influence on the responsiveness of tadpole tissues to induce TRbetaA mRNA during 24 h treatment with thyroxine (0, 1, 5, 10 nM T4) or T3 (0, 1, 5, 10 nM). Premetamorphic tadpoles were highly sensitive in their response to T4 and T3 treatments, whereas sensitivity to TH was decreased in early prometamorphic tadpoles and strongly diminished in late prometamorphic tadpoles. To examine the utility of TRbetaA gene expression analysis for detection of agonistic and antagonistic effects on T3 action, mRNA expression was assessed in premetamorphic tadpoles after 48 h of treatment with the synthetic agonist GC-1 (0, 10, 50, 250 nM), the synthetic antagonist NH-3 (0, 40, 200, 1000 nM), and binary combinations of NH-3 (0, 40, 200, 1000 nM) and T3 (1 nM). All tested concentrations of GC-1 as well as the highest concentration of NH-3 caused an up-regulation of TRbetaA expression. Co-treatment with NH-3 and T3 revealed strong antagonistic effects by NH-3 on T3-induced TRbetaA mRNA up-regulation. Results of this study suggest that TRbetaA mRNA expression analysis could serve as a sensitive molecular testing approach to study effects of environmental compounds on the thyroid system in X. laevis tadpoles.

Acetates↗
PubMed2000

Thyroid hormone receptor beta-deficient mice show complete loss of the normal cholesterol 7alpha-hydroxylase (CYP7A) response to thyroid hormone but display enhanced resistance to dietary cholesterol.

Thyroid hormone (T3) influences hepatic cholesterol metabolism, and previous studies have established an important role of this hormone in the regulation of cholesterol 7alpha-hydroxylase (CYP7A), the rate-limiting enzyme in the synthesis of bile acids. To evaluate the respective contribution of thyroid hormone receptors (TR) alpha1 and beta in this regulation, the responses to 2% dietary cholesterol and T3 were studied in TRalpha1 and TRbeta knockout mice under hypo- and hyperthyroid conditions. Our experiments show that the normal stimulation in CYP7A activity and mRNA level by T3 is lost in TRbeta-/- but not in TRalpha1-/-mice, identifying TRbeta as the mediator of T3 action on CYP7A and, consequently, as a major regulator of cholesterol metabolism in vivo. Somewhat unexpectedly, T3-deficient TRbeta-/- mice showed an augmented CYP7A response after challenge with dietary cholesterol, and these animals did not develop hypercholesterolemia to the extent as did wild-type (wt) controls. The latter results lend strong support to the concept that TRs may exert regulatory effects in vivo independent of T3.

Animals↗
PubMed1991

[Effects of whole-body microwave exposure on the plasma adrenocorticotropic hormone, thyroid-stimulating hormone and thyroid hormones in rats].

To investigate the effects of whole-body microwave exposure on plasma adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone (TSH), thyroxine (T4) and free triiodothyronine (T3) levels, rats weighing 267-306 g (light group) and 352-387 g (heavy group) were exposed to microwaves with a frequency of 2,450 MHz at the power densities of 5 and 10 mW/cm2 under an ambient temperature of 21 degrees C to 23 degrees C for an hour. Rectal temperatures were increased by 1.0 degrees C at 5 mW/cm2 and 2.1 degrees C at 10 mW/cm2 in the light group, and by 0.7 degrees C at 5 mW/cm2 and 1.5 degrees C at 10 mW/cm2 in the heavy group after microwave exposure. Plasma levels of ACTH increased significantly at 10 mW/cm2 in the light group and 5 and 10 mW/cm2 in the heavy group after microwave exposure. Plasma levels of TSH increased significantly at 10 mW/cm2 only in the light group. As for plasma levels of free T3, a significant decrease at 10 mW/cm2 was observed only in the heavy group. However, plasma levels of T4 did not change in either group after microwave exposure.

Adrenocorticotropic Hormone↗
PubMed1984

[Thyroid functions in nonthyroidal illness: specific changes in serum levels of thyroid hormones related in illness and the correlation between thyrotropin and free thyroid hormones in patients with nonthyroidal illnesses].

In order to assess the thyroid function of patients with nonthyroidal illness, 292 patients with nonthyroidal illness were employed in the present study. These patients were then subdivided into 6 groups according to their original illness. The groups consisted of patients with malignant illnesses (19 males and 10 females; mean age of 59.7 yr.), with chronic hepatitis (14 males and 8 females; mean age of 55.2 yr.), with liver cirrhosis (5 males and 6 females, mean age of 60.4 yr.), with uremia who had been receiving constant hemodialysis 2 approximately 3 times per week (52 males and 38 females; mean age of 48.1 yr.), with diabetes mellitus (50 males and 43 females; mean age of 52.3 yr.) and with cerebrovascular accident (21 males and 26 females; mean age of 74.9 yr.). In addition, 34 healthy persons (15 males and 19 females; mean age of 41.6 yr.) were also employed as controls. Because the differences between mean ages in these groups were significant, the relationship between age and thyroid function was examined. Significant positive correlations between age and total thyroxine (TT4) (r = 0.19; p less than 0.01), and reverse triiodothyronine (rT3) (r = 0.175; p less than 0.01) were found. A negative correlation was also found between age and total triiodothyronine (TT3) (r = 0.231; p less than 0.01). The serum levels of rT3 were elevated in patients with neoplasma and liver cirrhosis but significantly low in patients with uremia. These characteristic findings were correlated with the severity of each original disease such as % motarity, serum levels of cholinesterase, blood urea nitrogens and the blood sugar control in the diabetics. In these circumstances, multiple correlation analyses were performed in order to assess whether there might exist a negative feedback mechanism between thyrotropin and FT4/FT3. The highest partial correlation coefficient was obtained between thyrotropin and FT4. It might, therefore, be concluded that in patients with a nonthyroidal illness, decreased levels of serum thyroid hormones indicate not only the severity of the illness but also the supposed presence of a hypothyroid state.

Adult↗
PubMed1977

Modulation of pituitary thyrotropin releasing hormone receptor levels by estrogens and thyroid hormones.

The effect of estradiol and thyroid hormone treatment on pituitary TRH binding and TSH and PRL responses to the neurohormone was studied. A significant increase in the number of pituitary TRH binding sites was observed between 2 and 4 days after daily administration of estradiol benzoate with a plateau at 300% of control being reached at 7 days. Plasma PRL levels showed a similar early pattern of response. In animals rendered hypothyroid by a 2-month treatment with propylthiouracil or 1 month after surgical thyroidectomy, the level of pituitary TRH receptors was increased approximately 2-fold, this elevation being completely reversed by treatment with thyroid hormone. Estradiol-17beta administered with L-thyroxine partially reversed the inhibitory effect of thyroid hormone on TRH receptor levels in hypothyroid animals. The antagonism between estrogens and thyroid hormone is also apparent on the TSH response to TRH since estrogen administration can reverse the marked inhibition by thyroxine of the TSH response to TRH either partially or completely in intact and hypothyroid animals, respectively. The PRL response to TRH is 55 and 40% inhibited in hypothyroid and intact rats, respectively, by thyroid hormone when combined with estrogen treatment. The present data clearly show that estrogens and thyroid hormones can affect TSH and PRL secretion, the effect of estrogens being predominantly on PRL secretion while thyroid hormone affects mainly TSH. The close correlation observed between the level of TRH receptors and PRL and TSH responses to TRH suggests that estrogens and, to a lesser extent, thyroid hormones, exert their action by modulation of the level of receptors for the neurohormone in both thyrotrophs and mammotrophs.

Animals↗
PubMed1994

The variable clinical phenotype in thyroid hormone resistance syndrome.

Thyroid hormone resistance syndrome (RTH) is a rare disorder characterized by elevated levels of circulating free thyroid hormones, inappropriate TSH secretion, and reduced peripheral tissue responses to iodothyronine action. On the basis of clinical features, at least two different forms of RTH have been described: generalized resistance (GRTH) in which patients are asymptomatic with few clinical signs and pituitary resistance (PRTH) where patients present with some signs and symptoms associated with thyrotoxicosis. However, a review of the literature and our own experience indicates that there is a wide overlap of symptoms and signs exhibited by individuals with GRTH or PRTH. Assessments using biochemical and physiological indices of thyroid hormone action are useful, but limited by their lack of precision and also show an overlap between values recorded in GRTH and PRTH. In addition, we have observed significant temporal variations in clinical signs as well as in parameters of thyroid hormone action in the same individuals, with no correlation with their subjective symptoms. Recent genetic analyses indicate that patients with either GRTH or PRTH are heterozygous for mutations in the thyroid hormone receptor beta (TR beta) gene. Indeed, different clinical features have been observed in affected individuals within a kindred harboring the same Tr beta mutation, and identical mutations have been identified in unrelated kindreds classified as GRTH or PRTH. These data support the view that GRTH and PRTH are variable manifestations of a single genetic entity. Nevertheless, this clinical distinction will remain useful as a guide to the most appropriate treatment. The variable phenotypic spectrum of thyroid hormone resistance may be related to factors other than mutations in Tr beta that have yet to be elucidated.

Diagnosis, Differential↗
PubMed1993

Resistance to thyroid hormone.

Resistance to thyroid hormone encompasses a clinically heterogeneous group of conditions characterized by reduced responses of target tissues to a supply of thyroid hormone that under normal circumstances would be excessive. The syndrome of resistance to thyroid hormone is first suspected when serum thyroid hormone levels are found to be elevated in the presence of nonsuppressed serum thyrotropin (TSH). Clinical confirmation of the diagnosis requires the demonstration of the failure of full replacement doses of thyroid hormone to produce the expected suppressive effect on the secretion of TSH and a failure to induce appropriate responses in peripheral tissues.

Amino Acid Sequence↗
PubMed1984

Putative nuclear triiodothyronine receptors in tadpole erythrocytes: regulation of receptor number by thyroid hormone.

Putative thyroid hormone (TH) receptors have been detected in the nuclei of red blood cells (RBCs) from Rana catesbeiana tadpoles, and their binding characteristics have been examined. Nuclear T3 saturation analyses were carried out in vitro in intact RBCs suspended in phosphate-buffered amphibian Ringer. After incubation with T3, intact nuclei were obtained by centrifugation after lysing the cells in a sucrose-Tris-HCl buffer containing 0.2% saponin and then adding Triton X-100 (final concentration 0.125%) to the lysed mixture to reduce nonspecific binding to less than 10% of total binding. Scatchard analysis of equilibrium binding data revealed that RBCs from premetamorphic (first year) tadpoles contained 502 +/- 39 (SE) T3 binding sites per nucleus; in prometamorphic (second year) tadpoles the number had increased to 844 +/- 39. Development was also accompanied by some increase in the affinity of these sites; dissociation constant (Kd) = 1.8 +/- 0.39 X 10(-11) M and 0.95 +/- 0.108 X 10(-11) M in pre- and prometamorphic tadpoles, respectively. The number of sites per nucleus in both pre- and prometamorphic tadpole RBCs was greatly increased by pretreatment in vivo with either T3 or T4 for 6-10 days; a comparable number of sites per nucleus (2225 +/- 65) was observed after maximal stimulation by either hormone at both stages of development. Significant increases in receptor number were observed 10 days after injection of 0.03 nmol T3 or 0.06 nmol T4 into tadpoles weighing 13-15 g; maximal effects were obtained with 0.1 nmol T3 or 1.0 nmol T4. On the basis of these observations and the evidence that more TH is present in pro- than in premetamorphic tadpoles, it is suggested that the spontaneous increase in receptor number in RBC nuclei associated with progression from the pre- to prometamorphic phase is due, at least in part, to increased levels of endogenous TH.

Animals↗
PubMed2002

Persistence of oligodendrocyte precursor cells and altered myelination in optic nerve associated to retina degeneration in mice devoid of all thyroid hormone receptors.

Thyroid hormone (3,5,3'-triiodo-l-thyronine or T3) exerts a pleiotropic activity during central nervous system development. Hypothyroidism during the fetal and postnatal life results in an irreversible mental retardation syndrome. At the cellular level, T3 is known to act on neuronal and glial lineages and to control cell proliferation, apoptosis, migration, and differentiation. Oligodendrocyte precursor cells (OPC) found at birth in the optic nerves are self-renewing cells that normally differentiate during the first 3 weeks of rodent postnatal life into postmitotic myelinating oligodendrocytes. In vitro, the addition of T3 to OPC is sufficient to trigger their terminal differentiation. The present analysis of T3 receptor knockout mice reveals that the absence of all T3 receptor results in the persistence of OPC proliferation in adult optic nerves, in a default in myelination, and sometimes in the degeneration of the retinal ganglion neurons. Thus, T3 signaling is necessary in vivo to promote the complete differentiation of OPC.

Animals↗
PubMed1991

Regulation of c-erbA-alpha messenger RNA species in tadpole erythrocytes by thyroid hormone.

Putative thyroid hormone (TH) nuclear receptors have been detected in several tissues of Rana catesbeiana tadpoles. T3 receptor number (sites per nucleus) in red blood cells (RBCs) and tail increases substantially just before metamorphic climax or in response to exogenous TH; in contrast, receptor number in liver remains relatively constant. TH receptors in mammals and birds are thought to be encoded by a c-erbA gene. In the present study, two c-erbA cDNAs, one prepared from Xenopus laevis oocytes (XenTR alpha 1) and one prepared from Rana catesbeiana tail (RC12), were used to examine the c-erbA-related mRNA species in Rana catesbeiana tissues and determine their role in the TH induction of tadpole RBC receptor number. XenTR alpha 1 encodes a protein with T3-binding properties typical of TH receptors. RC12 is almost 99% homologous with XenTR alpha 1 at the amino acid level and contains all of the putative T3-binding region and most of the DNA-binding region. Using either cDNA as a probe, it was found that two major species of c-erbA-related mRNA species (2.6 and 4.0 kilobases) were clearly evident in tadpole RBCs, tail, and liver. A third, more diffuse band (approximately 5.0 kilobases) was observed in RBC and tail. In RBCs, but not in liver, the combined level of c-erbA-related mRNA species was increased during spontaneous metamorphosis or after administration of TH. Furthermore, the TH-induced increase in both c-erbA-related mRNA species and receptor number in RBCs was prevented if actinomycin-D was administered with TH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Thyroid hormone antibodies and Hashimoto's thyroiditis in mongrel dogs.

Abnormally elevated serum T3 concentrations measured by RIA were observed in 19 clinically euthyroid or hypothyroid mongrel dogs. The serum T4 concentrations in these sera were low, normal, or high. Measurement of the intensity of thyroid hormone binding to serum proteins was determined by equilibrium dialysis. A marked decrease in the percent free T3 was observed in these abnormal sera. Polyacrylamide gel electrophoresis, pH 7.4, of normal dog serum enriched with tracer 125I-labeled thyroid hormones demonstrated binding of [125I]T4 to transthyretin, thyroid hormone-binding globulin, and albumin and of [125I]T3 primarily to thyroid hormone-binding globulin. In all abnormal sera, polyacrylamide gel electrophoresis demonstrated strikingly higher binding of T3 to immunoglobulin (Ig). Eleven of 16 abnormal sera had minimal to moderate binding of T4 to Ig. The percent free T4 was lower only in dogs whose sera demonstrated markedly increased binding of T4 to Ig. All abnormal sera tested had positive antithyroglobulin antibodies, consistent with the diagnosis of autoimmune lymphocytic thyroiditis. As in humans, antibodies to thyroid hormones in dogs are more common in the presence of Hashimoto's thyroiditis and should be considered when elevated serum thyroid hormone concentrations are observed in the absence of clinical thyrotoxicosis. When an antibody to only one thyroid hormone is present, a marked discrepancy in the serum concentrations of T3 and T4 will be observed.

Animals↗
PubMed1975

Human lymphocyte binding and deiodination of thyroid hormones in relation to thyroid function.

The human lymphocyte has been investigated regarding its function as a thyroid hormone target cell. Binding and deiodination of the thyroid hormones were determined after simultaneous incubation of 131I-labelled L-thyroxine (131I-T4) and 125I-labelled L-triiodothyronine (125I-T3) with lymphocytes from healthy subjects, from hyperthyroid and primary hypothyroid patients before and after treatment. The mean percentages of binding, 8.0 +/- 0.5 (mean +/- SEM) for 131I-T4, and 9.7 +/- 0.4 for 125I-T3 in the control group, were increased in the hyperthyroids to 10.1 +/- 0.4 and 12.7 +/- 0.6 respectively, and in the hypothyroids to 10.9 +/- 0.7 and 12.8 +/- 0.6. All elevated values returned to normal with successful treatment. The mean percentage of deiodination, 12.0 +/- 1.7 for 131I-T4, and 6.5 +/- 0.9 for 125I-T3 in the control group, showed a threefold increase in the hyperthyroid patients, to 35.9 +/- 3.2 and 20.2 +/- 1.9 respectively and remained unaltered in the hypothyroid patients. The values of successfully treated hyperthyroid patients were normal and those of the treated hypothyroid patients below normal.

Adolescent↗
PubMed1999

Feedback regulation of thyrotropin-releasing hormone gene expression by thyroid hormone in the caudal raphe nuclei in rats.

Medullary TRH regulates autonomic activity, and altered thyroid status is associated with autonomic disorders. We investigated whether thyroid hormone exerts a negative feedback regulation on TRH gene expression in the medullary caudal raphe nuclei. Medullary pro-TRH messenger RNAs (mRNAs) were mainly located in the raphe pallidus and raphe obscurus neurons as shown by in situ hybridization and were significantly increased by 70% and 160-230% by Northern blot analyses in 24 h fasted rats at 1 and 3-5 weeks after thyroidectomy, respectively, when serum T4 levels were reduced by 75-87%. The increased pro-TRH mRNA on the 30th day after thyroidectomy was reversed to euthyroid levels by T4 replacement (2 or 4 microg/100 g x day). T4 injections (10 or 100 microg/100 g x day for 30 days) did not significantly influence medullary pro-TRH mRNA levels in sham-operated rats. Thyroidectomized rats fed normally showed a 500% increase in pro-TRH mRNA levels 30 days after the surgery, while those fasted for 24 h showed only a 180% increase. These data indicate that medullary TRH gene expression is enhanced during hypothyroidism due to the lack of negative feedback regulation by thyroid hormone, and this response is modulated by feeding state. These findings may have important relevance to understanding autonomic-related visceral alterations induced by hypothyroidism.

Animals↗
PubMed1998

Insulin-like growth factor I reduces thyroid hormone receptors in the rat liver. Evidence for a feed-back loop regulating the peripheral thyroid hormone action.

Tri-iodothyronine (T3) is known to be involved in the regulation of the growth hormone (GH)-insulin-like growth factor I (IGF-I) axis. In previous studies we demonstrated that IGF-I and GH reduced the metabolic response to T3 measured as the activity of two T3-dependent enzymes, mitochondrial alpha-glycerophosphate dehydrogenase (alpha-GPD) and cytosolic malic enzyme (ME) in cultured rat liver cells. In this study we analysed in vivo the effect of IGF-I administered to rats on the activity of alpha-GPD and ME. IGF-I (240 micrograms/100 g body weight (BW) every 12 h for 48 h) significantly diminished alpha-GPD (P < 0.01) and ME (P < 0.05) activities. Serum basal glucose concentration was not significantly modified 12 h after the administration of recombinant human IGF-I (240 and 480 micrograms/100 g BW every 12 h for 48 h). Under similar conditions, no significant change in serum total thyroxine (TT4) concentration was observed, although free thyroxine (FT4) was diminished (P < 0.02) and total T3 (TT3) was increased (P < 0.03). To explore the participation of the nuclear thyroid hormone receptor (THR) in the mechanism of IGF-I action we measured the maximal binding capacity and the affinity constant (Ka) of THR by Scatchard analysis, and concentrations of messenger RNAs (mRNAs) that code for the isoforms of THR present in the liver (beta 1, alpha 1 and alpha 2) by Northern blot. IGF-I (240 micrograms/100 g BW every 12 h for 48 h) significantly reduced maximal binding capacity to 37% of the control value (P < 0.01) without changes in the Ka. beta 1, alpha 1 and alpha 2 THR mRNAs were significantly reduced (P < 0.01) by 120-480 micrograms/100 g BW IGF-I administration every 12 h for 48 h. Time-course studies indicated that this effect was obtained 12 h after the administration of 240 micrograms/100 g BW IGF-I (P < 0.05). These results indicate that IGF-I administration to rats diminishes the metabolic thyroid hormone action in the liver by a mechanism that involves, at least in part, a reduction in the number of THRs and in their level of expression.

Animals↗
PubMed2003

Selective thyroid hormone receptor modulators.

Thyroid hormone regulates many important processes in vertebrates. Analysis of the symptoms that accompany hypo- and hyperthyroidism, the most common disorders of the thyroid, suggests that there are certain desirable biological effects brought about by an excess or deficiency of thyroid hormone, and that selective thyroid hormone receptor modulators (STRMs) would be potentially useful therapeutic agents. This review will provide an introduction to thyroid hormone biology, and will discuss the chemistry and pharmacology of the first generation STRMs.

Animals↗
PubMed1995

Interdependence of corticosterone and thyroid hormones in larval toads (Bufo boreas). I. Thyroid hormone-dependent and independent effects of corticosterone on growth and development.

In a previous study (Hayes et al. [1993] J. Exp. Zool., 266:206-215), we demonstrated that exogenous corticosterone (B) inhibited growth, and had varied effects on development and metamorphosis in the toad (Bufo boreas). The current study determined the relation between the actions of B and thyroid hormones on body growth (length and weight), tail growth and reduction (length and height), rear leg growth and differentiation, and foreleg emergence (FLE). Thiourea (Thio; a goitrogen) and metyrapone (MTP; a glucocorticoid synthesis inhibitor) were used to determine the role of endogenous hormones in growth and development. These inhibitors were also used in various combinations with the thyroid hormones, thyroxine (T4) and triiodothyronine (T3), to determine the extent to which B's actions depend on the thyroid hormones. B was ineffective at inducing tail reduction (length and height) in the presence of Thio, but B enhanced the effects of both thyroid hormones, suggesting that the actions of B on the tail were dependent on thyroid hormones. B inhibited body growth even in the presence of Thio, but did not enhance thyroid hormone's inhibition of growth. B alone stimulated foreleg emergence (FLE) and enhanced thyroid hormone's activity on FLE when B and the thyroid hormones were given in combination, but did not induce FLE in the presence of Thio. B stimulated rear leg development, but not in the presence of Thio, suggesting that this effect was due to interactions with thyroid hormones. Furthermore, MTP antagonized the stimulatory effect of T4 on rear leg development, suggesting that endogenous B also interacted with exogenous thyroid hormones.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗