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PubMed2005

Induction of pancreatic acinar cell proliferation by thyroid hormone.

Thyroid hormone is known to elicit diverse cellular and metabolic effects in various organs, including mitogenesis in the rat liver. In the present study, experiments were carried out to determine whether thyroid hormone is able to stimulate cell proliferation in another quiescent organ such as the pancreas. 3,5,3'-L-tri-iodothyronine (T3) added to the diet at a concentration of 4 mg/kg caused a striking increase in nuclear bromodeoxyuridine (BrdU) incorporation of rat acinar cells 7 days after treatment (the labeling index was 46.7% in T3-treated rats vs 7.1% in controls). BrdU incorporation was limited to the acinar cells, with duct cells and islet cells being essentially negative. The increase in DNA synthesis was accompanied by the presence of several mitotic figures. Histological examination of the pancreas did not exhibit any sign of T3-induced toxicity. Determination of the apoptotic index, measurement of the serum levels of alpha-amylase and lipase, and glycemia determination did not show any increase over control values, suggesting that the enhanced proliferation of acinar cells was a direct effect induced by T3 and not a regenerative response consequent to acinar or beta-cell injury. Additional experiments showed that DNA synthesis was induced as early as 2 days after T3 treatment (the labeling index was 9.4 vs 1.9% in controls) and was associated with increased protein levels of cyclin D1, cyclin A and proliferating cell nuclear antigen, with no substantial differences in the expression of the cyclin-dependent kinase inhibitor p27. The mitogenic effect of T3 on the pancreas was not limited to the rat, since extensive acinar cell proliferation was also observed in the pancreas of mice treated with T3 for 1 week (the labeling index was 28% in T3-treated mice vs 1.8% in controls). Treatment with three other ligands of nuclear receptors, ciprofibrate, all-trans retinoic acid and 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene, induced little or no pancreatic cell proliferation. These results demonstrated that T3 is a powerful inducer of cell proliferation in the pancreas and suggested that pancreatic acinar cell proliferation by selected agents may have potential for therapeutic use.

Administration, Oral↗

PubMed1979

Abnormal gamma globulin binding of thyroid hormones.

Thyroid hormone levels were studied in a thyrotoxic patient, who was treated with propylthiouracil. He had heavily increased triiodothyronine concentrations, measured by radioimmunoassay, in spite of only mild clinical symptoms of thyrotoxicosis. A moderately increased serum triiodothyronine concentration was observed in another patient, who was euthyroid and who had recently recovered from subacute thyroiditis. By gel electrophoresis and precipitation tests with human anti-IgG and anti-IgA, a binding to the gamma globulins of both triiodothyronine and thyroxine was detected in patient 1, and of triiodothyronine in patient 2. Such abnormal binding may result in serious errors in the determination of thyroid hormone concentration by radioimmunoassay.

Adult↗

PubMed2003

Depressed thermogenesis but competent brown adipose tissue recruitment in mice devoid of all hormone-binding thyroid hormone receptors.

We have examined the metabolic role of hormone-binding nuclear thyroid hormone receptors (TRs). Mice devoid of all hormone-binding TRs [TR alpha 1(-/-)beta(-/-) (TR-ablated mice)] had slightly decreased body temperature and much decreased basal metabolic rate, were still able to markedly increase metabolic rate in the cold, but were cold intolerant due to inadequate total heat production at low temperatures. A standard norepinephrine test showed that adrenergically induced thermogenesis could not be activated normally in the TR-ablated mice. This was not due to inadequate recruitment of brown adipose tissue, nor to the absence, decreased recruitment or dysfunction of the uncoupling protein-1. However, isolated brown fat cells were 10-fold desensitized, explaining the lack of response to standard adrenergic stimuli; cell culture experiments demonstrated that this desensitization was not an innate effect. Thus, the cold intolerance was probably not due to inadequate sympathetically induced nonshivering thermogenesis. Additionally, the results indicated that no metabolic effects of thyroid hormones could become manifest in the absence of nuclear TRs, that ligand-bound TRs were needed for euthermia and eumetabolism, but that TRs per se were not required for brown adipose tissue recruitment and uncoupling protein-1 gene expression.

Adipose Tissue, Brown↗

PubMed1988

Influence of marathon running on thyroid hormones.

Thyroid hormones were studied in 16 well-trained male amateur runners (mean age 31.8 years) before, immediately after, and 60 min and 22 h after marathon running. Free thyroxine (fT4), appraised by the free thyroxine index (fT4-I), was significantly increased immediately after and 1 h after the race compared with control values. Thyroid-stimulating hormone (TSH) was significantly increased immediately after the race, returned to the control value 1 h later, and was markedly decreased 22 h after the race. Free triiodothyronine (fT3) and free reverse triiodo-thyronine (frT3), appraised by the ratios triiodothyronine/-thyroxine binding globulin and reverse triiodothyronine/thyroxine binding globulin, respectively, showed contrary results. frT3 increased significantly after exercise, whereas fT3 decreased insignificantly. The peripheral conversion of thyroxine was additionally estimated by the ratios rT3/T3 and rT3/T. Both ratios were increased significantly after the run and remained elevated 22 h after the race. It is concluded that an increased TSH-regulated T4 secretion occurs during prolonged exercise as well as a change of the peripheral conversion process in favor of the hormonal inactive rT3. The latter condition remained still 22 h after the race.

Adolescent↗

PubMed1975

Effect of adrenal hormones on thyroid secretion and thyroid hormones on adrenal secretion in the sheep.

1. Previous work has shown that after stressful stimuli, sheep initially secrete increased amounts of thyroid hormone, at a time when adrenal secretion is also elevated. 2. This study was designed to evaluate (a) any short-term activation or inhibition of thyroid secretion by exogenous cortisol or ACTH administered in quantities comparable to those secreted after stress in sheep and (b) any short-term effect that exogenous thyroxine or triiodothyronine may have on the concentration of plasma cortisol in the sheep. 3. Thyroid activity was measured by determination of plasma protein bound 125I (PB125I) and total 125I in thyroid vein and mixed venous (jugular) blood. Plasma cortisol and thyroxine concentrations were measured by a competitive protein-binding assay at intervals for up to 5 hr after commencement of the experiment. 4. No evidence of an activation of thyroid secretion was found during cortisol or ACTH infusion, as monitored by thyroid vein PB125I. Similarly there was no evidence of any inhibition of thyroid function, as measured by continued secretion of thyroid hormones into thyroid vein blood. 5. No effect on plasma cortisol concentration due to thyroid hormone treatment was observed. 6. It was concluded that (a) elevated circulating corticosteroids in physiological concentrations have no short-term effects on thyroid activity in the sheep and (b) the short-term alterations in thyroid and adrenal cortical secretion observed during stress in the sheep could not be attributed to direct interaction of elevated thyroid hormone concentrations with adrenal cortical secretion.

Adrenal Glands↗

PubMed1988

Human recombinant interleukin-1 beta decreases plasma thyroid hormone and thyroid stimulating hormone levels in rats.

Thyroid function was investigated in rats treated sc with a single injection of human recombinant interleukin-1 beta (hrIL-1). In 5 h 12.5 micrograms hrIL-1 decreased total serum T4 levels by 30 +/- 2% (P less than 0.01) and serum T3 levels by 35 +/- 4% (P less than 0.001). However free T4 and T3 fractions increased markedly within the first 140 min by 162 +/- 20% (P less than 0.001) and by 55 +/- 4% (P less than 0.001) resulting in a 88 +/- 20% increase in the free T4 concentration (P less than 0.001) but no increase in the free T3 concentration. Serum TSH concentration fell in the 5 h after the hrIL-1 injection by 77 +/- 3% (P less than 0.001). A similar decrease was observed with 0.125 micrograms hrIL-1. Five hours of starvation did not change serum TSH levels, suggesting that the effect of hrIL-1 on TSH was not due to decreased food intake. In order to test whether the decrease in serum TSH was due to an intrapituitary increase in T3, hrIL-1 was injected in hypothyroid rats: the fall of serum TSH was not prevented and it fell in 5 h from 14.05 +/- 0.56 to 9.66 +/- 0.98 ng/ml (31%, P less than 0.01, n = 14). These results suggest that hrIL-1 acts independently of thyroid hormones. Peripheral metabolism of T4 was studied by implanting [125I]T4 secreting minipumps during 14 days. There was no difference in T4 plasma clearance rate between control and treated animals. The fall of serum T4 was therefore explained by decreased secretion and not by increased catabolism since ether link cleavage of T4 and changes in hepatic deiodinase could not be detected. We therefore suggest that hrIL-1 inhibits thyroid function mainly at the hypothalamic-hypophyseal level.

Animals↗

PubMed1980

Series on pharmacology in practice. 5. Thyroid hormones.

Thyroid hromones are among the most commonly prescribed medications. This article attempts a critical comparison of available preparations in the light of more recent information regarding thyroid physiology and, in particular, peripheral thyroid hormone economy. Indications and complications of therapy are reviewed. Present knowledge of thyroid physiology indicates that the use of L-thyroxine has advantages over other preparations in the treatment of hypothyroidism.

Chemical Phenomena↗

PubMed1986

Regulation of thyrotropin (TSH) bioactivity by TSH-releasing hormone and thyroid hormone.

The regulation of TSH biological activity by thyroid hormone and TRH was studied by comparison of pituitary and in vitro secreted TSH from normal and thyroidectomized rats that were alternatively treated with TRH either in vivo or in vitro. Normal and thyroidectomized (3 weeks postthyroidectomy), rats were injected with saline or TRH (100 micrograms) three times over 24 h. Pituitaries were incubated in vitro for 6 h, and six groups of samples from both pituitary and secreted TSH were analyzed: normal (n = 6), thyroidectomized (n = 6), normal and thyroidectomized groups treated with TRH in vitro (n = 2 each) with 10(-8) M TRH added to the incubation medium, and normal and thyroidectomized groups TRH treated in vivo, their incubation medium also supplemented with 10(-8) M TRH (n = 4 each). The biological activity of TSH in pituitary extracts and media was analyzed in terms of the ability to stimulate adenylate cyclase in human thyroid membranes. Thyroidectomy significantly decreased pituitary TSH bioactivity (70%) compared to normal, with no effect on secreted TSH in the medium. TRH, both in vivo and in vitro, when compared to the corresponding untreated groups, produced a significant increase in bioactive TSH in media from both normal (TRH in vivo, 131%; TRH in vitro, 139%) and thyroidectomized samples after TRH in vivo (158%). The TRH effect in the pituitary showed a significant increase in TSH bioactivity from normal samples treated with TRH in vivo (137%), whereas in thyroidectomized pituitary samples with TRH in vitro, TSH bioactivity was decreased (69%). These results indicate that thyroid hormone deficiency and TRH differentially regulate TSH bioactivity. Thyroid hormone deficiency induced a decrease in pituitary TSH bioactivity and favored the effect of TRH on secretion of more bioactive forms. TRH not only induced the formation of more bioactive forms but also stimulated their secretion into the medium.

Adenylyl Cyclases↗

PubMed1979

Serum concentrations of thyrotropin, thyroid hormones and thyroid hormone-binding proteins during acute and recovery stages of idiopathic respiratory distress syndrome.

A total number of 27 premature infants with idiopathic respiratory distress syndrome (IRDS) and 52 healthy controls with comparable gestational age and body weights were studied during the first month of life. In infants with IRDS a reduced thyrotropin (TSH) response to birth was suggested, as serum TSH was lower in IRDS patients than in controls during the first two days of life. Low serum concentrations of thyroid hormones were found in the acute stage of IRDS reaching minimal values by day 3--5. After that period an increase in thyroid hormone levels occurred. The serum T2 increased to the level of healthy prematures by day 6--10, whereas the serum T4 increased to normal levels by day 21--30. Serum concentrations of thyroxine-binding globulin (TBG) were significantly lower in IRDS patients than in healthy controls; a gradual increase to normal levels occurred during recovery. Serum prealbumin (TBPA) levels in IRDS infants increased rapidly after birth and exceeded levels of healthy infants. Serum albumin values were not significantly different in the two groups of infants. The serum T4/TBG ratios were low during recovery from IRDS.

Humans↗

PubMed2001

Uncoupling protein-3 is a molecular determinant for the regulation of resting metabolic rate by thyroid hormone.

Thyroid hormones increase energy expenditure, partly by reducing metabolic efficiency. The control of specific genes at the transcriptional level is thought to be the major molecular mechanism. However, both the number and the identity of the thyroid hormone-controlled genes remain unknown, as do their relative contributions. Uncoupling protein-3, a recently identified member of the mitochondrial transporter superfamily and one that is predominantly expressed in skeletal muscle, has the potential to be a molecular determinant for thyroid thermogenesis. However, changes in mitochondrial proton conductance and resting metabolic rate after physiologically mediated changes in uncoupling protein-3 levels have not been described. Here, in a study on hypothyroid rats given a single injection of T(3), we describe a strict correlation in terms of time course between the induced increase in uncoupling protein-3 expression (at mRNA and protein levels) and decrease in mitochondrial respiratory efficiency, on the one hand, and the increase in resting metabolic rate, on the other. First, we describe our finding that uncoupling protein-3 is present and regulated by T(3) only in metabolically relevant tissues (such as skeletal muscle and heart). Second, we follow the time course (at 0, 6, 12, 24, 48, 65, 96, and 144 h) of both uncoupling protein-3 mRNA levels and mitochondrial uncoupling protein-3 density in gastrocnemius muscle and heart. In both tissues, the maximal (12-fold) increase in uncoupling protein-3 density was reached at 65 h. The resting metabolic rate [lO(2)(kg(0.75))(-1)h(-1)] showed the same time course, and at 65 h the increase vs. time zero was 45% (1.316 +/- 0.026 vs. 0.940 +/- 0.007; P < 0.001). At the same time point, gastrocnemius muscle mitochondria showed a significantly higher nonphosphorylating respiration rate (nanoatoms of oxygen per min/mg protein; increase vs. time zero, 40%; 118 +/- 4 vs. 85 +/- 9; P < 0.05), whereas the membrane potential decreased by 8% (168 +/- 2 vs. 182 +/- 4; P < 0.05). These data are diagnostic of mitochondrial uncoupling. The results reported here provide the first direct in vivo evidence that uncoupling protein-3 has the potential to act as a molecular determinant in the regulation of resting metabolic rate by T(3).

Animals↗

PubMed1990

Na(+)-K+ pump in rat muscle: effects of hypophysectomy, growth hormone, and thyroid hormone.

We investigated the effects of growth hormone and thyroid hormone on the synthesis of Na(+)-K+ pumps in rat soleus muscle. Hypophysectomized rats were treated for 11 days with saline, human growth hormone (hGH; 140 micrograms/day), thyroxine (T4; 3 micrograms/day), or hGH plus T4. Age-matched nonhypophysectomized control rats received no treatment. The concentration of Na(+)-K+ pumps was reduced by 75% in the hypophysectomized rats. Treatment with hGH alone or combined with T4 restored the growth rate, whereas T4 alone did not stimulate growth. In contrast, the synthesis of Na(+)-K+ pumps was only responsive to T4 treatment when given alone or in combination with hGH. The concentration of Na(+)-K+ pumps increased around threefold in the T4-treated groups and showed full normalization to the control level after 11 days of treatment. It is concluded that growth hormone does not play any major role in the de novo synthesis of Na(+)-K+ pumps in skeletal muscle. More important, thyroid hormone, also at physiological doses, seems to be the major endocrine factor determining the concentration of Na(+)-K+ pumps in skeletal muscle.

Animals↗

PubMed1985

Metabolic responses during modified fasting and refeeding. The role of sympathetic nervous system activity and thyroid hormones.

Thyroid hormones, sympatho-adrenomedullary activity and metabolic responses have been studied in eight healthy obese subjects during modified fasting (0.8 MJ, 200 kcal/d) for 14 d, followed by hypocaloric-carbohydrate refeeding (2.4 MJ, 600 kcal/d) for 3 d. In the week preceding modified fasting, the subjects received a 7.2 MJ (1800 kcal) diet daily containing 20 mmol sodium, in order to distinguish the effects of salt depletion from those of energy restriction. Sodium (20 mmol/d) and potassium (80 mmol/d) were kept constant throughout the study. During modified fasting a low T3-high rT3 state developed; concomitantly a marked decrease in sympatho-adrenomedullary activity (assessed by 24-h urinary excretion of catecholamines) was observed. Upon refeeding plasma T3 increased and plasma rT3 decreased, but not completely to pre-fast values. Upon refeeding urinary catecholamine excretion markedly increased. A strong inverse relationship was found between the marked decrement of both thermogenic hormones and the catabolism of protein. No correlation between these parameters was found during brief refeeding. The observed decline of both thermogenic hormones may represent an adaptation to protect tissues from the catabolic effect of these substances during severe energy deficiency.

Adolescent↗

PubMed1973

Stimulation of mitochondrial adenosine diphosphate uptake by thyroid hormones.

Thyroid hormone administered in vivo increased carrier-mediated (atractyloside-sensitive) ADP uptake by rat liver mitochondria. 3 Days after a single large dose of triiodothyronine (20 mug/100 g of body weight), mitochondrial uptake of ADP measured at 6 degrees was 2.35 +/- 0.17 nmol/min per mg of protein, compared with an uptake of 1.81 +/- 0.19 nmol/min per mg of protein in mitochondria from untreated rats (P < 0.025). Cyanide (1.33 mM) had no effect on ADP uptake by mitochondria from either untreated or triiodothyronine-treated animals. Uptake of ADP by mitochondria from thyroidectomized rats treated with thyroxine for 7 days was 2.89 +/- 0.40 nmol/min per mg in mitochondria from thyrotoxic rats (20 mug of thyroxine per 100 g per day) and 1.98 +/- 0.22 nmol/min per mg in mitochondria from euthyroid rats (2 mug of thyroxine per 100 g per day) (P < 0.025). Mitochondria from both untreated and thyroid hormone-treated rats displayed a highly significant linear correlation between ADP uptake and ADP-dependent (i.e., state 3 minus state 4) oxygen consumption. There was, however, no difference in respiratory control ratios between mitochondria from euthyroid and thyrotoxic animals. Administration of dinitrophenol (2 mg/100 g) also stimulated carrier-mediated ADP uptake, but respiratory control of mitochondria from dinitrophenol-treated animals was virtually abolished. Triiodothyronine in vitro, at concentrations of 100 and 0.1 nM, appeared to inhibit rather than stimulate the uptake of mitochondrial ADP. The relationship between these observations and the clinical manifestations of thyrotoxicosis is discussed from the point of view of the possible effects of increased mitochondrial ADP transport on oxidative phosphorylation and adenosyl nucleotide metabolism.

Adenosine Diphosphate↗

PubMedDate not supplied

[Control of muscular bioenergetics by the thyroid hormones].

Thyroid hormones control the expression of genes coding for myosin isoforms, the Na-K ATPase pumps and the Ca-ATPase canals of the sarcoplasmic reticulum. This explains the increase of contractility and relaxation of skeletal muscles observed in hyperthyroidism, as opposed to hypothyroidism. Control of key-enzymes of the main energetic pathways accounts for inhibition of oxidative metabolisms in hypothyroidism and excessive glycolysis recruitment in hyperthyroidism. In both cases muscle performance is reduced, with accumulation of lactic acid at exercise. This is due to defective pyruvate oxidation and proton expulsion in hypothyroidism, and to acceleration of glycolysis in hyperthyroidism. These abnormalities partly explain why subjects with dysthyroidism are intolerant to exertion.

Energy Metabolism↗

PubMed1990

Differential and tissue-specific regulation of the multiple rat c-erbA messenger RNA species by thyroid hormone.

Thyroid hormone (T3) has been shown to regulate the level of its receptor in a number of tissues and cell lines. Recently, proteins encoded by the protooncogene c-erbA have been identified as T3 receptors. In the rat, four c-erbA gene products have been isolated, three of which, r-erbA alpha-1, r-erbA beta-1, and r-erbA beta-2, encode biologically active T3 receptors; the fourth, r-erbA alpha-2, may play an inhibitory role in T3 action. The present work examines the molecular nature of T3 receptor autoregulation using probes specific for each c-erbA mRNA. Rats were rendered hypothyroid with propylthiouracil and then treated with either saline or T3. Northern blot analyses reveal marked tissue-specific and differential regulation of the multiple c-erbA mRNAs by T3. In the pituitary the levels of r-erbA beta-1 mRNA increase, whereas the levels of the pituitary-specific r-erbA beta-2 mRNA decrease with T3 treatment. In heart, kidney, liver, and brain the levels of r-erbA beta-1 are unaffected by thyroidal status. The levels of both r-erbA alpha mRNAs decrease with T3 treatment in all tissues examined except for the brain, where there is no change. In addition, we find that changes in the mRNAs encoding specific subpopulations of T3 receptors do not always parallel changes in total nuclear T3 binding. Differential regulation of the specific c-erbA mRNA species could have important consequences for T3 action.

Animals↗

PubMed2004

Both thyroid hormone receptor (TR)beta 1 and TR beta 2 isoforms contribute to the regulation of hypothalamic thyrotropin-releasing hormone.

Thyroid hormones (TH) are essential regulators of vertebrate development and metabolism. Central mechanisms governing their production have evolved, with the beta-TH receptor (TRbeta) playing a key regulatory role in the negative feedback effects of circulating TH levels on production of hypothalamic TRH and hypophyseal TSH. Both TRbeta-isoforms (TRbeta1 and TRbeta2) are expressed in the hypothalamus and pituitary. However, their respective roles in TH-dependent transcriptional regulation of TRH are undefined. We confirmed the preferential role of TRbeta vs. TRalpha isoforms in TRH regulation in wild-type mice in vivo by using the TRbeta preferential agonist GC-1. We next determined the effects of tissue-specific rescue of TRbeta1 and TRbeta2 isoforms by somatic gene transfer in hypothalami of TRbeta null (TRbeta(-/-)) mice. TH-dependent TRH transcriptional repression was impaired in TRbeta(-/-) mice, but was restored by cotransfection of either TRbeta1 or TRbeta2 into the hypothalamus. TRbeta1, but not TRbeta2, displayed a role in ligand-independent activation. In situ hybridization was used to examine endogenous TRH expression in the paraventricular nucleus of the hypothalamus of TRbeta(-/-) or TRalpha null (TRalpha(o/o)) mice under different thyroid states. In contrast to published data on TRbeta2(-/-) mice, we found that both ligand-independent TRH activation and ligand-dependent TRH repression were severely impaired in TRbeta(-/-) mice. This study thus provides functional in vivo data showing that both TRbeta1 and TRbeta2 isoforms have specific roles in regulating TRH transcription.

Animals↗

PubMed2005

Potential involvement of mammalian and avian uncoupling proteins in the thermogenic effect of thyroid hormones.

Thyroid hormones (THs) have long been known to be involved in the control of thermoregulation in birds and mammals. In particular, they are reported to play a role in the regulation of heat production. The underlying mechanisms could be the stimulation of the nuclear and mitochondrial transcription of several genes involved in energy metabolism and/or a direct action on the activity of components of the mitochondrial respiratory chain. Attention has recently been focussed on a subfamily of mitochondrial anion carriers called uncoupling proteins (UCPs). These proteins are suspected to be involved in a partial dissipation of the mitochondrial proton electrochemical gradient that would uncouple phosphorylations from oxidations and hence produce heat. However, the involvement of uncoupling mechanisms in thermogenesis and particularly in the thermogenic effect of TH is still unclear. The thermogenic role of UCP1, specifically expressed in brown adipose tissue, and its regulation by TH in rodents is quite well recognised, but the involvement in heat production of its mammalian homologues UCP2, ubiquitously expressed, and UCP3, muscle and adipose tissue-specific, as well as the role of the muscular avian UCP (avUCP), are to be further investigated. The expression of the UCP2 and UCP3 genes was shown to be enhanced by TH in muscle of several rodent species, and to be increased in situations where thermogenesis is stimulated, whereas results are more contrasted in pig. There is now increasing evidence that the physiological role of the mammalian UCP3 and UCP2 is rather related to lipid oxidation and/or prevention of reactive oxygen species accumulation than to heat production by uncoupling. The expression of avUCP was also recently demonstrated to be strongly regulated by thyroid status in chicken, and overexpressed in experimental conditions favouring high triiodothyronine concentrations and thermogenesis. However, its real uncoupling activity and contribution to thermogenesis remain to be established.

Animals↗

PubMed1981

Thyroxine-binding globulin deficiency in early childhood. Postnatal changes in serum concentrations of thyroid hormones and thyroid hormone-binding proteins.

Serial determinations of serum thyroxine (T4), triiodothyronine (T3), thyrotropin (TSH), thyroid hormone-binding globulin (TBG), prealbumin (TBPA) and albumin were performed in a euthyroid girl with TBG deficiency and in her mother for a period of 22 months after delivery. At 8 days old the child had a serum TBG concentration around 50% of normal level which remained essentially unchanged during infancy. Total serum T4 and T3 concentrations were low, the free serum T4, free serum T3 and serum TSH concentrations were normal. The mother had received thyroid hormone from the age of 15 years. Her serum TBG level at 6 weeks post partum was similar to that of non-pregnant adults but decreased to about 50% of normal level, indicating a TBG deficiency. She remained euthyroid after withdrawal of T4 therapy. Serum TBPA and albumin concentration were normal in mother and child. An X-linked inheritance of the TBG deficiency was suggested from a study of the family.

Adult↗