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PubMed1981

[Effect of anti-thyroid antibodies on thyroid hormone secretion].

Secretory thyroid function was studied in animals with experimental autoimmune thyroiditis and in rats with passive immunization by antithyroid antibodies. The lowering of colloid endocytosis and thyroglobulin proteolysis accompanied by complete suppression of total thyroxin secretion stimulation was shown to occur in autoimmune thyroiditis. Injection to the rats of antibodies in the form of IgG gamma 2 fraction led to the reduced colloid output from the follicles, diminished secretion of triiodothyronine and to a pronounced suppression of thyroxin secretion stimulation. It is concluded that the lowering of colloid endocytosis and proteolytic enzymes is caused by insufficient production of TSH. Antithyroid antibodies should be treated as responsible for suppressed thyroxin secretion into the blood.

Animals↗
PubMed1982

Studies on the range of tissue protein synthesis in pigs: the effect of thyroid hormones.

The effects of thyroid hormones on the range of tissue protein synthesis in growing pigs using the constant infusion technique with [14C]lysine were studied. 2. During a 6 h infusion, samples were taken from blood and, at the end of the infusion, from liver, pancreas, stomach, small and large intestines, kidney cortex, kidney medulla, muscle and skin. 3. Lower relative specific radioactivities of free leucine and lysine in several tissues were observed in the hormone-treated group than in the untreated one. 4. The range of protein synthesis rate and the daily amount of protein synthesized in tissues was higher in all tissues after application of thyroid hormones. 5. Assuming that the organs analysed represented 70% of the total trichloroacetic acid-precipitable protein of the pig, the estimated range of daily protein synthesis was 251-490 and 312-880 g in untreated and hormone-treated pigs respectively.

Animals↗
PubMed1992

Transcript levels for nuclear-encoded mammalian mitochondrial respiratory-chain components are regulated by thyroid hormone in an uncoordinated fashion.

Thyroid hormone is one of the few known physiological regulators of mammalian mitochondrial biogenesis. Although it exerts a global effect on biogenesis, it does so by regulating the expression of a limited number of unidentified mitochondrial proteins. We have investigated these hormone-regulated proteins in rat liver. Hormone injection induced a 30-fold increase in the levels of cytochrome-c1 mRNA after 3 d. In addition, the mRNA for the growth-activated adenine-nucleotide translocator, ANT2, was increased 13-fold and that for the ATPase N,N'-dicyclohexylcarbodiimide-binding protein increased 4-5-fold. Mitochondrial transcripts of cytochrome-oxidase subunit I also increased. No changes were found in the mRNA levels for the F1-ATPase beta-subunit or cytochrome oxidase IV. A single low dose of triiodothyronine induces rapid increases in cytochrome-c1 and ANT2 mRNA species which parallel changes in the activity of the hormone-responsive malic enzyme, but are earlier than other mitochondrial biogenetic events. These data strengthen the view that thyroid hormone regulates synthesis of specific components within each respiratory-chain complex and that these products apparently play key roles in inner-membrane biogenesis and assembly. The significance of ANT2 induction is also discussed with respect to the rapid respiratory response induced by thyroid hormone.

Adenosine Triphosphatases↗
PubMed2004

[Mood disorders, psychopharmacology and thyroid hormones].

For more than 40 years thyroid hormones and mood disorders have been associated. Some psychiatric symptoms are produced by thyroid illnesses and there is a frequent association of thyroid dysfunction with mood disorders. Therefore, routine thyroid function assessment in patients with mood disorders and the treatment of sub-clinical thyroid dysfunctions is recommended. The usefulness of adding thyroid hormones to antidepressive treatment in euthyroid patients to obtain a potentiation effect has been probed repeatedly. The most common strategy is potentiation with T3, but high doses of T4 have been also used in patients with resistant depression. Thyroid hormones exert their action in the central nervous system through a variety of mechanisms: modulation of gene expression of several groups of proteins, some of them with known physiopathological implications in mood disorders and the influence over serotonin and noradrenergic neurotransmission, known to be one of the modes of action of antidepressants. Finally, it is also important to stress the complex relationship between psychiatric drugs, deiodinases and thyroid hormones, that can potentially help to understand the mechanisms of action of these drugs.

Central Nervous System↗
PubMed2004

Thyroid hormone binding protein abnormalities in patients referred for thyroid disorders.

BACKGROUND & OBJECTIVES: Thyroid hormone binding protein (THBP) abnormalities are the major cause of discordance in commonly performed total thyroxine (T4) and thyrotropin (TSH) estimations, though these do not interfere with thyroid hormone action. Determination of such abnormalities in patients showing discordant thyroid function tests (TFTs) is diagnostically important as it eliminates equivocal assessment of thyroid function and treatment especially where proper methodology for free T4 (FT4) estimation is not available. This study was undertaken to analyse the THBP abnormalities in the population attending thyroid clinic. Family members of affected patients were also screened to study the inheritance of quantitative TBG abnormalities. METHODS: Blood samples of 15000 consecutive patients over a period of 4 years (1994-1997) were tested for thyroid function. THBP abnormalities were studied using polyacrylamide gel electrophoresis autoradiography. Serum thyroxine binding globulin (TBG), free and total T4, total tri-iodothyronine (TT3) were assayed by radioimmunoassay methods. RESULTS: In our screening of 15,000 thyroid patients over a four year period, we found the presence of complete and partial TBG deficiency and TBG excess to be 1:2,500, 1:200 and 1:15,000 respectively. Our study on the families of three affected patients revealed X-chromosome linked inheritance pattern of TBG deficiency in two families and TBG excess in one family. INTERPRETATION & CONCLUSION: Our study suggests that it would be beneficial to rule out THBP abnormalities before interpreting results of TFTs, particularly when there is large discrepancy between T4 and TSH levels. In case of inherited THBP abnormalities, the family members of the affected individual should also be screened to avoid misdiagnosis and erroneous treatment in case they develop thyroid dysfunction in future.

Autoradiography↗
PubMed1997

Effect of melatonin on serum cholesterol and phospholipid levels, and on prolactin, thyroid-stimulating hormone and thyroid hormone levels, in hyperprolactinemic rats.

The effects of melatonin treatment and pituitary transplants on serum total and free cholesterol levels, cholesterol esterification index, phospholipid levels and prolactin, thyroid-stimulating hormone (TSH), thyroxine (T4) and triiodothyronine (T3) levels were examined in rats. Male rats were grafted an anterior pituitary under the kidney capsule or were sham-operated on day 30th of life. Thirty days later, the rats received 4 daily s.c. injections of melatonin (25, 50 or 100 microg/rat) or vehicle, 2 h before lights off, and were killed 15 h after the last injection, and after a 24-hour fasting period. In pituitary-grafted rats, a decrease in serum free cholesterol with unmodified total cholesterol levels, and thus an augmented cholesterol esterification index, occurred. Pituitary-grafted rats showed also an increase in serum phospholipids. In control, but not in pituitary-grafted rats, melatonin injection decreased free cholesterol without modifying total cholesterol levels. Melatonin treatment (50 microg/day or greater) normalized the augmented serum phospholipid levels found in pituitary-grafted rats and increased serum phospholipids in control rats. Melatonin injection also reduced the high serum prolactin and T3 levels found in pituitary-grafted rats, and decreased T4 concentration in control rats. Neither melatonin nor pituitary grafts modified serum TSH concentration. The results demonstrate that melatonin counteracts in part lipid disturbances of hyperprolactinemic rats and lowers free plasma cholesterol and augmented serum phospholipids in control rats.

Animals↗
PubMed1988

The hypothyroid (hyt/hyt) mouse: a model system for studying the effects of thyroid hormone on developmental changes in gene expression.

Thyroid hormone has been implicated as an important factor in rodent development. We have used a strain of mice with a recessive mutation producing congenital primary hypothyroidism (C.RF/J-hyt/+) to study the effects of thyroid hormone on developmental changes in the expression of genes encoding a number of proteins involved in lipid metabolism and transport. Total cellular RNA was prepared from the small intestine and liver of hyt/hyt mice and their unaffected littermates (+/?) at various times during postnatal development. RNA blots were probed with apolipoprotein A-I, A-II, A-IV, B, and E cDNAs plus cDNAs encoding the low density lipoprotein receptor, 3-hydroxy-3-methylglutaryl coenzyme A reductase, and three cytoplasmic hydrophobic ligand-binding proteins (two fatty acid-binding proteins and a protein that binds all-trans-retinol). Hypothyroidism results in small changes (1.5- to 5-fold) in the concentration of many of these mRNAs in liver and small intestine between postnatal days 15 and 50. A much greater tissue-specific effect was noted on apolipoprotein B (apoB) gene expression. In euthyroid +/? animals, apoB mRNA levels fall by a factor of 30 in liver between days 20 and 35 without a comparable decrease in the small intestine. This liver-specific decrease does not occur in hyt/hyt animals. The normal decrease in hepatic apoB mRNA levels is accompanied by a decrease in plasma apoB-100 but not apoB-48. No reduction in either form of plasma apoB was noted in hyt/hyt animals. Mutant hyt/hyt mice given thyroxine from birth to 35 days had liver apoB mRNA levels comparable to those in +/? littermates. In contrast, hepatic apoB mRNA concentrations did not fall to normal levels in hyt/hyt mice given thyroxine from postnatal days 15 to 35. All treatment groups have comparable levels of plasma corticosteroids. These data suggest that (i) there is a critical period or a required response time during postnatal development for thyroid hormone action on apoB gene expression, (ii) thyroid hormone's effect on apoB is tissue specific, and (iii) the hyt/hyt mouse represents a useful system to evaluate the developmental effects of thyroid hormone on specific gene expression.

Animals↗
PubMed1991

Hyperthyroidism due to familial pituitary resistance to thyroid hormone: successful control with 3, 5, 3' triiodothyroacetic associated to propranolol.

We herein describe a family with thyroid hormone resistance. Thyroid hormones and basal TSH were elevated. Pituitary tumor or abnormality in thyroid hormone binding proteins were ruled out by appropriate tests. Mother and sister of the propositus presented similar abnormal hormonal features but no hyperthyroidism. Initially the patient was treated with carbimazole (30 mg/day): three months later a dramatic increase in the size of the thyroid gland and in TSH levels (12.5 to 28 mU/l) were noted. Thereafter, dextrothyroxine (D-T4) and 3, 5, 3'-triiodothyroacetic acid (TRIAC) were given consecutively and treatment was accompanied by a decrease of TSH levels (2 mU/l) but thyroid hormone remained elevated. The symptoms and signs of hyperthyroidism improved with the addition of propranolol (30-60 mg/day). In conclusion, the present report describes a new family with the syndrome of THR and variable degrees of involvement among relatives. We suggest the usefulness of TRIAC therapy to decrease TSH levels and propranolol to improve thyrotoxicosis due to pituitary resistance to thyroid hormone.

Adolescent↗
PubMed1994

Annual variations in serum thyroid-stimulating hormone and thyroid hormones and in their responses to thyrotrophin-releasing hormone in the reindeer.

The reindeer in its natural habitat is subject to great annual variations in ambient temperature, illumination and nutrition. To ascertain the effect of these environmental factors on thyroid function, serum thyroid-stimulating hormone (TSH), thyroxine (T4), tri-iodothyronine (T3) and reverse T3 (rT3) concentrations were measured four times a year (2 June, 8 October, 21 November, and 24 February) in 14 animals housed outdoors at latitude 69 degrees 10'N. They all showed statistically significant (P < 0.05) seasonal changes. Serum TSH and T4 were highest in February (623 +/- 30 ng/ml and 287 +/- 19 nmol/l respectively). TSH was lowest in October (318 +/- 47 ng/ml) and T4 in November (199 +/- 19 nmol/l). The T3 concentration was highest in November (3.0 +/- 0.3 nmol/l) and lowest in June (1.8 +/- 0.2 nmol/l). In contrast, rT3 was highest in June (3.6 +/- 1.2 nmol/l) and lowest in November (1.9 +/- 0.6 nmol/l). Thus, there was an inverse relationship between T3 and rT3 (linear regression r = -0.406, P < 0.01). TSH, T4, T3 and rT3 responses to exogenous thyrotrophin-releasing hormone (synthetic TRH; 500 micrograms i.m.) were determined in ten animals. The magnitude of their response to TRH was significantly (P < 0.05) dependent on the time of year. When compared with the control level all the parameters rose significantly (P < 0.05). The greatest rise in serum TSH occurred in October (219 +/- 151%) and the smallest in February (66 +/- 53%).(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Nutritional Physiological Phenomena↗
PubMed2002

Thyroid hormone, brain development, and the environment.

Thyroid hormone is essential for normal brain development. Therefore, it is a genuine concern that thyroid function can be altered by a very large number of chemicals routinely found in the environment and in samples of human and wildlife tissues. These chemicals range from natural to manufactured compounds. They can produce thyroid dysfunction when they are absent from the diet, as in the case of iodine, or when they are present in the diet, as in the case of thionamides. Recent clinical evidence strongly suggests that brain development is much more sensitive to thyroid hormone excess or deficit than previously believed. In addition, recent experimental research provides new insight into the developmental processes affected by thyroid hormone. Based on the authors' research focusing on the ability of polychlorinated biphenyls to alter the expression of thyroid hormone-responsive genes in the developing brain, this review provides background information supporting a new way of approaching risk analysis of thyroid disruptors.

Brain↗
PubMed2000

Gene regulation by thyroid hormone.

Regulation of gene expression by thyroid hormones (T3, T4) is mediated via thyroid hormone receptors (TRs). TRs are DNA-binding transcription factors that function as molecular switches in response to ligand. TRs can activate or repress gene transcription depending on the promoter context and ligand-binding status. In most cases, in the absence of ligand, TRs interact with a corepressor complex containing histone deacetylase activity, which actively inhibits transcription. The binding of ligand triggers a conformational change in the TR that results in the replacement of the corepressor complex by a coactivator complex containing histone acetyltransferase activity, through which the chromatin structure is remodeled, thereby leading to activation of transcription. In addition, the finding that several TR-interacting coregulators act more directly on the basal transcriptional machinery suggests that mechanisms independent of histone acetylation and deacetylation also are involved in TR action.

Animals↗
PubMed1993

In vivo stimulation of thyroid hormone release by rabbit antibodies with thyroid stimulating activity raised against the mutated receptor peptide TSH-R-HIS17.

The present study was designed to examine whether thyroid stimulating antibodies (TSAb) against the mutated or non-mutated peptide of human TSH receptor stimulates release of thyroid hormones in mice in vivo. We generated antibodies against mutated TSH receptor peptide TSH-R-HIS17 and non-mutated TSH receptor peptide TSH-R-ASP17 immunizing the peptides to rabbits. We isolated immunoglobulin G (IgG) from these antibodies and injected iv into male ddy mice. Control mice were injected iv with bTSH or TSAb-negative normal rabbit IgG. Serum T3 and T4 concentrations were elevated after the administration of bTSH in a dose-dependent manner. Serum T3 and T4 concentrations were significantly elevated after the injection of IgG from the rabbit antibodies with TSAb activity produced against TSH-R-HIS17. However serum T3 and T4 remained within normal levels after the injection of IgG from the rabbit antibodies without TSAb activity toward TSH-R-ASP17. The present data offer in vivo support of the IgG with TSAb activity interaction with the TSH receptor of the thyroid and raise the possibility that TSAb against mutated human TSH receptor peptide might be contributed to induce thyroid hyperfunction.

Amino Acid Sequence↗
PubMed1985

Influence of endogenous T3-autoantibodies on thyroid hormone measurements in a woman with transient postpartum thyroiditis.

Unreliable estimates of serum total T3 due to the presence of autoantibodies against T3 were observed in a woman who developed thyrotoxicosis followed by transient hypothyroidism after childbirth (postpartum thyroiditis). The T3 autoantibody levels changed during the postpartum period in a similar way to the thyroid microsomal antibodies. The total T3 values were constantly low, whereas the measurement of free T3 by the Amerlex analogue method deviated from the expected only at the time of maximal antibody levels. Thus, evaluation of thyroid function may be complicated by the simultaneous presence of thyroid hormone autoantibodies and transient postpartum thyroiditis.

Adult↗
PubMed1986

The effect of benziodarone on the thyroid hormone levels and the pituitary-thyroid axis.

The effect of benziodarone on the levels of thyroid hormones in the serum has not attracted interest, in spite of the prolific literature on the related drug amiodarone. It is shown here that benziodarone administration has several effects, mainly similar to amiodarone, but some possibly opposite and inappropriate. Nine normal volunteers received benziodarone, 100 mg three times daily for 14 days. Before and 1, 3, 7 and 14 days after continuous administration the following estimates were obtained: serum T4, T3, rT3 and TSH, both basal (TSH0) and 30 min after iv administration of TRH (TSH30), the difference being calculated as delta TSH. Serum T4 remained relatively constant. Serum T3 decreased significantly from the 1st to the 14th day (eg. before 2.15 +/- 0.12 nmol/l, at 3 days 1.45 +/- 0.07). Serum rT3 increased significantly from the 1st to the 14th day (eg. before 0.71 +/- 0.16 nmol/l, at 7 days 2.61 +/- 0.19). Serum TSH0 and TSH30 decreased significantly on the 1st and 3rd day. Later they increased, and TSH0 at 14 days was significantly higher than the pre-treatment value. Our results suggest that benziodarone has an amiodarone-like action in diverting the peripheral metabolism of T4 towards rT3 rather than T3. However, the effects on the pituitary-thyroid axis are not similar to those previously reported by others and ourselves about amiodarone, and these merit further research.

Adult↗
PubMed2005

Alternate pathways of thyroid hormone metabolism.

The major thyroid hormone (TH) secreted by the thyroid gland is thyroxine (T(4)). Triiodothyronine (T(3)), formed chiefly by deiodination of T(4), is the active hormone at the nuclear receptor, and it is generally accepted that deiodination is the major pathway regulating T(3) bioavailability in mammalian tissues. The alternate pathways, sulfation and glucuronidation of the phenolic hydroxyl group of iodothyronines, the oxidative deamination and decarboxylation of the alanine side chain to form iodothyroacetic acids, and ether link cleavage provide additional mechanisms for regulating the supply of active hormone. Sulfation may play a general role in regulation of iodothyronine metabolism, since sulfation of T(4) and T(3) markedly accelerates deiodination to the inactive metabolites, reverse triiodothyronine (rT(3)) and T(2). Sulfoconjugation is prominent during intrauterine development, particularly in the precocial species in the last trimester including humans and sheep, where it may serve both to regulate the supply of T(3), via sulfation followed by deiodination, and to facilitate maternal-fetal exchange of sulfated iodothyronines (e.g., 3,3'-diiodothyronine sulfate [T(2)S]). The resulting low serum T(3) may be important for normal fetal development in the late gestation. The possibility that T(2)S or its derivative, transferred from the fetus and appearing in maternal serum or urine, can serve as a marker of fetal thyroid function is being studied. Glucuronidation of TH often precedes biliary-fecal excretion of hormone. In rats, stimulation of glucuronidation by various drugs and toxins may lead to lower T(4) and T(3) levels, provocation of thyrotropin (TSH) secretion, and goiter. In man, drug induced stimulation of glucuronidation is limited to T(4), and does not usually compromise normal thyroid function. However, in hypothyroid subjects, higher doses of TH may be required to maintain euthyroidism when these drugs are given. In addition, glucuronidates and sulfated iodothyronines can be hydrolyzed to their precursors in gastrointestinal tract and various tissues. Thus, these conjugates can serve as a reservoir for biologically active iodothyronines (e.g., T(4), T(3), or T(2)). The acetic acid derivatives of T(4), tetrac and triac, are minor products in normal thyroid physiology. However, triac has a different pattern of receptor affinity than T(3), binding preferentially to the beta receptor. This makes it useful in the treatment of the syndrome of resistance to thyroid hormone action, where the typical mutation affects only the beta receptor. Thus, adequate binding to certain mutated beta receptors can be achieved without excessive stimulation of alpha receptors, which predominate in the heart. Ether link cleavage of TH is also a minor pathway in normal subjects. However, this pathway may become important during infections, when augmented TH breakdown by ether-link cleavage (ELC) may assist in bactericidal activity. There is a recent claim that decarboxylated derivates of thyronines, that is, monoiodothyronamine (T(1)am) and thyronamine (T(0)am), may be biologically important and have actions different from those of TH. Further information on these interesting derivatives is awaited.

Alanine↗
PubMed1990

Cold exposure elevates cellular levels of messenger ribonucleic acid encoding thyrotropin-releasing hormone in paraventricular nucleus despite elevated levels of thyroid hormones.

Cold exposure increases blood levels of TSH and thyroid hormones by stimulating the secretion of TRH from the median eminence. Thyroid hormones reduce TRH release and cellular levels of TRH mRNA. Using quantitative in situ hybridization to measure changes in cellular levels of various neuropeptide mRNAs, the present studies demonstrate that cold exposure also increases cellular levels of TRH mRNA in neurons of the paraventricular nucleus (PVN), supporting the concept that TRH mRNA levels are reflective of TRH secretion in these neurons. The effect of cold appeared to be specific for TRH expression in the PVN, because cold exposure did not influence cellular levels of TRH in the reticular thalamic nucleus or beta-actin and oxytocin mRNAs in the PVN. Cellular levels of mRNA encoding CRH were elevated by cold exposure. This latter observation is predictable based on the cold-induced activation of the hypothalamic-pituitary-adrenal axis. There was a 24-h rhythm and a time of day difference in the effect of cold on TRH mRNA levels in the PVN. Time of day differences in the effect of cold on CRH mRNA levels were not apparent. Cold exposure appeared to elevate TRH mRNA levels in all neurons of the PVN, indicating that the neurally mediated effect of cold on TRH expression can override the inhibitory effects of circulating T3 within the same neuronal population.

Actins↗
PubMed1996

Effects [correction of Effecs] of the thyroid hormone (T3) on astrocytes.

Thyroid hormones have profound effects on growth and development. In the brain L-3,5,3'-triiodothyronine (T3), the bioactive hormone, is involved with the harmonious development acting in neuronal and glial cell differentiation. T3 acts on the cells by interacting with nuclear receptors that can regulate the expression of several genes. Astrocytes also show receptors to the hormone. We reported herein data on the effects of T3 on astrocytes. We have verified that T3 has a morphological effect on cultured cortical astrocytes with rearrangement of GFAP filaments, and induces proliferation in the cultured cerebellar astrocytes of newborn rats. We discuss here the effects of T3 on astrocytes, considering the possibility that thyroid hormone prepares the astrocytes to interact with neurons.

Animals↗
PubMed1993

[Is it appropriate to treat thyroid nodules with thyroid hormone?].

The appropriateness of treating thyroid nodules with thyroid hormone is being debated: in fact, the development of nodules is not caused by an iodothyronine deficiency or a desuppression of TSH, and T4 seems to be able to regain control on cell proliferation. A very great number of authors have reported their experience with suppression of thyroid nodules with thyroid hormone, but treatment efficacy has been variably appreciated (9 to 69% regression). On the other hand, the four randomized prospective studies available at present, which analyze the evolution of nodules, especially on ultrasonography, have not demonstrated that hormone therapy is more effective than a placebo. The methodology of these studies is not free from criticism, and other prospective surveys are required, especially to establish whether this treatment is innocuous and whether some varieties of nodules may be more amenable to hormone therapy than others.

Humans↗