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PubMed2003

Effects of temperature on photoperiodically induced reproductive development, circulating plasma luteinizing hormone and thyroid hormones, body mass, fat deposition and molt in mountain white-crowned sparrows, Zonotrichia leucophrys oriantha.

The mountain white-crowned sparrow, Zonotrichia leucophrys oriantha, breeds in subalpine meadows throughout many mountainous regions of western North America. Mathematical analysis of 20 years of egg-laying dates at Tioga Pass, California (3030m elevation) indicated a highly predictable breeding season suggesting that precise environmental cues such as the annual change in day length were important for regulating reproductive function. Additionally, it appeared that there was sufficient yearly variation in the timing of breeding to suggest that other environmental cues may also be important for regulating adjustments in reproductive development and regression. Captive populations of Z. l. oriantha showed strong responses in gonadal development following transfer to longs days (15L 9D) and low temperature (5 degrees C) slowed down photoperiodically induced gonadal growth and subsequent regression, in both males and females. High temperature of 30 degrees C tended to accelerate gonadal development and regression whereas gonadal development was intermediate in a group exposed to 20 degrees C. Prior exposure to these temperature regimes while on short days (9L 15D) had no effect on body mass, fat, or plasma levels of luteinizing hormone (LH) and thyroid hormones. Curiously there was no effect of temperature on photoperiodically induced rises in LH in either sex despite marked effects on gonadal growth. Brood patch development was also enhanced in females exposed to 30 degrees C. Corticosterone levels measured in a subset of plasma samples from this experiment indicated no effect of temperature suggesting that the retarded gonadal development at 5 degrees C was not a result of thermal stress. Although there was a robust effect of photostimulation on thyroid hormone levels in blood of both sexes, temperature treatment had no effect on tri-iodothyronine (T3) concentrations. However, plasma levels of thyroxine (T4) were lower initially at 5 degrees C versus 20 and 30 degrees C treatments. This may be related to the protracted gonadal cycle at 5 degrees C versus the truncated gonadal cycle at 30 degrees C. Molt score, an indication of post-reproductive state and onset of photorefractoriness, was delayed in birds exposed to 5 degrees C. Body mass, and to a lesser extent fat score, tended to be lowest in birds exposed to 5 degrees C compared with those at 20 and 30 degrees C. These results demonstrate that ambient temperature significantly affected photoperiodically induced gonadal development and regression in these birds. The endocrine mechanisms underlying these effects require further study.

Adipose Tissue↗

PubMed1994

Desethylamiodarone is a noncompetitive inhibitor of the binding of thyroid hormone to the thyroid hormone beta 1-receptor protein.

It has been hypothesized that amiodarone (A), a potent antiarrythmic and antianginal drug, induces a local hypothyroid-like condition in extrathyroidal tissues. This might be related to competitive antagonism of A for the thyroid hormone receptor reported in some studies but denied in others. These conflicting results are presumably due to the poor solubility of A in a hydrophilic environment. We, therefore, studied the effect of the drug and its major metabolite, desethylamiodarone (DEA), on the in vitro binding of thyroid hormone (T3) to its receptor protein using the rat beta 1-thyroid hormone receptor expressed in Escherichia coli. A and DEA stayed in solution up to 10(-4) M when 0.05% Triton X-100 was added to the incubation buffer, as evidenced by a recovery of 80-90% for both chemicals, as measured by HPLC. DEA, but not A, had a clear inhibitory effect on the binding of T3 to its receptor (IC50, 1-3 x 10(-5) M). Scatchard analysis in the presence of DEA demonstrated a dose-dependent decrease in the Ka as well as the maximum binding capacity. Lineweaver-Burke analysis indicated noncompetitive inhibition. Plots of the intercepts of Lineweaver-Burke plots vs. DEA concentration were linear (y = 0.334 + 0.098x), giving a Ki of 30 microM for the binding of DEA to the occupied receptor. Plots of the slopes vs. inhibitor concentration were parabolic (y = 3.01 + 0.06x + 0.16x2), indicating a progressively stronger effect of DEA on the unoccupied receptor as concentrations rise. This preference for the unoccupied receptor is reflected in experiments that show a progressive loss of T3 binding when the receptor was incubated for increasing periods with DEA before adding T3. We conclude that DEA is a noncompetitive inhibitor of the binding of T3 to the beta 1-thyroid hormone receptor protein, interacting preferably with the unoccupied T3 receptor.

Amiodarone↗

PubMed1989

The anterior pituitary content of neuromedin U-like immunoreactivity is altered by thyrotrophin-releasing hormone and thyroid hormone status in the rat.

In this study we have examined the effects of TRH, thyroid hormones and dopamine on the rat anterior pituitary content of neuromedin U-like immunoreactivity. Oral administration of TRH (20 mg/100 g per day) to euthyroid animals evoked a fivefold increase in peptide content after 12 days of treatment. This effect was found to be dependent upon circulating levels of thyroid hormone, since administration of TRH to thyroidectomized animals failed to show a similar effect without simultaneous treatment with tri-iodothyronine. The possibility that the TRH-induced increase in anterior lobe neuromedin U content reflected alterations in prolactin secretion or synthetic rate was also examined. Treatment of euthyroid animals with a dopamine agonist and antagonist was, however, without effect. These results demonstrate a unique relationship between TRH and thyroid hormone levels in increasing the anterior lobe content of neuromedin U immunoreactivity.

Animals↗

PubMed1990

A nuclear factor that enhances binding of thyroid hormone receptors to thyroid hormone response elements.

Recent studies from this laboratory have demonstrated the presence of thyroid hormone response elements (TREs) in the 5'-flanking region of the rat alpha and TSH beta subunit genes. Using an avidin-biotin complex DNA binding assay, we have shown that these TREs bind the thyroid hormone (T3) receptor present in nuclear extracts of GH3 cells, as well as the in vitro synthesized Hc-erbA beta, which has been identified as a member of the family of T3 receptors. The binding of Hc-erbA beta to the alpha subunit TRE can be enhanced 3-4-fold by including GH3 nuclear extract in the binding assay. Binding to the TRE present in the TSH beta gene or the rat growth hormone gene was similarly enhanced, although to a lesser degree. The enhanced binding activity is trypsin-sensitive and heat labile, and is not reproduced by the addition of histones, bovine serum albumin, or cytosol instead of nuclear extract. Gel exclusion chromatography suggests a molecular size of approximately 65,000 Da. This protein, which is present in several different cell types, is also able to complement binding of the rat erbA alpha-1 and the pituitary-specific erbA beta-2 forms of the receptor. These data suggest that the binding of the T3 receptor to a TRE is augmented by another nuclear protein, which may be involved in the mechanism of action of thyroid hormone.

Animals↗

PubMed1979

Changes in serum concentrations of thyroid hormones and thyroid hormone-binding proteins during early infancy. Studies in healthy fullterm, small-for-gestational age and preterm infants aged 7 to 240 days.

Serum concentrations of thyrotropin (TSH), thyroxine (T4), triiodothyronine (T3), thyroxine-binding globulin (TBG), prealbumin (TBPA) and albumin (Alb) were determined in 492 blood samples from 127 fullterm (FT), 91 small-for-gestational age (SGA) and 88 preterm (PT) healthy infants aged 7 to 240 days. Serum T4 decreased about 20% during the first month of life. In infants aged 7--49 days, serum T4 concentrations were significantly lower in SGA than in FT infants, and even lower values were found in PT infants. Serum T3 increased 50--70% reaching maximal values by 50--79 days of life. Serum T3 levels were higher in FT than in SGA infants throughout the observation period. In PT infants serum T3 increased from low values to levels which exceeded those of SGA and FT infants by 120--240 days of life. Serum TSH level did not change with age and was less than or equal to 5 mU/l in all infants. Serum TBG values were high compared to normal adult values and did not change significantly with age. Comparable serum TBG values were found in FT, SGA and PT infants. Serum TBPA increased with age. Serum TBPA increased gradually in FT infants. In SGA infants serum TBPA increased from low values to levels which by 120--240 days of life exceeded those of PT and FT infants. In PT infants a decrease in serum TBPA appeared before the rise commenced. Serum Alb increased gradually in FT, SGA and PT infants during the observation period. Serum Alb in PT infants aged 30--119 days was lower than those in FT infants with similar ages. These physiological changes in serum concentrations of thyroid hormones and hormone-binding proteins during early infancy should be considered when interpreting thyroid function tests in infants with various maturity.

Age Factors↗

PubMed1991

[Effects of yin-tonics and yang-tonics on serum thyroid hormone levels and thyroid hormone receptors of hepatic cell nucleus in hyperthyroxinemic and hypothyroxinemic rats].

Hyperthyroxinemia model was made by giving thyroid tablet suspension to Wistar rats and hypothyroxinemia model was made by thyroidectomy. We measured serum thyroid hormone levels by RIA and the parameters of triiodothyronine receptors in rat hepatic cell nucleus by radio-ligand binding assay: Maximal binding capacity (Bmax) and Dissociation constant (Kd). It is found that (1) Yin-tonics can lower serum thyroid hormone levels and Bmax of hepatic nuclear T3R of hyperthyroxinemia rat from 167.14 +/- 25.62 fmol/100 micrograms DNA to 98.98 +/- 15.24 fmol/100 micrograms DNA, P less than 0.001. (2) Both Yang-tonics I and II can raise serum thyroid hormone levels of hypothyroxinemia rats, but not Bmax of hepatic nuclear T3R. Yang-tonics I even lowers Bmax. All the Chinese herbs have no effect on the Kd of rat hepatic nuclear T3R. The results may have some value in studying the effects of Chinese medical drugs.

Animals↗

PubMed1990

Seasonal variations in prolactin, growth hormone and thyroid hormones and the prolactin surge at ovulation do not affect litter size of ewes during pregnancy in the oestrous or the anoestrous season.

Injection of bromocriptine from 5 days before until 5 days after mating clearly suppressed the periovulatory prolactin surge in ewes in the anoestrous and oestrous season but did not change the litter size significantly. Progesterone, GH, TSH or thyroid hormone concentrations were not influenced by the bromocriptine treatment. The progesterone concentrations were lower during the first weeks after mating in the anoestrous season compared to the oestrous season, while there was no difference between pregnant and non-pregnant ewes. During later gestation this seasonal difference was only observed in the non-pregnant ewes. At the same time there was a clear difference between pregnancy and non-pregnancy in both seasons. The prolactin, GH and thyroid hormone values also varied significantly during gestation. Since these patterns are identical in pregnant and non-pregnant ewes, the fluctuations are due to environmental factors and not to pregnancy or altered progesterone concentrations. In the anoestrous season prolactin, GH, T4 and T3 levels were higher than in the breeding season, while rT3 showed the opposite pattern. The TSH concentration did not differ between the two seasons. These results suggest that seasonal variations in prolactin, GH and thyroid hormones or the periovulatory prolactin surge do not affect litter size of ewes during pregnancy in the oestrous or the anoestrous season.

Animals↗

PubMed1994

Intracellular iodination of thyroglobulin in filter-polarized thyrocytes leads to the synthesis and basolateral secretion of thyroid hormone.

Thyroid follicles perform several functions that depend upon epithelial polarity: secretion of thyroglobulin (Tg) to the apical lumen, uptake of iodide for Tg iodination, and the manufacture of thyroid hormone for delivery to the bloodstream. In this report we examine Tg processing by thyroid epithelial monolayers cultured on porous filters. Basolateral 125I uptake resulted in thyrotropin-dependent radiolabeling of Tg in cells and apical medium. Polarized thyrocytes iodinated exogenous gamma globulins (IgG), demonstrating labeling in the apical extracellular space. Apical catalase addition inhibited the appearance of apical [125I]IgG and [125I]Tg, but had no effect on cell-associated [125I]Tg, indicating additional iodination of Tg in an intracellular compartment. A similar conclusion was drawn from radioiodination experiments at 20 degrees C. Intracellular iodination was selective for Tg forms receiving prior Golgi carbohydrate modifications. During a 2-h chase, [125I]Tg was exported from cells to apical medium, while modest amounts of thyroxine were secreted with a majority to the basolateral medium. Neither radioiodination at 20 degrees C nor apical catalase addition blocked formation or secretion of [125I]thyroxine during the chase. Thus in filter-grown thyroid epithelial cells, prior to apical extracellular iodination, intracellular iodination of Tg begins the process leading to formation of thyroxine.

Animals↗

PubMedDate not supplied

Renal artery resistance index, thyroid hormones, and thyroid volume in the early kidney transplants recipients.

BACKGROUND: Thyroid hormones could affect renal function, and, on the other hand, renal dysfunction may affect thyroid function. Disturbances of concentrations of thyroid hormones are often associated with thyroid gland enlargement. The aim of the study was to assess the function and morphology of the thyroid (volume and hormones concentration) and kidney function after transplantation (creatinine concentration and resistance index [RI] of transplant artery). MATERIAL AND METHODS: The group included 13 females, 19 males; aged 19-69 years, mean 44.75 +/- 14.8 years after transplantation with stable graft function. Thyroid volume, renal artery RI, creatinine concentration, and concentrations of T3, rT3, FT3, FT4, and TSH were estimated the day before surgery, and at 1, 3, 6, and 10 days after transplantation. RESULTS: The statistical analysis revealed a negative correlation between delta RI (difference between RI at 3 and 6 days after transplantation) and serum creatinine concentration, 10 days after transplantation (r = -0.63; P < 0.01). We also observed a negative correlation between creatinine serum concentration at 10 days after transplantation and delta thyroid volume (Delta Vol; r = - 0.48; p < .05), a positive correlation between delta FT4 (Delta FT4) serum concentration, and delta creatinine (Delta Crea; r = 0.73; P < .001). CONCLUSIONS: The dynamics of RI changes in the transplant kidney artery between 3 and 6 days after transplantation may predict graft function. Together with improved kidney function at 10 days after transplantation, we observed a regression of goiter.

Adult↗

PubMed1999

Correlations of plasma growth hormone with somatostatin, gonadal steroid hormones and thyroid hormones in rainbow trout during sexual recrudescence.

The study explores the interrelationships among growth hormone (GH), somatostatin-14 (SRIF), non-esterified fatty acids (NEFA), gonadal steroid hormones and thyroid hormones (THs) in sexually recrudescent rainbow trout (Oncorhynchus mykiss) to examine aspects of the complex set of physiological changes associated with gonadal growth and maturation. Females exhibited significant decreases in plasma SRIF, NEFA and triiodo-L-thyronine (T3) concentrations, and a significant increase in plasma GH concentration associated with gonadal maturation, whereas in males, only SRIF and NEFA concentrations showed significant changes during testicular maturation. The declining SRIF levels during gonadal recrudescence may indicate a role for the hormone in the energy repartitioning processes that occur in both sexes at this time. Correlation analysis of plasma variables revealed a direct correlations between plasma NEFA and 17 beta-estradiol (E2) in females, an inverse correlation between NEFA and testosterone (T) in males, inverse correlations between GH and SRIF in both males and females, and inverse correlations between THs and SRIF concentrations in females. These marked gender differences in correlations likely reflect the different physiological challenges faced by the two sexes and emphasizes the need to consider gender, as well as maturity when studying the interactions of hormones.

Animals↗

PubMed1993

Dominant negative inhibition by mutant thyroid hormone receptors is thyroid hormone response element and receptor isoform specific.

The heterogeneity of tissue-specific manifestations of generalized resistance to thyroid hormone (GRTH) could result from differential interactions between the mutant thyroid hormone (T3) receptor-beta (TR beta) on T3 response elements (TREs) in different T3-responsive genes. To explore this hypothesis, the mutant TR beta associated with kindred A, P448H; a TR beta mutant, P448L; and a comparable TR alpha mutant (P398H) were tested for intrinsic function and for inhibition of wild-type TR alpha- and -beta-induced expression from four structurally distinct TREs, the rGH ABC*, the rGH palindrome (PAL), the rat malic enzyme (ME), and the chicken lysozyme silencer F2 (F2). The relative function of the mutants was similarly reduced on the four TREs studied and was T3 concentration dependent. The TR alpha mutant retained the intrinsically greater potency characteristic of this isoform, but remained impaired with respect to wild-type TR alpha even at 500 nM T3. In general, dominant negative inhibition of wild-type TR alpha and -beta function was dependent upon the T3 concentration, as expected from the decreased affinity for ligand conferred by this mutation. A T3 concentration sufficient to relieve the inhibition of wild-type TR function on the ABC*, PAL, and ME TREs (50 nM) had no effect on inhibition of the F2 TRE by the mutant TRs. Receptor isoform preferential inhibition was observed on the ABC*, PAL, and ME TREs by the mutant TRs. Thus, both TRE structure and the isoform of endogenously active receptor could determine the degree of inhibition of a specific gene in GRTH individuals. Further, the lack of dominant negative potentials does not explain the absence of TR alpha mutations in GRTH kindreds.

Animals↗

PubMed1995

Desethylamiodarone is a competitive inhibitor of the binding of thyroid hormone to the thyroid hormone alpha 1-receptor protein.

Desethylamiodarone (DEA), the major metabolite of the potent antiarrythmic drug amiodarone, is a non-competitive inhibitor of the binding of thyroid hormone (T3) to the beta 1-thyroid hormone receptor (T3R). In the present study, we investigated whether DEA acts in a similar way with respect to the alpha 1-T3R. The chicken alpha 1-T3R, expressed in an E. coli system, was incubated in the presence or absence of DEA with [125I]T3 in buffer containing 0.05% Triton X-100, 0.05% BSA and 1% ethanol (v/v) in order to solubilise DEA. DEA, but not amiodarone, inhibited T3 binding in a dose-dependent manner; the IC50 value was 3.5 x 10(-5) M. Scatchard analyses in the presence of DEA demonstrated a dose-dependent decrease in Ka values, but no change in MBC. Lineweaver-Burk plots clearly indicated competitive inhibition by DEA. Pre-incubation of the alpha 1-receptor with DEA decreased maximal [125I]T3 binding, which was independent of the duration of pre-incubation. In conclusion, in contrast to the beta 1-T3R, where DEA acts as a non-competitive inhibitor, we now report as a new finding the competitive action of DEA to the alpha 1-T3R.

Amino Acid Sequence↗

PubMed1982

Changes of pyruvate dehydrogenase in rat brain with thyroid hormones.

Thyroid hormone deficiency increased the activity of PDHa (active) in three regions of the rat brain with insignificant changes in the total form; a regional variation was also observed. Treatment of thyroidectomized rats with triiodothyronine restored the enzyme activity to almost control values after 60 days of thyroidectomy in all the three regions. Administration of T3 to control animals decreased the PDHa by 70% without affecting the total form. Results are discussed in relation with insulin sensitivity of various tissues.

Animals↗

PubMed1981

A possible explanation of myxedema and hypercholesterolemia in hypothyroidism: control of lysosomal hyaluronidase and cholesterol esterase by thyroid hormones.

Thyroid hormones control the levels of the lysosomal enzymes, cholesterol esterase and hyaluronidase, in rat liver, skeletal muscle and skin. Activities of these enzymes decreased to approximately 40-50% of normal levels in liver cell fractions, skeletal muscle homogenates and skin homogenates from thyroidectomized rats. Treatment of hypophysectomized rats with L-triiodothyronine increased the activities of cholesterol esterase and hyaluronidase approximately 2-fold in liver cell fractions. The low levels of hyaluronidase and cholesterol esterase in thyroidectomized rats may account for the accumulation of mucopolysaccharides in skin and for the elevation of serum cholesterol levels in hypothyroid patients.

Acid Phosphatase↗

PubMed1993

Selenium deficiency, thyroid hormone metabolism, and thyroid hormone deiodinases.

Much research into the functions of selenium in the cell has concentrated on its role in selenium-containing glutathione peroxidases. However, selenium was recently shown to be an essential component of type I iodothyronine 5'-deiodinase in rats, which converts thyroxin to the more biologically active hormone 3,5,3'-triiodothyronine. Thus, selenium-deficient rats have low tissue deiodinase activities and abnormal thyroid hormone metabolism. The discovery of this function for selenium in thyroid hormone metabolism has important implications for the interpretation of the effects of selenium deficiency, especially in individuals with an adequate vitamin E status.

Animals↗

PubMed1990

Induction of ventricular morphogenesis and atrial natriuretic factor synthesis by thyroid hormone.

Thyroid hormones have been shown to increase atrial natriuretic peptide (ANP) synthesis in atria both in vitro and in vivo. In this study the effects of triiodothyronine (T3) administration on primary cultures of 6-day-old atrial and ventricular myocytes were studied. Levels of immunoreactive (ir-) ANP were determined by radioimmunoassay over 9 days of culture in cells cultured in the presence and absence of 10(-8) M T3. The proportion of immunostained nuclei was also determined and changes in cell characteristics noted over this time. Over 9 days T3 had no effect on the proportion of atrial cells immunostained for ANP, while cell and medium content of ir-ANP in treated wells doubled that of the untreated. In treated ventricular myocytes, cell and medium ir-ANP similarly increased; in addition, the proportion of immunostained cells increased by 1-2 orders of magnitude. The formation of dendritic processes was enhanced in these cultures, reflected in increased rates of spontaneous contractility. Thus it would appear that the 6-day-old myocardium exhibits profound differences in response to T3 administration, in that ventricular cells dedifferentiate and undergo morphological changes which are not seen in atriocytes.

Animals↗

PubMed1998

Levels of MyoD protein expression following injury of mdx and normal limb muscle are modified by thyroid hormone.

Thyroid hormone (T3) affects muscle development and muscle regeneration. It also interacts with the muscle regulatory gene MyoD in culture and affects myoblast proliferation. We studied the localization of MyoD protein using a well-characterized polyclonal antibody for immunohistochemistry. Relative numbers of myogenic precursor cells per field were identified by their MyoD expression during muscle regeneration in normal and mdx dystrophic mice, with particular reference to the expression in mononuclear cells and myotubes at various T3 levels. In regeneration by normal muscles, relatively few MyoD+ nuclei per field were present in mononuclear cells of euthyroid and hypothyroid mice. MyoD staining of mononuclear cell nuclei was approximately doubled in fields of regenerating muscles of normal hyperthyroid compared to euthyroid mice, and was observed in precursors that appeared to be aligned before fusion into myotubes. In mdx regenerating muscle, twofold more mononuclear cells positive for MyoD were present in all three treatment groups compared to normal muscles regenerating under the same conditions. Localization was similar to the pattern in normal euthyroid mice. However, in muscles regenerating in hyperthyroid mdx mice, both mononuclear cell nuclei and centrally located nuclei in a subpopulation (about 15%) of new myotubes formed after the crush injury were intensely stained for MyoD protein. The changes observed are consistent with reports on T3-induced alteration of muscle repair, and propose a link between MyoD regulation and the accelerated differentiation during regeneration under high T3 conditions. (J Histochem Cytochem 46:59-67, 1998)

Animals↗

PubMed2005

Modulation of mitochondrial transition pore components by thyroid hormone.

Thyroid hormone (TH) modulates metabolic efficiency by controlling the coupling of mitochondrial oxidative phosphorylation. However, its uncoupling mode of action is still enigmatic. Treatment of Jurkat or GH3 cells with T3 is reported here to result in limited, Cyclosporin A-sensitive mitochondrial depolarization, conforming to low conductance gating of the mitochondrial transition pore (MTP). MTP protein components induced by T3 treatment were verified in T3-treated and hypothyroid rat liver as well as in Jurkat cells. T3 treatment resulted in increase in mitochondrial Bax and Bak together with decreased mitochondrial Bcl2. T3-induced mitochondrial depolarization was aborted by overexpression of Bcl2. In contrast to Bax-Bcl2 family proteins, some other MTP components were either not induced by T3 (e.g. voltage-dependent anion channel) or were induced, but were not involved in Cyclosporin A-sensitive MTP gating (e.g. Cyclophilin D and adenine nucleotide translocase-2) Hence, TH-induced mitochondrial uncoupling may be ascribed to low conductance MTP gating mediated by TH-induced increase in mitochondrial proapoptotic combined with a decrease in mitochondrial antiapoptotic proteins of the Bax-Bcl2 family.

Animals↗