• Korean Journal of Veterinary Research
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• v.38 no.3
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• pp.508-517
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• 1998

There is evidence that the sympathetic nervous system exerts a control on thyroid function via an adrenergic innervation of thyroid cells. Although it is clear that the inhibitory effects of catecholamines result from an activation of ${\alpha}_1$-adrenoceptors, the mechanisms involved in ${\alpha}_1$-stimulation are not fully understood. The effects of methoxamine and protein kinase C (PKC) activator on the release of thyroxine ($T_4$) from mouse thyroid were studied to clarify the role of PKC in the regulation of $T_4$ release in vitro. The glands were incubated in the medium, samples of the medium were assayed for $T_4$ by EIA kits. Methoxamine inhibited the TSH-stimulated $T_4$ release. This inhibition was reversed by prazosin, an ${\alpha}_1$-adrenergic antagonist. Futhermore, the inhibitory effect of methoxamine on the $T_4$ release stimulated by TSH was prevented by chloroethylclonidine, an ${\alpha}_{1b}$-adrenoceptor antagonist, but not by WB4101, an ${\alpha}_{1a}$-adrenoceptor antagonist. Also methoxamine inhibited the forskolin-, cAMP- or IBMX-stimulated $T_4$ release. These inhibition were reversed by PKC inhibitors, such as staurosporine and $H_7$. PMA, a PKC activator, completely inhibited the TSH-stimulated $T_4$ release, and its inhibition was reversed by staurosporine and $H_7$, but not by chelerythrine. R59022 (a diacylglycerol kinase inhibitor), like methoxamine, also inhibited the TSH-stimulated $T_4$ release, and its inhibition was also reversed by staurosporine. The present study suggests that methoxamine inhibition of $T_4$ release from mouse thyroid can be induced by activation of the ${\alpha}_{1b}$-adrenoceptors and that it is mediated through the ${\alpha}_1$-adrenoceptor-stimulated PKC formation.

• Korean Journal of Veterinary Research
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• v.39 no.6
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• pp.1073-1080
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• 1999

Previous studies suggested that the inhibition of thyroxine ($T_4$) release by ${\alpha}_1$-adrenoceptor and muscarinic receptor stimulation results in activated protein kinase C (PKC) from mouse and guinea pig thyroids. In the present study, the effect of carbachol, methoxamine, phorbol myristate acetate (PMA), and R59022 on the release of $T_4$ from the mouse, rat, and guinea pig thyroids was compared to clarify the role of PKC in the regulation of the release of $T_4$. The thyroids were incubated in the medium containing the test agents, samples of the medium were assayed for $T_4$ by EIA kits. Forskolin, an adenylate cyclase activator, chlorophenylthio-cAMP sodium, a membrane permeable analog of cAMP, and isobutyl-methylxanthine, a phosphodiesterase inhibitor, like TSH (thyroid stimulating hormone), enhaced the release of $T_4$ from the mouse, rat, and guinea pig thyroids. Methoxamine, an ${\alpha}_1$-adrenoceptor agonist, inhibited the TSH-stimulated release of $T_4$ in mouse, but not rat and guinea pig thyroids. In contrast, carbachol, a muscarinic receptor agonist, inhibited the release of $T_4$ in guinea pig, but not mouse and rat thyroids. These inhibition were reversed by prazosin, an ${\alpha}_1$-adrenoceptor antagonist or atropine, a muscarinic antagonist or $M_1$- and $M_3$-muscarinic antagonists, in mouse or guinea pig thyroids. In addition, staurosporine, a PKC inhibitor, reversed methoxamine or carbachol inhibition of TSH stimulation. Furthermore, PMA, a PKC activator, and R59022, a diacylglycerol (DAG) kinase inhibitor, inhibited the TSH-stimulated release of $T_4$ in mouse, rat, and guinea pig thyroids. These inhibition were blocked by staurosporine. These findings suggest that the activation of receptor or DAG inhibits TSH-stimulated $T_4$ release through a PKC-dependent mechanism in thyroid gland.

• The Korean Journal of Nuclear Medicine
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• v.7 no.2
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• pp.1-12
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• 1973

The most commonly used methods for determining thyroxine binding globulin(TBG) concentration as the total thyroxine-binding capacity utilize electrophoretic seperation of serum. Although technically simple, the electrophoretic method is time consuming and is limited in the number of samples which can be run in a single assay. The author presented a single $T_4$ load ion exchange resin method as an approach to simplify the technique as with clinical practicability and results were analyzed. For construction of the standard curves, serum mixtures were diluted with barbital buffer.which effectively blocked $T_4$-binding to TBPA. For each serum dilution, a constant amount of $T_4-^{125}I$ and increments of unlabelled $T_4$ were added. After incubation in water bath, resin beads were dispensed to the samples which binded all $T_4$ not bound to TBG. The radioactivity in the supernatant was counted in the gamma scintillation counter. Each standard curve was plotted from the percent counts in the supernatant and total $T_4$ in each tube. Unknown samples were diluted to 1:40 and ran at a single $T_4$ loading concentration, and the TBG capacity of the samples was able to be read on the standard isobars. The following results were obtained. 1) Mean and standard deviation for TBG capacity in normal population was $28.6{\pm}5.09{\mu}g\;T_4/100ml$. 2) $24.9{\pm}3.87{\mu}g\;T_4/100ml$ in hyperthyroidism showed low TBG capacity comparing to normal population.(p<0.025) 3) $31.0{\pm}2.40{\mu}g\;T_4/100ml$ in hypothyroidism showed high TBG capacity tendency comparing to normal population. 4) Reversed correlationship existed between TBG capacity and $T_3$ resin uptake(r=-0.624), TBG capacity and serum $T_4$ value (r=-0.859), and TBG capacity and free thyroxine index(r=-0.623). The author assumes that this method of assay is considerably simpler in instrumentation and technique than any other assays traditionally being used, and seems to be more practical for routine clinical laboratory use.

• Clinical and Experimental Pediatrics
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• v.45 no.6
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• pp.796-799
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• 2002

A child diagnosed with congenital hypothyroidism after newborn screening and follow up thyroid function test at 1 month of life in another general hospital demonstrated euthyroid state with thyroxine( $T_4$) supplementation until the age of 22 months of life, when he was transferred to our hospital, where he was diagnosed as thyroxine binding globulin(TBG) deficiency with low $T_4$ and TBG. Withdrawal of $T_4$ at age of 26 months was associated with hyperthyrotropinemic hypothyroidism. This patient is a case of TBG deficiency associated with hypothyroidism, and in rare instances, TBG deficiency may lead to hypothyroidism requiring hormone supplementation.

• The Journal of Internal Korean Medicine
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• v.21 no.3
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• pp.399-407
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• 2000

This study was carried out to examine if Haejohwan (HJ) inhibits oxidant-induced lipid peroxidation and therby produces protective effect against thyroxine-induced hyperthyroid rats. Triiodothyronine $(T_3)$, thyroxine $(T_4)$, lipid peroxidation, xathine oxidase activities and type conversion ratio were increased in thyroxine treated group. However, they were decreased in HJ extract's pre-applied group. Glutathione level, activities of glutathione peroxidase, glutathione Stransferase and glutathione reductase were decreased in thyroxine treated group. But, they were increased in HJ extract's pre-applied group. These results suggest that in thyroxine-induced hyperthyroid rats HJhas an increase in the activities of oxygen free radical scavenging enzymes and inhibition of xanthine oxidase activities, and prevents lipid peroxidation.

• Korean Journal of Animal Reproduction
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• v.11 no.1
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• pp.16-21
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• 1987

We describe a simple, solid-phase chemiluminescence immunoassay for the meausrement of serum T4. An immunoglobulin G fraction of antibody to thyroxine was passively absorbed onto the walls of polystyrene tubes. The labeled antigen was thyroxine-aminobutylethylisoluminol. After the bindings reaction (37$^{\circ}C$ for 1 hour), the solution is removed by aspiration and the antibody-bound fraction was washed once with buffer. Sodium hydroxide (5mol/1,200${mu}ell$) was added and the mixture incubated for 30 minutes at 6$0^{\circ}C$. Luminescence was initiated by oxidation of the label with micropeeroxidase-hydrogen peroxide and the signal of light emission was intergrated for 10 sec. The light yield was inversely proportional to the concentration of T4 in the standard or sample. An evaluation of the method gave the following values sensitivity of calibration curve 7.5$\pm$2.8 nmol/l (mean$\pm$SD). The intra-assay precision (CV%) was 8.9, 7.3 and 5.4. The inter-assay precision (CV%) was 10.2, 8.1 and 7.1. When seum samples were assayed for T4, the results obtained by solid-phase CIA and the conventional RIA agreed well(n=3.5, r=0.954).

• Journal of the Korean Society of Food Science and Nutrition
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• v.26 no.3
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• pp.507-513
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• 1997

This study was carried out to examine whether kimchi has hypolipidemic effect and to know how it exert lipid-lowering effect in rats. Male Sprague-Dawley rats were fed with kimchi-fee diet, or 3%, or 5%, or 10% kimchi diets for 6 weeks. Plasma cholesterol level was lowered in rats fed all concentrations of kimchi diets, and plasma triglyceride(TG) level was lowered in 10% kimchi diet group compared with that of control significantly(p<0.05). Th intake of kimchi lowered VLDL-cholesterol and VLDL-TG levels, whereas increased HDL-cholesterol level significantly(p<0.05). LDL-cholesterol level was lowered only in 5% kimchi diet group and LDL-TG level was lowered in all kimchi diet groups compared with those of control significantly (p<0.05). the intake of 5% and 10% kimchi diets also lowered the levels of hepatic cholesterol, TG, total lipid, and apolipoprotein B, whereas increased the levels of fecal total fat, cholesterol, TG, and apolipoprotein A-1 significantly(p<0.05). Triiodothyronine(T$_3$) level was elevated in rats fed kimchi diet, whereas thyroxine(T$_4$) level was not affected by kimchi treatment. These observations support that the intake of kimchin in rats loweres plasma and hepatic lipid levels by increasing the excretion of TG and cholesterol through feces, by the elevation of T$_3$ level, and by the altered lipoprotein metabolism.

• Clinical and Experimental Pediatrics
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• v.49 no.6
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• pp.677-685
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• 2006

Purpose : This study aimed to investigate whether exogenous thyroxine($T_4$) treatment to alcohol-fed dams would ameliorate the detrimental effects of alcohol on the postnatal development of neuropeptide-Y(NPY)-containing neurons of the cerebral cortex and hippocampus of the offspring. Methods : Time-pregnant rats were divided into three groups. An alcohol-fed group A received 35 calories of liquid alcohol diet daily from gestation day 6; control group B was fed a liquid diet in which dextrin replaced alcohol isocalorically; and alcohol＋$T_4$ group C received 35 calories of liquid alcohol diet and exogenous thyroxine subcutaneously. The features of the growth and maturation of rat brain tissue were observed at 0, 7, 14, 21 and 28 postnatal days via immunohistochemistry. Results : Group C showed prominent NPY immunoreactivity in the cerebral cortex compared to group A and B at P7. In group C, NPY-containing neurons were widely distributed in the all layers of cerebral cortex after P14. Also, numerical decreases of NPY-containing neuron were not found according to increasing age in group C. A decrease of NPY-containing neurons, however, was clearly observed in group A compared to group C at P28. In the hippocampus, similar patterns appeared in groups B and C after P7. Especially, in groups B and C, NPY-containing fibers formed plexus in the cerebral cortex and hippocampus at P14. Conclusion : These results suggest that the increase of NPY synthesis caused by maternal administration of exogenous thyroxine may convalesce fetal alcohol effects, one of the effects of the dysthyroid state following maternal alcohol abuse.

• Korean Journal of Veterinary Research
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• v.38 no.4
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• pp.712-719
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• 1998

Thyroid function is mainly regulated through cAMP and phophatidylinositol, and it is well known that TSH-stimulated thyroxine ($T_4$) release is inhibited by catecholamine from mouse thyroids via the ${\alpha}_1$-adrenoceptor stimulation. Previous study has established that the inhibition of $T_4$ release by ${\alpha}_1$-adrenoceptor stimulation results in activated protein kinase C (PKC). The purpose of this study was to determine if ion transport systems are involved in the inhibition of $T_4$ release elicited by ${\alpha}_1$-adrenergic agonist in mouse thyroids. TSH-, IBMX- and cAMP analogue-stimulated $T_4$ release were significantly inhibited by methoxamine, R59022 (diacylglycerol kinase inhibitor), and MDL (adenylate cyclase inhibitor). TSH-stimulated $T_4$ release could be inhibited by Bay K 8644 and cyclopiazoic acid, but not by verapamil and tetrodotoxin. The addition of nifedipine ($Ca^{2+}$ channel blocker), tetrodotoxin and lidocaine ($Na^+$ channel blockers), but not amiloride (EIPA) and ryanodine, completely blocked the inhibitory effects of methoxamine on $T_4$ release. TSH-stimulated $T_4$ release was also inhibited by benzamil ($Na^+-Ca^{2+}$ exchange inhibitor). TSH-, IBMX- and cAMP-stimulated $T_4$ release were inhibited by methoxamine or R59022, these effects were reversed by nifedipine. but not by verapamil. Furthermore, nifedipine reversed the inhibitory effects of benzamil and R59022 on TSH-stimulated $T_4$ release. These data suggest that the observed ${\alpha}_1$-adrenoceptor-mediated inhibition of $T_4$ release in mouse thyroids is the result of an increase in intracellular $Na^+$ or $Ca^{2+}$ effected via activation of fast $Na^+$ or nifedipine-sensitive $Ca^{2+}$ channels, and that $Na^+-Ca^{2+}$ exchange may play an important role in reducing thyroid hormone by increasing intracellular $Ca^{2+}$.

• Korean Journal of Animal Reproduction
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• v.16 no.4
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• pp.353-361
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• 1993

This study was taken to examine external changes, behavioral changes, and endocrine changes such as estradiol-17$\beta$, progesterone, T4 and T3 of female Oreochromis niloticus living in 0$\textperthousand$, 10$\textperthousand$, 20$\textperthousand$, and 30$\textperthousand$ salt concentrations, respectively. The results obtained in these experiments were summarized as follows. In seawater obtained in these experiments were summarized as follows. In seawater challenge test, any fish didn't die in each group such as 10$\textperthousand$, 20$\textperthousand$ and 30$\textperthousand$. When fish were adapted from 0$\textperthousand$ to 10$\textperthousand$, 20$\textperthousand$ and 30$\textperthousand$, external body color of fish changed from dark-striped to light-grey color. At the same time, thyroxine and triiodothyronine concentrations significantly(P<0.05) increased, and then were at the highest level in 30 salinity. When fish were adapted from 0$\textperthousand$ to 10$\textperthousand$, feed intake of fish started from the fourth day. From 0$\textperthousand$ to 10$\textperthousand$, 20$\textperthousand$ and 30$\textperthousand$, estradiol-17$\beta$ levels were increased gradually. When fish was adapted from 0$\textperthousand$ to 10$\textperthousand$, 20$\textperthousand$ and 30$\textperthousand$, the levels of each progesterone didn't show significant change, and especially showed the lowest peak in 20$\textperthousand$. The greatest thyroxine activity(T4) was observed in 30$\textperthousand$. The levels of and triiodothyronine(T3) significantly changed in all salinities, and its level was at the highest peak in 30$\textperthousand$ salinity. Correlation coefficients between serum progesterone and triiodothyronine in 10$\textperthousand$ and 30$\textperthousand$ were ＋0.677 and ＋0.843, respectively. Correlation coefficient of serum thyroxine(T4) and triiodothyronine(T3) individuals in 10$\textperthousand$ was ＋0.768, and ＋0.843, respectively.