• 대한핵의학회지
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• 제12권2호
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• pp.23-31
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• 1978

Hyperthyroidism may be defined as those clinical conditions which result from an increase in the circulating levels of one or both thyroid hormones. Hyperthyroidism in broad sense could be classified with toxic diffuse goiter, toxic adenomatous goiter, and toxic multinodular goiter on the basis of the circulating thyroid hormone levels. For this study, the subject included 94 cases with hyperthyroidism were presented in 77 with toxic diffuse goiter, 8 with toxic adenomatous goiter, and 9 with toxic multinodular goiter on the levels of $^{125}IT_3$ resin uptake rate and serum thyroxine ($T_4$). The observed results were as follows: 1) In the cases of hyperthyroidism including toxic diffuse goiter, toxic adenomatous goiter, and toxic multinodular goiter, 20.21% of the patients were male and 79.79% female. The majority of the patients were in 2nd to 4th decades of their lives. 2) There were objective signs clearly manifested in hyperthyroidism including toxic diffuse goiter and toxic adenomatous goiter which were rare in the multinodular goiter. The clinical signs in toxic diffuse and toxic adenomatous goiter included wide pulse pressure, tachycardia, systolic murmur, exophthalmos, tremor and warm skin etc. (Table 3.) 3) The most freauent complaints of the patients with hyperthyroidism were palpitation, weight loss, increased appetite, perspiration, heat intolerance, nervousness, exertional dyspnea, and menstrual disturbance etc. (Table 4.) There was no clear difference in the incidence of symptoms between toxic diffuse goiter and toxic adenomatous goiter, but there was clear difference between toxic multinodular goiter. 4) Considering of results of $^{125}IT_3$ resin uptake rate and serum $T_4$ level in toxic diffuse goiter, toxic adenomatous goiter and toxic multinodular goiter, $^{125}I\;T_3$ resin uptake rate was $49.15{\pm}9.94%$ (mean) and serum $T_4\;21.29{\pm}7.04ug/dl$ (mean) in toxic diffuse goiter. In toxic multinodular goiter, $^{125}I\;T_3$ resin uptake rate was $32.47{\pm}6.74%$ (mean) and serum $T_4$ level $11.03{\pm}5.0ug/dl$, and then there was clear difference in the results of $^{125}I\;T_3$ resin uptake rate and serum $T_4$ between toxic diffuse goiter and toxic multinodular goiter. The levels of $^{125}I\;T_3$ resin uptake rate and serum $T_4$ in toxic adenomatous goiter were $40.32{\pm}13.08%$ (mean), $15.47{\pm}8.25ug/dl$ (mean) respectively, so there was no clear difference between toxic diffuse goiter and toxic adenomatous goiter. 5) There was no significant differnece in length and width performed with thyroid scanning in toxic diffuse goiter, toxic adenomatous goiter, and toxic multinodular goiter.

• BMB Reports
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• 제42권9호
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• pp.568-573
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• 2009

Fatty acid oxidation (FAO) defects cause abnormal lipid accumulation in various tissues, which provides an opportunity to uncover novel genes that are involved in lipid metabolism. During a gene expression study in the riboflavin deficient induced FAO disorder in the chicken, we discovered the dramatic increase in mRNA levels of an uncharacterized gene, ANKRD9. No functions have been ascribed to ANKRD9 and its orthologs, although their sequences are well conserved among vertebrates. To provide insight into the function of ANKRD9, the expression of ANKRD9 mRNA in lipidperturbed paradigms was examined. The hepatic mRNA level of ANKRD9 was repressed by thyroid hormone ($T_3$) and fasting, elevated by re-feeding upon fasting. However, ANKRD9 mRNA level is reduced in response to apoptosis. Transient transfection assay with green fluorescent protein tagged- ANKRD9 showed that this protein is localized within the cytoplasm. These findings point to the possibility that ANKRD9 is involved in intracellular lipid accumulation.

• Journal of Nutrition and Health
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• 제35권2호
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• pp.207-212
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• 2002

Acetyl-CoA carboxylase (ACC) is the enzyme that controls no devo fatty acid biogynthesis, and this enzyme catalyzes the carboxylation pathway of acetyl-CoA to malonyl-CoA. Acetyl-CoA carboxylase gene expression was regulated by nutritional and hormonal status. The present study was performed to identify the regulation mechanism of ACC gene promoter I. The fragments of ACC promoter I -1.2-kb region wert recombined to pGL3-Basic vector with luciferase as a reporter gene. The primary hepatocytes from the rat were used to investigate the hormonal regulation of ACC promoter I activity. ACC PI (-1.2)/Luc plasmid was trtransferred into primary hepatocytes using lipofectin. Activity of luciferase was increased two-fold by 10-9M, three-fold by 10-8M, 10-6M, 3.5-fold by 10-6M, and 4.5-fold by 10-7M insulin treatment, respectively. In the presence of dexamethasone (1 $\mu$M), the effects of insulin increased about 1.5-fold, showing the additional effects of dexamethasone. Moreover, the activity of luciferase increased with insulin+dexamethasone, insulin+T3, dexamethasone+T3, and dexamethasone+insulin+T3 treatment approximately 6-, 4-, 6.5-, and 10-fold, respectively. Therefore it can be postulated that 1) these hormones coordinately regulate acetyl-CoA caroxylase gene expression via regulation of promoter activity, 2) the -1.2-kb region of ACC promoter I may have the response element sequences for insulin, dexamethasone, and T3.

• Clinical and Experimental Pediatrics
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• 제45권6호
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• pp.796-799
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• 2002

티록신 결합글로불린 결핍증은 대부분 갑상선기능저하증을 동반하지 않으므로 갑상선 호르몬 보충 요법이 필요 없으나 드문 예에서 유리 티록신 농도가 정상치 보다 낮게 유지되고, 중추 신경계에 대한 갑상선 호르몬의 부족에 의해 갑상선 자극호르몬이 정상치 보다 증가하는 경우가 있다. 이런 경우는 티록신 결합글로불린의 결핍 정도가 갑상선기능저하증을 유발할 수 있을 정도로 갑상선 호르몬의 이동과 갑상선 밖의 호르몬 저장에 영향을 주는 것이므로 갑상선호르몬의 보충요법이 필요하게 된다. 저자들은 갑상선기능저하증을 동반하여 갑상선 호르몬의 투여가 필요한 중증의 티록신 결합글로불린 결핍증 1례를 보고하는 바이다.

• Journal of Yeungnam Medical Science
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• 제29권2호
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• pp.77-82
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• 2012

AMP-activated protein kinase (AMPK) is an important cellular fuel sensor. Its activation requires phosphorylation at Thr-172, which resides in the activation loop of the ${\alpha}1$ and ${\alpha}2$ subunits. Several AMPK upstream kinases are capable of phosphorylating AMPK at Thr-172, including LKB1 and CaMKK${\beta}$ ($Ca^{2+}$/calmodulin-dependent protein kinase kinase${\beta}$). AMPK has been implicated in the regulation of physiological signals, such as in the inhibition of cholesterol fatty acid, and protein synthesis, and enhancement of glucose uptake and blood flow. AMPK activation also exhibits several salutary effects on the vascular function and improves vascular abnormalities. AMPK is modulated by numerous hormones and cytokines that regulate the energy balance in the whole body. These hormone and cytokines include leptin, adiponectin, ghrelin, and even thyroid hormones. Moreover, AMPK is activated by several drugs and xenobiotics. Some of these are in being clinically used to treat type 2 diabetes (e.g., metformin and thiazolidinediones), hypertension (e.g., nifedipine and losartan), and impaired blood flow (e.g., aspirin, statins, and cilostazol). I reviewed the precise mechanisms of the AMPK activation pathway and AMPK-modulating drugs.

• 대한수의학회지
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• 제20권1호
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• pp.17-24
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• 1980

In order to know the effects of thyroid hormone on the bursa of Fabricius in chicken, the bursae were studied with the light microscope after administration of thyroxine(TX) or propylthiouracil(PPT). Macroscopically, the bursa of TY-treated group showed increase in size and thickened folds. while those of the PPT-treated group decrease in size, compared with those of control group. In the light microscopic studies, the bursa of Fabricius of the TX-treated group showed active cell-divisions in the medulla, and increased number of pyroninophilic large lymphocytes and plasma cells containing PAS positive materials in the cytoplasms. On the other hand, the bursa from PPT-treated group revealed decreased number of lymphocytes, significant increase of necrotic lymphocytes in the follicles, and the proliferation of the interfollicular connective tissues. A large number of pyroninophilic lymphocytes and plasma cells were also appeared in the spleen of the TX-treated group.

• 대한핵의학회지
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• 제15권1호
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• pp.37-43
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• 1981

Congenital hypothyroidism due to organification defect was first reported by Haddad and Sidbury in 1959. The organification defect is easily proved by perchlorate discharge test. We experienced a patient who had large goiter, growth and mental retardation, and revealed positive reponse to perchlorate discharges test, and the surgical biopsied specimen showed Huerthle cell adenoma, which was probably due to chronic stimulation of thyroid stimulating hormone, or coexisted incidentally. Described here a case of congenital hypothyroidism due to organification defect associated with Huerthle cell adenoma, with review of some literatures.

• 대한한의학회지
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• 제18권1호
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• pp.399-410
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• 1997

In order to investigate the effects according to the concentration(o, 30, 60 and $120{\mu}g/350{\sim}400g$: saline group, I-group, II-group and III-group) of Labiatae Herba Prunellae Acua-acupuncture on the bilateral loci Taechung(LR3) in hyperthyroidism rats induced by sodium triiodothyronine injection, triiodothyronine(T3), thyroxine(T4), thyroid- stimulating hormone(TSH) and total cholesterol were observed. The results were summarized as follows; 1. The increases of the serum T3 were inhibited significantly by II-group and III-group compared with the control group. 2. The decreases of the serum T4 were inhibited significantly by I-group, II-group and III-group compared with the control group. The I-group and II-group compared with the saline group is significantly different. 3. The decreases of the serum TSH were inhibited significantly by II-group and III-group compared with the control group. The II-group compared with the saline group is significantly different. 4. The decreases of the serum total cholesterol were inhibited significantly by I-group, II-group and III-group compared with the control group. The II-group and III-group compared with the saline group is significantly different.

• 한국동물학회지
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• 제36권4호
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• pp.487-495
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• 1993

TRH (Thvrotropin-Releasing Hormone) known to regulate the transcription of the TSH (Thyroid-Stimulating Hormones gene in pituitary cells, but little is understood about the mechanism(sl involved. re present study was attempted to elucidate the role of Ca2+ movement through the voltage-gated channels in the regulation of TSH gene transcription. The c-fos is one of immediate early genes and used as model system for the investigation of signaling pathwavs involved in various stimuli. The changes of c-fos mRNA levels were determined after treatment of various agents using Northern and slot hybridization analysis. The c-fos mRNA was rapidly and transiently induced by TRH (about 3-fold) in GH3 cells and this induction was repressed by calcium chelating agent (EGTA), calcium channel blocker (verapamil) anti protein kinase C inhibitor (aminoacridine). The abilities of forskolin (adenvlate cvclase activators, PMA (protein kinase C activator), and A23187 (calcium ionophore) to affect c-ios gene transcription, either alone or in combination with TRH were tested in the same cells. All of them significantly increased the level of c-fos mRUA. However, no additive relationship was observed in all combined treatments except forskolin. These results suggest that TRH action on the c-fos gene activation is mediated by calcium influx as well as through protein kinase C.

• 한국임상수의학회지
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• 제35권1호
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• pp.19-21
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• 2018

A 7-year-old female American cocker spaniel presented with chronic regurgitation and megaesophagus on radiography at a local hospital. Dry and coarse hair coat, tail alopecia, and bradycardia were observed during physical examination. Mild, non-regenerative anemia was indicated by complete blood count (CBC) analysis. Concurrent hypercholesterolemia and hypertriglycemia were indicated by biochemistry tests. Decreased levels of total and free thyroxine (T4) and increased canine thyroid stimulating hormone (cTSH) levels were also detected. Megaesophagus was confirmed by radiographic examination. Based on the results, a diagnosis of hypothyroidism with megaesophagus was made. The patient was initially treated with levothyroxine sodium at a dosage of 0.02 mg/kg twice a day. After two weeks of treatment for hypothyroidism, the dilated esophagus returned to its original size and no further regurgitation was observed. No relapse was observed during two months of follow-up.