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Young Kil Choi  (Choi YK) 49 Articles
Retraction: Multi-country Study on the Prevalence and Clinical Features of Peripheral Arterial Disease in Type 2 Diabetic Patients Who are at High Risk for Atherosclerosis.
Sang Youl Rhee, Seungjoon Oh, Young Kil Choi, Doo Man Kim, Bong Yun Cha, Hyun Chul Lee, Seung Woo Ha, In Kyu Lee, Tae Sun Park, Min Young Chung, In Joo Kim, Moon Kyu Lee, Sung Soo Koong, Kyung Soo Park, Kyung Wan Min, Young Seol Kim
J Korean Endocr Soc. 2007;22(6):478-478.   Published online December 1, 2007
DOI: https://doi.org/10.3803/jkes.2007.22.6.478
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Comparison of Common Carotid Artery Intima-Media Thickness between Subclinical Hypothyroidism and Euthyroidism.
Kyung Sun Park, Jung Im Rue, Soo Kyung Kim, In Jae Kim, Sang Wook Lim, Seok Won Park, Yu Lee Kim, Dong Hoon Cha, Yong Wook Cho, Young Kil Choi, Sang Jong Lee
J Korean Endocr Soc. 2006;21(6):490-496.   Published online December 1, 2006
DOI: https://doi.org/10.3803/jkes.2006.21.6.490
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AbstractAbstract PDF
BACKGROUND
Common carotid artery intima-media thickness (IMT), which is increased in patients with overt hypothyroidism, is an independent risk factor of the atherosclerosis-related disease. This study was performed to compare serum lipid level and common carotid artery IMT among patients with overt hypothyroidism, subclinical hypothyroidism and euthyroidism. METHODS: Patients with newly-diagnosed subclinical (n=32) and overt (n=32) hypothyroidism were selected for this study. All of the patients and an age- and sex-matched euthyroidism cohort were checked for clinical characteristics and serum lipid levels. Common carotid artery IMT was also measured using high resolution B-mode ultrasonography. RESULTS: Statistically significant differences were observed between the total cholesterol levels of patients with subclinical hypothyroidism and those with euthyroidism. When common carotid artery IMT measured by ultrasonography, subclinical (0.67 +/- 0.11 mm) and overt (0.71 +/- 0.12 mm)) hypothyroidism showed significantly increased mean IMT compared to that of euthyroidism (0.58 +/- 0.07 mm, P < 0.05, respectively), but no differences were found between subclinical and overt hypothyroidism. CONCLUSION: We concluded that subclinical hypothyroidism is related to increased common carotid artery IMT as well as dyslipidemia. Therefore, we recommend that treatment principle of subclinical hypothyroidism be established through large-scale, prospective studies performed to determine the effect of thyroid hormone replacement on the reduction of common carotid artery IMT.

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  • The Effect of Brief Thyroid Functional Changes on Arterial Stiffness in Patients Who Preparing Radioactive Iodine Administration
    Ho-Su Kim, Jae-Hoon Jung, Jung Hwa Jung, Soo Kyoung Kim, Sungsu Kim, Jeong Rang Park, Rock Bum Kim, Jong Ryeal Hahm
    International Journal of Thyroidology.2015; 8(2): 161.     CrossRef
  • Changes of Body Composition, Blood Concentrations of Lipid Profiles and Thyroid Hormone After Exercise Training in Hypothyroid-induced Rat
    Kijin Kim
    The Korean Journal of Obesity.2012; 21(1): 65.     CrossRef
Multi-country Study on the Prevalence and Clinical Features of Peripheral Arterial Disease in Type 2 Diabetic Patients Who are at High Risk for Atherosclerosis.
Sang Youl Rhee, Seungjoon Oh, Young Kil Choi, Doo Man Kim, Bong Yun Cha, Hyun Chul Lee, Seung Woo Ha, In Kyu Lee, Tae Sun Park, Min Young Chung, In Joo Kim, Moon Kyu Lee, Sung Soo Koong, Kyung Soo Park, Kyung Wan Min, Young Seol Kim
J Korean Endocr Soc. 2006;21(4):290-301.   Published online August 1, 2006
DOI: https://doi.org/10.3803/jkes.2006.21.4.290
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AbstractAbstract PDF
BACKGROUND
PAD-SEARCH (Peripheral Arterial Disease-Screening and Evaluation of diabetic patients in Asian Regions Characterized by High risk factors) is the first international study to investigate the prevalence of peripheral arterial disease (PAD) in Asian type 2 diabetic patients and to demonstrate the relationships between the putative risk factors and PAD in this population. METHODS: A total of 6,625 type 2 diabetic patients (2,873 males and 3,752 females aged 50 and older) were enrolled in PAD-SEARCH in Korea, China, Taiwan, Hong Kong, Indonesia, Thailand and Philippines from October 2003 to March 2004. The Fukuda vascular profile VS-1000(TM) was used to determine the ankle-brachial index (ABI) and the brachial-ankle pulse wave velocity (baPWV). RESULTS: The mean patient age was 63.7 +/- 8.2 years and the mean duration of diabetes was 10.3 +/- 8.0 years. 1,172 (17.7%) subjects were diagnosed as PAD by the ABI (< or = 0.9). Subjects with PAD had a significantly longer duration of diabetes or hypertension, a higher HbA1c level and a significantly lower mean BMI than did the non-PAD subjects. In terms of the lipid profiles, triglyceride was the only significant variable. Notably, the mean ABI and baPWV in the females were significantly poorer than the age matched males for the in subjects with a normal ABI. However, the mean ABI and baPWV in males were significantly poorer than those of the age matched females for the subjects with PAD. On the multivariate analysis, gender, age, BMI, smoking status, duration of diabetes and a previous history of cerebrovascular disease were identified as the independent risk factors of PAD. CONCLUSION: These findings suggest that PAD is a common complication in Asian type 2 diabetic patients. Therefore, PAD screening and treatment should be emphasized for Asian diabetic patients with high risk factors.
A Case of Non-islet Cell Tumor Hypoglycemia.
Yun Tae Chae, Il Jun Hwang, Kyung Hee Ryu, Eun Hyang Ko, Jung Im Rue, Soo Kyung Kim, Seok Won Park, Yoo Ri Kim, Yong Wook Cho, Young Kil Choi, Sang Jong Lee
J Korean Endocr Soc. 2006;21(1):74-78.   Published online February 1, 2006
DOI: https://doi.org/10.3803/jkes.2006.21.1.74
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AbstractAbstract PDF
Mesenchymal tumors including hemangiopericytomas, hepatocellular tumors, adrenal carcinomas, and a variety of other large tumors have been reported to produce excessive amounts of insulin-like growth factor (IGF) type II precursor, which binds weakly to insulin receptors and strongly to IGF-I receptors, leading to insulin like actions. In addition to increased IGF-II production, IGF-II bioavailability is increased due to complex alterations in circulating binding proteins. The authors of this article diagnosed non-islet cell tumor hypoglycemia from an 81-year-old male patient suffering from repetitive fasting hypoglycemia while he has not received any treatment for pulmonary hemangiopericytoma diagnosed in the past. Moreover, this topic is getting reported as the authors have experienced a significant improvement of catamnesis by a treatment with glucocorticoid.

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  • A Case of Epithelioid Hemangioendothelioma of the Pelvic Retroperitoneum with Hypoglycemia
    Ji Ryang Kim, Yun Kyung Jeun, Kee Tae Park, Yang Ho Kang, Seok Man Son, In Ju Kim, Yong Ki Kim, Kyung Un Choi, Kwang Jae Lee
    Journal of Korean Endocrine Society.2007; 22(6): 440.     CrossRef
Role of Thigh Muscle in the Carotid artery Intima-Media Thickness and Insulin resistance.
ll Jun Hwang, Kyung Sun Park, Yun Tae Chae, Kyeh Dong Shi, Soo Kyung Kim, Seok Won Park, Yu Lee Kim, Yong Wook Cho, Young Kil Choi, Sang Jong Lee
J Korean Endocr Soc. 2005;20(5):452-459.   Published online October 1, 2005
DOI: https://doi.org/10.3803/jkes.2005.20.5.452
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AbstractAbstract PDF
BACKGROUND
There have been recent reports that the fat distribution within skeletal muscle and the amount of muscle mass are associated with insulin resistance and the development of type 2 diabetes mellitus (T2DM). This study evaluated the impacts of visceral fat and thigh muscle from patients with T2DM and healthy subjects on atherosclerosis and insulin resistance. METHODS: Forty-two patients with newly-developed T2DM and 11 healthy subjects were selected for the study. The diabetic patients were subdivided into two groups, those under 40 years of age, as the young T2DM (n=21) group, and 40 years-old or greater, as the old T2DM (n=21) group. CT scans were obtained for all patients at the L4-L5 level and at the mid-portion between the greater trochanter and upper margin patella. The carotid intima-media thickness (IMT) was also measured using high resolution B-mode ultrasonography. RESULTS: The mean visceral fat area (VFA) in the old T2DM group was 169.4+/-13.2cm2, which was significantly greater than that found in the healthy subjects (67.9+/-7.92cm2, P<0.001) and young T2DM group (127.1+/-10.4cm2, P<0.05). The mean visceral fat to normal density muscle area ratio (VMNR) in the old T2DM group was 1.50+/-0.19, which was greater than in the healthy subjects (0.46+/-0.52, P<0.001) and young T2DM group (1.01+/-0.10, P<0.05). The total thigh muscle areas in the young and old T2DM groups were smaller than that in the healthy subjects, but without statistical significance. VMNR showed a positive correlation with the IMT and HOMA-IR. However, the total thigh muscle area was negatively correlated with the IMT. The normal density muscle area also showed significant negative correlations with the IMT and HOMA-IR. In a multiple regression analysis, age and VMNR were the most important independent risk factors of an increased carotid IMT. CONCLUSION: This study showed that the role of thigh muscle, as well as that of visceral fat, played a very important role in the occurrence of atherosclerosis. VMNR was found to be an especially important independent factor for an increased carotid IMT.

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  • High fat stores in ectopic compartments in men with newly diagnosed type 2 diabetes: an anthropometric determinant of carotid atherosclerosis and insulin resistance
    S-K Kim, S-W Park, I-J Hwang, Y-K Lee, Y-W Cho
    International Journal of Obesity.2010; 34(1): 105.     CrossRef
Gene Expression of the Somatostatin Receptors, Gi2 alpha and Pit-1 alpha in GH3 Cells Permanently Transfected with a Mutant Gs alpha Gene.
Cheol young Park, In myung Yang, Eun hee Kim, Sook jin Sohn, Mee sook Ryu, Jeong taek Woo, Sung woon Kim, Jin woo Kim, Young seol Kim, Young kil Choi, Seung joon Park
J Korean Endocr Soc. 2002;17(2):170-182.   Published online April 1, 2002
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BACKGROUND
Cyclic AMP stimulates the expression of the somatostatin (SRIF) receptor (sst1-5) and human growth hormone (GH)-secreting pituitary tumors with the gsp oncogene which increases intracellular cAMP levels, and shows a good inhibitory response of the GH to SRIF. Taken together, we hypothesized that the gsp oncogene may increase the SRIF receptor expression or and factors related to the postreceptor signal transduction of the SRIF, in order to enhance its responsiveness to SRIF. To test this hypothesis, we investigated if the gsp oncogene could increase the sst1, sst2, Gi2 alpha, and pit-1 alpha gene expression in GH3 cells. METHODS: GH3 cells were permanently transfected with the plasmid expressing Gs alpha gene, where the arginine of codon 201 was replaced with histidine. Intracellular cAMP levels and GH concentrations were measured by radioimmunoassays. Gene expressions of the sst1, sst2, Gi2 alpha, and pit-1 alpha were determined by RT-PCR. RESULTS: Intracellular cAMP levels and medium GH release were increased by 1.7 and 2.7-fold in GH3 cells expressing the gsp oncogene, respectively. In GH3 cells expressing the gsp oncogene, the sst1 mRNA levels were decreased, whereas those of the sst2, Gi2 alpha and pit-1 alpha mRNA were increased. A 4-h forskolin (10 M) stimulation remarkably increased the sst1 and sst2 mRNA levels in GH3 cells expressing wild and mutant Gs alpha . However, forskolin did not affect the Gi2 alpha and pit-1 alpha mRNA levels. In contrast, SRIF (1 M, 2 h) decreased the sst2 mRNA levels only in GH3 cells expressing the gsp oncogene. CONCLUSION: These results suggest that higher expressions of sst2, Gi2 alpha, and pit-1 alpha, induced by the gsp oncogene may be a mechanism by which gsp-positive pituitary tumors show a greater response to SRIF. The discrepancy between these and in vivo results should be explored further.
Gene Expression of Somatostatin Receptor (Subtype 2 & 5), Gi2 alpha and Pit-1 in GH-secreting Pituitary Adenomas.
Mee sook Ryu, In myung Yang, Cheol young Park, Jeong taek Woo, Sung woon Kim, Jin Woo Kim, Young seoul Kim, Young kil Choi, En hee Kim, Seung joon Park, Kook gi Kim
J Korean Endocr Soc. 2002;17(2):158-169.   Published online April 1, 2002
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BACKGROUND
Mutation of Gs protein subunit (gsp oncogene), detected in about 30~40% of growth hormone (GH)-secreting pituitary tumors, is associated with an increased long-acting somatostatin analog octreotide sensitivity. However, the mRNA expression of somatostatin receptor (sst) was not changed in the GH-secreting pituitary tumor, regardless of whether they were gsp oncogene positive or negative. This suggests that the expression of genes coding for Gi2 alpha , Pit-1 and the other factors involved in the regulation of secretory activity in somatotrophs is likely to be altered in gsp oncogene positive tumors. We observed the impact of the gsp oncogene on the expression of the genes coding for Gi2 alpha, Pit-1 and sst (2&5) in GH-secreting pituitary tumors. METHODS: The GH response to octreotide was examined in 13 acromegalic patients before transsphenoidal adenomectomy. Genomic DNA and RNA were extracted from fresh frozen tumor tissues. PCR was performed to amplify and sequence the region between codon 184 and 251 that includes exons 8 and 9 of the Gs gene. Sst2, sst5, Gi2 alpha and Pit-1 mRNA levels were measured by semi-quantitative RT-PCR. RESULTS: Sst2 and sst5 mRNA transcripts were detected in all tumors (7 gsp +, 6 gsp-). The amount of sst transcripts varied considerably varied between the tumors. There were no significant differences in sex, age, tumor size, grade or basal GH levels. Pit-1 and sst2 mRNA levels were not different. In contrast, Gi2 alpha mRNA levels were significantly higher in gsp (+) while sst5 mRNA levels were higher in gsp (-). CONCLUSION: These data suggests that gsp oncogene may increase Gi2 alpha levels but decrease sst5 mRNA levels. However, Pit-1 and sst2 mRNA expression may not be affected by gsp oncogene. The increased expression of the Gi2 alpha gene might be an inhibitory compensatory response to the action of gsp oncogene.
The Significance of Plasma ADH in Differential Diagnosis of Central Diabetes Insipidus.
Ho Jong Lee, In Myung Yang, Sun Kee Min, Jung Hyun Noh, Cheol Young Park, Seung Joon Oh, Deog Yoon Kim, Jung Taek Woo, Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Young Kil Choi
J Korean Endocr Soc. 2001;16(4-5):438-446.   Published online October 1, 2001
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BACKGROUND
Although the water restriction test(WRT) has been used as a standard test for the differential diagnosis of diabetes insipidus(DI), the measurement of plasma ADH concentration is also known to be useful method for differential diagnosis. Recent studies have shown that some patients with idiopathic central DI(CDI) were found to have a lesion on follow-up imaging studies. There have been no report in Korea on plasma ADH measurement for the differential diagnosis of DI, nor on follow-up imaging study of the idiopathic CDI. METHODS: We retrospectively reviewed the clinical and laboratory findings of 26 patients(12 men, 14 women, age 9-65 years) with CDI, including pituitary MRI or CT scan, who had been diagnosed with WRT and had undergone plasma ADH concentration measurement. RESULTS: 1) Clinical features of the patients with complete CDI did not differ from those of patients with partial CDI. 2) Maximal urine osmolality of complete CDI and partial CDI were 168+/-69mOsm/kg and 431+/-141mOsm/kg, respectively, and the percentage increase in the urinary osmolality after ADH injection was 209+/-149% and 29+/-17%, respectively. 3) Among the 26 patients, 10 patients had their plasma ADH measured. Nine patients in this group were diagnosed as CDI by WRT and plasma ADH concentration of the 9 was compatible for CDI. The plasma ADH level was also inappropriately low in one patient who had been diagnosed with primary polydipsia by WRT, the patient was diagnosed as partial CDI. 4) The findings of follow-up MRI revealed isolated thickening of the pituitary stalk in two cases of idiopathic CDI diagnosed initially with MRI. CONCLUSION: This study suggests that the measurement of plasma ADH can ensure a better differential diagnosis between partial CDI and primary polydipsia, and that the patients with idiopathic CDI should be examined regularly with MRI brain scan, including the pituitary gland.
The Combined Pituitary Stimulation Test in Patients Suffered from Massive Postpartum Hemorrhage.
Sang Hwa Kim, In Myung Yang, Cheol Young Park, Seung Joon Oh, Deog Yoon Kim, Jeong Taek Woo, Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Sun Woo Kim, Young Kil Choi
J Korean Endocr Soc. 2001;16(1):39-53.   Published online February 1, 2001
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BACKGROUND
ackground: Sheehan's syndrome secondary to severe postpartum hemorrhage is one of the major causes of pituitary insufficiency in Korea. Most of these patients do not manifest symptoms or signs of gross endocrinopathies. Earlier detection of pituitary insufficiency is of clinical importance. The combined pituitary stimulation test that uses the four hypothalamic releasing hormones is a rapid, safe, and effective way to evaluate anterior pituitary function. However, the criteria for a normal response has not been established in Korea. METHODS: Combined anterior pituitary stimulation tests were performed on fourteen healthy women who had no history of endocrine disease. Combined tests of anterior pituitary reserve were done no forty-five patients who suffered from massive postpartum hemorrhage which required transfusing, along with subsequent shock or changing consciousness and in thirty-nine patients who experienced mild postpartum hemorrhage. RESULTS: 1) In the severe hemorrhage group, thirty-three of forty-five women (73.3%) showed blunted responses in more than one of the anterior pituitary hormones in the combined pituitary stimulation tests. However, in the mild hemorrhage group, only eighteen of thirty-nine women (46.2%) demonstrated blunted responses of more than one of the anterior pituitary hormones. 2) In the severe hemorrhage group, the TSH response was blunted in twenty-five patients (55.6%), prolactin in eleven patients (24.4%), ACTH in ten patients (22.2%), LH in ten patients (22.2%), GH in nine patients (20%), and FSH in five patients (11.1%). 3) The results of combined pituitary stimulation tests in the normal control group were different from the results of other studies. CONCLUSION: It is recommended that the women who experienced a severe postpartum hemorrhage should be evaluated by using the combined pituitary stimulation test. Moreover, criteria for a normal response to the combined pituitary stimulation test should be established in Korea.
Effect of Acute Hyperglycemia - and Isoproterenol - induced Hypothalamic Somatostatin Release on the Thyroid Hormone Releasing Hormone - induced Thyroid Stimulating Hormone Secretion.
Cheol Young Park, In Myung Yang, Seung Joon Oh, Deog Yoon Kim, Jeong Taek Woo, Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Young Kil Choi
J Korean Endocr Soc. 2000;15(4-5):486-492.   Published online January 1, 2001
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BACKGROUND
Acute hyperglycemia stimulates somatostatin (SRIH) release from the hypothalamus, and which in turn suppress growth hormone (GH) secretion and thyroid stimulating hormone (TSH) from the anterior pituitary gland. Beta-adrenergic pathway is known to stimulate the hypothalamus SRIH release. Recently, We demonstrated that isoproterenol, a beta-adrenergic agonist, had an additional suppressive effect on the suppression by glucose of GHRH-stimulated GH response. Therefore, the present study aimed to determine whether isoproterenol has an additional suppressive effect on the suppression by glucose of TRH-stimulated TSH response. METHODS: Seven healthy young men, aged 24 to 27 years, were studied. Four different TRH stimulation tests were carried out. (Test 1) TRH (Hoechst AG, Germany), 200 microgram bolus, was given intravenously at 0 minute. (Test 2) Glucose, 100 g, was given orally 30 min before TRH administration. (Test 3) Isoproterenol(Isuprel, Sanofi Winthrop, USA), 0.012 pg/kg, was infused continuously for 120 min after TRH administration. (Test 4) After pretreatment with glucose as Test 2, isoproterenol and TRH were administered as Test 3. RESULTS: Oral glucose ingestion significantly suppressed the TRH-stimulated TSH secretion. Isoproterenol infusion significantly suppressed the TRH-stimulated TSH secretion. Glucose-induced suppression of the TSH response was significantly greater than that by isoproterenol. 1soproterenol infusion after glucose pretreatment did not show any additional suppressive effect on the glucose-induced suppression of TSH response to TRH. CONCLUSION: The results suggest that isoproterenol infusion in addition to glucose pretreatment before the TRH stimulation test is not necessary for the development of stronger stimulation test for the hypothalamic somatostatin secretion.
Thyrotropin-releasing Hormone(TRH) Receptor Gene Expression in GH3 Cells Permanently Transfected with a Mutant Gs alpha Gene.
Seung Joon Park, In Myung Yang, Sung Vin Yim, Joo Ho Chung, Jee Chang Jung, Kye Chang Ko, Young Seol Kim, Young Kil Choi
J Korean Endocr Soc. 2000;15(1):46-54.   Published online January 1, 2001
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BACKGROUND
Gs alpha gene mutation, that constitutively increases intracellular cAMP, is found in some acromegalic patients. It was demonstrated that increased intracellular cAMP levels suppress the expression of rat TRH receptor (TRH-R) mRNA. We previously demonstrated that transient expression of a mutant Gs alpha gene suppress the rat TRH-R gene expression in the cultured rat growth hormone-secreting tumor cell line (GH3), whereas TRH-R gene expression in adenomas with Gs alpha gene mutation (gsp oncogene) did not differ from that in tumors without the mutation. The discrepancy suggests the possibilities that the effect of permanent expression of mutant Gs alpha gene on TRH-R gene expression is different from that of transient expression of the mutant gene and hypothalamic hormones including TRH regulate the gene expression. METHODS: We investigated whether permanent expression of the mutant-type Gs alpha does not suppress the TRH receptor gene expression in GH3 cells, and whether TRH suppresses the gene expression by using reverse transcription-polymerase chain reaction (RT-PCR) and in vitro transcription. RESULTS: Permanent expression of a mutant-type Gs alpha increased basal cAMP levels up to 1.7-fold relative to the controls, whereas the wild-type cell line did not show increased cAMP levels. Permanent expression of a mutant-type Gs alpha increased TRH receptor mRNA level up to 2.8 fold compared with the controls. Treatment of the permanently transfected GH3 cells with TRH suppressed TRH-R gene expression more prominently compared to the wild type GH3 cells. CONCLUSION: These results suggest that permanent expression of mutant Gs alpha enhances the expression of TRH-R in GH-secreting pituitary tumors with gsp oncogene, but the gene expression may also be regulated by other factors including TRH.
The Effect of Slow Release Lanreotide in Korean Acromegalic Ratients.
Sang Hwa Kim, In Myung Yang, Kwang Sik Seo, Eul Soon Im, Seung Joon Oh, Deog Yoon Kim, Jeong Taek Woo, Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Sun Woo Kim, Young Kil Choi
J Korean Endocr Soc. 1999;14(3):458-471.   Published online January 1, 2001
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BACKGROUND
Previous studies have shown that somatostatin analogues such as octreotide are effective in suppressing GH and IGF-I levels in acromegaly. The recent availability of slow release lanreotide could avoid the inconveniences associated with either repeated subcutaneous injections or continuous infusions. We investigated the effects of the SR-lanreotide on clinical, biochemical and safety responses in five patients with acromegaly. And we investigated whether the response of the GH level to acute adrninistration of octreotide predicts the response after 12 weeks of treatment with the SR-lanreotide and whether the identification of gsp oncogene could be used as a therapeutic and prognostic clue in treatment with the SR-lanreotide. METHODS: We studied the effects of SR-lanreotide 30 mg administered intramuscularly biweekly for 12 weeks in five Korean acromegalic patients. Subjective improvements in the clinical symptoms of acromegaly and adverse reactions were recorded. During SR-lanreotide treatment, serum GH, IGF-I and IGFBP-3 concentrations were evaluated just before the next injection of the SR-lanreotide. Before the start of SR-lanreotide therapy the sensitivity of GH secretion to the octreotide was tested by measuring the effect of the acute response to 0.1 mg intravenously on plasma GH levels followed until 6 hours after administration of octreotide. Direct polymerase chain reaction sequencing of the gsp oncogene were performed. We compared the responses to SR-lanreotide in patients harboring gsp-positive and gsp-negative somatotroph adenomas. RESULTS: The treatment with SR-lanreotide for 12 weeks could suppress the GH level by more than 50% in four of five patients and normalize the IGF-I in two patients. No correlation was found between the GH level and IGF-I level at the end of the study. The IGFBP-3 level correlated with the IGF-I level in three of five patients. Although the initial GH response to octreotide tended to correlate with the IGF-I response after SR-lanreotide treatment, the results were statistically insignificant. The patients with gsp-positive tumor tended to show a better response to SR-lanreotide. During treatment, there was a reduction in the percentage of patients complaining of joint pain, fatigue, digital paresthesia, and hyperhydrosis. Changes in soft tissue swelling were documented by decreases in finger circumference. The common adverse events were abdominal discomfort, loose stool, and diarrhea. These events were decreased progressively. No patients discontinued the treatment of SR-lanreotide due to adverse events. CONCLUSION: This study showed that SR-lanreotide is effective in controlling acromegalic symptoms as well as GH and IGF-I hypersecretion. This treatment was well tolerated and more convenient for the patients. Further studies are required for clinical outcome of long-term SR-lanreotide treatment and cost-effective analysis.
Analysis of Glucocorticoid Response Element and TPA Response Element of Rat Thyrotropin-Releasing Hormine Gene by Site-Directed Mutagenesis.
Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Young Kil Choi, In Myoung Yang, Jung Taek Woo, Woon Won Chung
J Korean Endocr Soc. 1999;14(2):278-292.   Published online January 1, 2001
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BACKGROUND
We previously demonstrated that a GRE/TRE composite sequence, which is located between 200 bp and 220 bp relative to the transcriptional start site of rat TRH gene, is responsible for the dexamethasone (DEX)- and TPA-induced transcriptional activation, and the transcriptional activation by DEX is mediated by interaction between glucocorticoid receptor (GR) and a TRE-binding transcriptional factor such as c-Jun. However, a non-specific binding with the transciption factors can not be excluded as the mutants used in the previous report could not inhibit the binding of GR and c-Jun completely, and it remains unclear which one of the two TRE-like sequences is critical for the interaction of the two transcription factors. METHODS: Luciferase expressing plasmids that contain a part of rat TRH promoter including the composite GRE sequence or its mutants were transfected into HeLa cells by Fugene 6. After the cells were incubated overnight with DEX or/and TPA, the luciferase activity was measured in a chemiluminometer. A gel retardation assay was performed after binding of the labeled composite sequence or its mutants with GR and c-Jun. RESULTS: DEX and TPA increased the transcriptional activity of the wild type composite sequence by 3 folds and 4 folds, respectively, and the combined stimulation increased the activity by 10 folds. The mutants of which all 6 nucleotides of the GRE half site were replaced and removed almost did not bind to GR and eould not enhance the transcriptional activity at all in response to DEX. The GRE-deleted mutant bound to c-Jun with a remarkably lower affinity and showed a lower response to TPA, whereas the GRE-replaced mutant bound to c-Jun with a similar affinity and showed a similar response to TPA compared to those of the wild type. In response to the combined simulation with DEX and TPA, the mutants showed 30-40% of the trancriptional activity of the wild type. Basal transcriptional activity of all the TRE mutants was significantly lower than that of the wild type. While they almost could not bind to c-Jun, their binding affinity to GR was comparable to that of the wild type. Whereas the DEX- and TPA-induced transcriptional activity of 5 TRE mutant was 10% and 15% of that of the wild type, it responded to those agents in a similar pattern as the wild type. The 3 TRE mutant and the mutant of both TRE sites did not respond to DEX and TPA. The GRE-deleted mutant hardly formed the DNA-protein complex as did the wild type, while the GRE -replaced mutant could form the complex in a less amount with nuclear extract of HeLa celL CONCLUSION: These results suggest that GRE/TRE composite sequence of rat TRH gene specifically binds to GR and c-Jun, providing a site for interaction between the two transcription factors, and that both TRE sites play an important role in basal transcription, and that the 3 TRE site is more critical in the interaction between GRE and TRE for DEX-induced transcriptional activation. (J Kor Endocrinol 14:278-292, 1999)
The Characterization of Glucocoritcoid Response Element(GRE) on the Promoter of Thyrotropin-Releasing Hormone(TRH) Gene.
Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Young Kil Choi, In Myoung Yang, Jung Taek Woo, Woon Won Chung
J Korean Endocr Soc. 1999;14(2):265-277.   Published online January 1, 2001
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BACKGROUND
We previously demonstrated that the promoter of rat TRH gene has GRE half site (TGTTCT) between -210 bp and -205 bp flanking with similar sequences of TPA response element (TRE), TAGTCA, at a distance of several base pairs from the GRE half site. It promps us to hypothesize that this composite GRE/TRE sequence can provide a site for interaction between glucocorticoid receptor (GR) and c-Jun. Thus, we investigated whether the composite sequence mediates transcriptional regulation induced by dexamethasone (DEX) and 12-O-tetradecanoyl phobol-13-acetate (TPA), and whether it binds GR and c-Jun. METHODS: A luciferase expressing plasmids that contain a part of rat TRH promoter including the composite sequence or their mutants were transfected into HeLa cells by Fugene 6. After the cells were incubated overnight with DEX and TPA, the luciferase activity was measured in a chemiluminometer. A gel retardation assay was performed after binding of the labeled composite sequence or its mutants with GR and c-Jun. RESULTS: DEX increased the transcriptional activity of the plasmid containing the wild type GRE by 2.5 folds, and TPA increased the transcriptional activity by 4 folds. The simultaneous stimulation with DEX and TPA synergistically increased the transcriptional activity by 10 folds. Two mutants whose GRE half sits were altered showed no responses to DEX, and suppressed the TPA-induced or both agents-induced transcriptional activity by 50%. Two mutants whose TRE-like sites were altered suppressed the DEX-induced transcriptional activity by 20%, TPA-induced trarptional activity by 25%, and both agents-induced transcriptional activity by 50%. Gel retardation assay showed that the composite sequence fonned a complex with GR and its mutants bound to GR with remarkably less affinity. c-Jun also bound to the composite sequence to form two cornplexes with less affinity compared to the AP-1 consensus sequence. The mutants of the TRE-like sequence bound to c-Jun with a significantly lower affinity compared to that of the wild type. Simulateous binding of the composite sequence with GR and c-Jun did not form any larger complex. The complex of GR and the composite sequence was much smaller than that formed by c-Jun, suggesting that GR binds to the composite sequence as a monomer. CONCLUSION: These results suggest that the composite sequence of GRE half site and TRE-like site on the promoter of rat TRH gene provides binding sites for GR and c-Jun, which mediate the interaction between two signal transduction pathways. (J Kor Soc Endocrinol 14:265-277, 1999)
Effect of Isoproterenol on the Glucose-induced Hypothalamin Somatostatin Release.
Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Young Kil Choi, In Myoung Yang, Jung Taek Woo, Chul Young Park, Sun Woo Kim, Jung Hyun Ro, Sang Hwa Kim, Seung Joon Oh, Duk Yoon Kim
J Korean Endocr Soc. 1999;14(2):255-264.   Published online January 1, 2001
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BACKGROUND
Acute hypoglycemia stimulates somatostatin (SRIH) release from the hypothalamus, and which in turn suppress growth hormone (GH) secretion from the anterior pituitary gland. However, the exact mechanism of glucose increases the hypothalamic SRIH secretion is not well known. Beta-adrenergic pathway is known to stimulate the hypothalamus SRIH release. We, therefore, hypothesized that the glucose-induced SRIH release may be mediated by the stimulation of the central beta-adrenergic system, and investigated to determine whether a beta-adrermgic aganist, isoproterenol, contribute the suppressive effect of glucose on the GHRH-induced GH secretian. METHODS: Ten healthy young men, aged 23 to 26 years, were studied. Four endocrinological tests were carried out. (Test 1) GHRH (Bachem, CA, U.S.A.), 100pg bolus, was given intravenously at 0 minute. (Test 2) Glucose 100 gm dissolved in water, was given orally at -30 minute and GHRH was administered as Test 1. (Test 3) Isoproterenol (Isuprel, Sanofi Winthrop, USA), 0.012 mg/kg, wasinfused continuously between 0 minute and 120 minute, and GHRH was administered as Test 1. (Test 4) Isoproterenol, 0.012 mg kg was infused continuously between 0 minute and 120 minute, and glucose and GHRH were administered as Test 2. RESULTS: Oral glucose ingestion significantly suppressed the GHRH-induced GH secretion. The acute hyperglycemia significantly suppressed GHRH-induced GH secretion. The pretreatments with isoproterenol significantly suppressed the GHRH-induced GH levels. The pretreatment with glucose and isoproterenol suppressed the GHRH-induced GH levels more compared to those induced by glucose in Test 2. The GH levels in Test 4 did not significantly differ from those in Test 3. CONCLUSION: The results of this study suggests that the hypothalamic somatostatinergic activity induced by the oral glucose administeration is not mediated by the beta-adrenergic pathway in normal men. (J Kor Soc Endocrinool 14:255-264, 1999)
Relationship between the Expression of Growth Hormone-Releasing Hormone Receptor Gene and Endocrinologic Profiles in GH-Secreting Pituitary Adenomas.
Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Young Kil Choi, Seung Joon Park, In Myoung Yang, Jung Taek Woo, Mi Sook Ryu, Chul Young Park, Sun Woo Kim
J Korean Endocr Soc. 1999;14(2):241-254.   Published online January 1, 2001
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BACKGROUND
Growth hormone-releasing hormone (GHRH) plays a key role in the regulation of the proliferation and differentiation of somatomammotroph cells as well as secretion of GH. The actions of GHRH are mediated through the GHRH receptor (GHRH-R) that is a G protein coupled receptor with seven transmembrane domains. It has been demonstrated that alternative splicing occurs in the third cytoplasmic domain of rat and human GHRH-R mRNA, However, the clinical significance of the altemative splicing remains to be unsolved. To find an insight into the clinical significance, we investigate the correlation between the GHRH-R gene expression and a variety of clinical clinical and endocrinological findings in 11 acromegalic patients. METHODS: Eleven acromegalic patients (3 males and 8 females, mean age 43.5 years) were included in this study. Six endocrine tests were carried out to evaluate the GH seeretory function of tumors. Invasiveness of tumors were evaluated by preoperative MRI findings on the basis of Hardys classification. Sequence the gsp oncogene and estimate the GHRH-R gene expression by RT-PCR and in vitro transcription. RESULTS: Three different sized cDNA fragments, 250 bp, 700 bp and 810 bp, were found after RT-PCR. The amount of 250 bp fragment was higher than those of the other two fragments. The clinical findings (age, size, GH level, frequency of paradoxical response to TRH or GnRH, octreotide response, hypothalamic somatostatinergic activity) of the group with high expression of the 250 bp fragment did not significantly differ from those of the group with low expression. The GHRH-R gene expression of tumors with gsp oncogene did not significantly differ from that of tumors without gsp oncogene. CONCLUSION: These results suggest that the expression of GHRH-R gene may not be an important determinant for tumor growth, and the lower GH response to GHRH of tumors with gsp oncogene may not be attributed to the lower expression of GHRH-R gene. The expression of GHRH-R is likely to be regulated by a certain property of tumors for GH secretion and growth.
Cytotoxic T Lymphocyte Antigen-4 (CTla-4) Polymorphism in Korean Autoimmune Thyroid Disease.
Dong Kuen Lee, Young Seol Kim, Jeong Taek Woo, Sung Woon Kim, In Myung Yang, Jin Woo Kim, Young Kil Choi, Jeong Ryung Paeng
J Korean Endocr Soc. 1999;14(1):40-52.   Published online January 1, 2001
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BACKGROUND
The cause of autoimmune thyroid diseases (AITD), including Graves disease and Hashimotos thyroiditis, is largely unknown. To identify the genes responsible, most attention has been focussed on the HLA regions in the early studies. However, these studies have repeatedly shown a weak association between AITD and the HLA-DR3 in Caucasians. To understand and find out the mechanisms underlying the development of AITD, a search for non-HLA linked susceptibility genes is important. A recent study from American population have indicated an association between a polymorphism of CILA-4 gene and Graves disease. To clarify the relationship of the CTLA-4 polymorphism and AITD, the allele frequency of CTLA-4 gene from the patients with Graves disease and with Hashimotos thyroiditis in Korean papulation were analysed. METHODS: The CTLA-4 exon 1 polymorphism (49, A/G) was analysed by PCR-based, RFLP (Restriction Fragment Length Polymorphism) from 92 women and 37 men with Graves disease and 50 women and 9 men with Hashimotos thyroiditis diagnosed. Also, 287 healthy controls including 155 women and 132 men with no clinical evidence or family history of thyroid disease were enrolled. RESULTS: 1) In the group of Graves disease, there was significantly more patients with alanine homozygote (GG) than in control group (P<0.0005, RR=1.40). However, there was not significant with threonine homozygote (AA) between two groups (P=0.052). In the group of Hashimotos thyroiditis, no significant differences were found between all homozygotes and heterozygote. 2) In the group of Graves disease, there were significantly more patients with alanine homozygote (GG) (P<0.0001, RR=1.85) and significantly fewer patients with threonine homozygote (AA) than in the group of Hashimoto's thyroiditis (P<0.005, RR 0.25). CONCLUSION: Regardless of sex difference, alanine homozygote (GG) at exon 1 (codon 17) of CTLA-4 is associated with Graves disease in Korean population, which suggests genetic susceptibility is some role in the pathogenesis of Graves disease.
Gene Expression of Somatostatin Receptor Subtype 2 and 5 in GH-Secreting Pituitary Adenomas.
Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Young Kil Choi, Seung Joon Park, In Myoung Yang, Jung Taek Woo, Kook Ki Kim
J Korean Endocr Soc. 1997;12(4):508-517.   Published online January 1, 2001
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BACKGROUND
SSTR2 and SSTR5 are most frequently observed in GH-secreting pituitary tumors, and SSTR5 is believed to be more specific to mammosomatotroph lineage. Octreotide binds with high affinity to those two types. There is no report that investigates the quantitative comparison of the two subtype gene expressions, and the correlation between their gene expressions and GH response to octreotide in GH-secreting pituitary adenomas. METHOD: GH response to octreotide was examined in 8 acromegalic patients before transsphenoidal adenomectomy. Genomic DNA and RNA were prepared from fresh frozen tumor tissues. PCR was performed to amplify and sequence the region between codon 184 and 251 that includes exons 8 and 9 of the Gas gene. mRNAs of SSTR2 and SSTRS were quantitated by the comparative RT-PCR and in vitro transcription. RESULTS: The in vitro transcripts of SSTR2 and SSTR5 cDNA were detected in all tumors. The amount of SSTR transcripts was considerably variable between the tumors. The amount of SSTR5 transcript was significantly smaller than that of SSTR2 transcript (0.07+-0.02 vs. 0.87+-0.10), and they did not show any correlation . There was no signicant difference in sex, age, tumor size and grade, basal GH levels, and the GH responses to octreotide between the group with high and low SSTR gene expression. No significant correlation was found between the GH response to octreotide and the amount of SSTR2 transcript, wherease the amount of SSTR5 transcripts showed a tendency of negative correlation with the octreotide response. Tumors with gsp oncogene showed significantly higher response to octreotide than those without the oncogene. The amount of SSTRS transcript in gsp-positive tumors was significantly smaller than in gsp-negative tumors (0.03+-0.01 vs. 0.12+-0.03). CONCLUSION: These results suggest that SSTRS gene expression is lower than that of SSTR2 in GH-secreting adenomas. It is probably attributed to the binding of somatostatin to SSTR5 which has a higher affinity to the hypothalamic somatostatin, Tumors with gsp-oncogene is likely to express a higher density of SSTR5 than those without the oncogene.
Effect of Ga2 gene mutation on the Expression of Thyrotropin-Releasing Hormone ( TRH ) Receptor Gene in GH3 Cells.
Seung Joon Park, In Myung Yang, Jeong Hwa Ryu, Joo Ho Chung, Jee Chang Jung, Kye Chang Ko, Young Seol Kim, Young Kil Choi
J Korean Endocr Soc. 1997;12(3):357-363.   Published online January 1, 2001
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Expression of TRH Receptor Gene in GH-Secreting Piruitary Adenomas.
In Myung Yang, Seung Joon Park, Jeong Wha Ryu, Joo Ho Chung, Mee Sook Ryu, Jeong Taek Woo, Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Young Kil Choi
J Korean Endocr Soc. 1997;12(3):349-356.   Published online January 1, 2001
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Background
To test the hypothesis that Galphas gene mutation may suppress the expression of TRH-R gene, we investigated whether hTRH-R gene expression is lower in human GH-secreting pituitary adenomas with Galphas mutation than in tumors without the mutation. Method: TRH-induced paradoxical response of GH was observed in 8 acromegalic patients. The mutation of gene was identified by direct sequencing of the genomic DNA prepared from GH-secreting pituitary adenomas. The expression of hTRHT mRNA was quantitated by RT-PCR. Results: The transcript of hTRH-R gene was detected in 6 of 8(75%) tumors. Three of these(50%) showed the paradoxical GH response to TRH and the other three patients did not show the response. The relative expression of hTRH-R mRNA in the tumors from patients with the paradoxical response of GH to TRH did not differ from that in the tumors from patients without the paradoxical response. Direct PCR sequencing of Galphas disclosed a mutant allele and a normal allele only at codon 201 in 4 of 8 tumors. The paradoxical response to TRH was observed in 2 of 4 patients without the mutation, and 2 of 4 patients with the mutation. The hTRH-R gene expression of pituitary adenomas did not differ between the tumors without the mutation and those with mutation. Conclusion: This study suggests that the expression of TRH-R gene is not likely to be a main determinant for the paradoxical response of GH to TRH, and that Galphas mutation does not seem to suppress the gene expression of TRH-R in GH secreting adenoma.
A Case of Multiple endocrine neoplasia type 2a.
Seung Jae Hong, In Myung Yang, Jeong Taek Woo, Jin Woo Kim, Young Seol Kim, Young Kil Choi, Yong Sun Yun, Chung Hwan Lee, Seong Ho Lee, Deok Yoon Kim, Sung Weon Kim
J Korean Endocr Soc. 1997;12(2):328-337.   Published online January 1, 2001
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Multiple endocrine neoplasia type2a (MEN type2a) is a dominantly inherited cancer syndrome which is characterized by medullary thyroid carcinoma, pheochromocytoma and parathyroid hyperplasia or adenoma. Recent reports show that DNA analysis will be introduced into screening of MEN type2a families. Regular prospective screening and appropriate surgical intervention can reduce the morbidity and mortality due to MEN type2a. We experienced a case of MEN type 2a in a 46-year-old female patient. She had undergone bilateral adrenalectomy due to pheochromocytoma, followed by a total radical thyroidectomy, which revealed medullary thyroid carcinoma of the both thyroid gland and parathyroid hyperplasia.
A Study of Point Mutations of Human Insulin-like Growth Factor - 1 (IGF - 1) Promoter Gene in Familial Short Stature (FSS) Patients.
In Myung Yang, Jeong Taek Woo, Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Young Kil Choi, Hyun Ha Chang, In Kyung Jung, Tae Kwan Park
J Korean Endocr Soc. 1996;11(4):500-509.   Published online November 7, 2019
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Background
FSS is a normal variants in Korea, but some of them had defect of noctumal GH pulse i.e. neurosecretory dysfunction. Although Korean children had strikingly got higher final height in the last decade. We are interested in what kinds of differences were existed in FSS group. Previous study showed theres no difference of GH related biochemical markers between normal and FSS group, like IGF-I, IGFBP-3 etc. We analyzed molecular difference in FSS group. Methods: We screened 23 FSS patients and 16 normal controls to IGF-I gene prornoter region with PCR-SSCP (single strand conformation polymorphisrn) method and sequenced 1 FSS patients who had abnormal SSCP band. Results: We found 1 out of 23 patients with abnormal SSCP band (none for 16 controls). Their IGF-I promoter gene were sequenced with modified Maxam-Gilbert method. One subject had 2 point mutations(+8 and +74). Conclusion: We found point mutations of IGF-I promoter in FSS group, This position was regarded as HNF(hepatic nuclear factor)-3 binding sites. We needed more study for the detection of its biological function according io linear growth with in vivo and in vitro study.
Effect of Dexamethasone and Deflazacort on the Function and Gene Expression of the Primary Cultured Human Osteoblast-Like Cells.
Hyun Koo Yoon, In Myung Yang, Sung Woon Kim, Soung Seol Kim, Young Kil Choi, Ho Yeon Chung, Young Soon Kang, In Gul Moon, Chang Hoon Yim, Sang Woo Kim, Ki Ok Han, Hak Chul Chang, In Kwon Han
J Korean Endocr Soc. 1996;11(4):479-491.   Published online November 7, 2019
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Background
Chronic use of glucocorticoid is known to result in osteoporosis. Deflazacort (DFZ), a synthetic glucocorticoid, has been reported to have bone sparing properties in vivo eompared to dexamethasone(DEX). Not only the direct effect of DFZ on human osteoblast but the mechanism by which the drug spares bone remains unclear. This study, therefore, is aimed to investigate the direct effect of DFZ on the proliferation and differentiation of human osteoblast as well as on the gene expression of osteocalcin and osteoblast as well as on the gene expression of osteocalcin and growth factor produced in osteoblast. Methods: Human osteoblast-like cells were cultured from a piece of the tibia removed during selective orthopedic surgery for patients without metabolic bone diseases. The morphological iden- tification of osteoblast-like cell was performed under the light microscope after alkaline phosphatase staining. Cell proliferation rate was determined by [3H] thymidine incorporation into DNA. Cell differentiation was determined by alkaline phophatase activity. mRNA expression was quanti- tatively measured by the competitive reverse transcription-polymerase ehain reaction(RT-PCR). Results: The cultured cells demonstrated 1,25-dihydroxyvitamin D3-induced increases in alkaline phophatase activity and osteocalcin mRNA expression which are the properties of osteoblast. Twenty six percent of the cultured cells were identified as osteoblast-like cells by alkaline phophatase staining. After 24hr incubation with DEX or DFZ, the [3H) thymidine incorporation was significantly inhibited by 100nM DEX or DFL Alkaine phophatase activity was significantly increased by 100nM DEX. Osteocalcin mRNA was significantly decreased by both glueocorticoids. While DEX significantly suppressed expression of asteocalcin mRNA at 10nM and 100nM, DFZ did so only at 100nM. IGF-I mRNA was significantly decreased by 100nM DEX. Conclusion: These results suggest that the inhibitory effect of DFZ on the cell proliferation and protein synthesis is less than that of DEX, which might be responsible for the bone sparing effect of DFZ in vivo.
Expression of Exon 1 and 6 of Indulin-like Growth Factor - 1 (IGF - 1) Gene in Thyroid Tissues.
Sung Woon Kim, Hyun Ha Chang, In Kyung Jung, Jeong Taek Woo, In Myung Yang, Jin Woo Kim, Soung Seol Kim, Young Kil Choi
J Korean Endocr Soc. 1996;11(4):409-417.   Published online November 7, 2019
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Background
Goiter has been a common problem in the thyroid disease. The exact mechanism of goiter had not been clarified yet, but some goiters were increased with TSH(thyrotropin releasing hormone) dependent manner. TSH might be a major influencing factor for increasing size of goiter(goitrogen) and theres many cofactors those influenced to goiter size. One of the rnost prominent growth factor as a goitrogen is a IGF-I(insulin-like growth factor-I). IGF-I play a great role as a cofactor of goitrogen with TSH. This study, therefore, is aimed to investigate intracellular activation of IGF-I gene promoter in the surgical specimens of thyroid tumor. Methods: We used surgical specimen of various thyroid tissues from normal to malignant along its cell nature. Actually we used normal liver tissue as a IGF-I control tissue, normal thyroid, benign adenoma, and papillary thyroid cancer tissue with its malignat nature. We checked Mrna expression of whole IGF-I and IGF-I exon 6 by Northern blot method, and IGF-I, promoter 1 expression by RT-PCR-transcription method. Autoradiographied signals were analysed with densitometer. Results: We found whole IGF-I mRNAs were expressed with alternate splicing in exon 1, 2 and exon 4, 5 respectively. Striking events of IGF-I transcription were multiple tranascription initiatian in Pl and P2, and 3 sites for polyadenylation in exon 6. Four or more Mrna bands in Northern blot analysis of IGF-I(0.8, 1.4, 4.2, and 7.8kb) were noted. In low molecular weight IGF-I Mrna did not change their signal intensity with tissues, but exan 6(7.8kb) signals were significantly increased to its hepatic expression levels in malignant tissue. IGF-I, exon 1 expression by RT-PCR-T7 transcription was strikingly increased in thyroid cancer tissue, but exon 6 expression was not a great expession. Conclusion: One possible guess for this expression discrepancy of each exon may be originated from different Mrna degradation of each IGF-I signals. We need more preeise experiment for Mrna degradation speed of IGF-I.
Increased Somatostatinergic Activity Induced by Acute Hyperglycemia is Not Mediated by Stimulation of the Beta-adrenergic System.
Seung Jae Hong, In Myung Yang, Gyu Choon Lee, Jeong Taek Woo, Sung Woon Kim, Jin Woo Kim, Soung Seol Kim, Young Kil Choi
J Korean Endocr Soc. 1996;11(4):383-390.   Published online November 7, 2019
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No abstract available.
Insulin Like Growth Factor-I and Insulin Like Growth Factor Binding Protein-3 in Human Thyroid Cystic Fluids.
In Myung Yang, Jeong Taek Woo, Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Young Kil Choi, Byoung Joon Kim, Seung Joon Oh
J Korean Endocr Soc. 1995;10(4):395-404.   Published online November 7, 2019
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In the thyroid tissue, thyrotrophin(TSH) and IGF-I played major role of the goitrogen. But the evidences and precise mechanism of these two factors were not known so much. Actually local secretion of thyroid IGF-I was originated from its fibroblasts mainly. We guessed major roles of IGFs in the thyroid tissue were local paracrine effect of thyroid cells proliferation and differentiation which concert with TSH. Recently, some reporters described the source of thyroid IGF-I were partly from thyroid follicular cells and its action were synergistic with TSH. We measured TSH, IGF-I and IGFBP-3 from sera and thyroid cystic fluids in 36 patients with simple thyroid cyst and examined into correlation between TSH, IGF-I and IGFBP-3.1) According to cyst/serum TSH ratio, we classified two groups(Group I; c/s TSH <1, n=19. Group II; c/s TSH >1, n=17). This classification criteria means that cystic TSH level were increased than that of serum or not.2) The serum TSH, IGF-I and IGFBP-3 levels are not difference between group I and II.3) Cystic TSH were dependent on the serum TSH in Group I, but negative correlation in Group II. In Group II, cystic TSH was significant increased.4) Serum IGF-I were positive correlation in each Group5) In Group II, cystic IGF-I was not exceed than those of serum IGF-I, but some cystic IGFBP-3 were more increased than those of serum.6) In Group II, cystic IGFBP-3 increased than serum TSH, and cystic IGFBP-3 was positive correlation with cystic TSH and cystic IGF-I.As these data suggested that cystic TSH and cystic IGF-I levels may influence cystic IGFBP-3 level. The main effect for maintenance of cyst was mediated by cystic TSH and cystic IGFBP-3. But the cystic IGFBP-3 has major role for thyroid cyst than cyst TSH.
Identification of TPA - Response Element (TRE) in the Rat Thyrotropin - Releasing Hormone (TRH) Gene.
Woon Won Jung, Young Kil Choi, In Myung Yang, Kwang Sik Seo, Jeong Taek Woo, Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Young Kil Choi, Seung Joon Park
J Korean Endocr Soc. 1994;10(3):200-213.   Published online November 6, 2019
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There are two potential imperfect copies of the TRE consensus sequence between -47 and -113bp position on 5' upstream of the rat TRH gene. The upstream element(5'-TGcCgTCA-3') is located between -101 bp and -94 bp, and the downstream element(5'-TGAcCTCA-3') is positioned between -59bp and -52bp relative to the stranscription start site. The downstream variant differs from the consensus sequence of TRE(AP-1)(5'-TGACTCA-3'), by addition of one nucleotide. As there is no direct evidence that TPA stimulates the transcription of rat TRH gene, and there is no study to define TRE of the rat TRH gene, we performed Northern blot assay, transient gene expression study and gel shift assay to identify TRE. TRH mRNA expression of CA77 cells was increased about 2-2.5 fold 30 min after TPA stimulation. When PC12 cells were stimulated by TPA after transfection of the plasmids containing serially deleted 5'upstream of the rat TRH gene ligated to luciferase gene, the transcription of luciferase gene was increased more than 3.2 fold with the plasmid pTRH(-600/84)Luc and pTRH(-113/84)Luc. However, the transcriptional activation was remarkably decreased less than 1.6 fold with pTRH(-77/84)Luc, pTRH(-47/84)Luc, and pTRH(6/84)Luc. The plasmid containing the sequence of -108/-79 did not show any significant activation in both of basal and TPA-stimulated transcription, whereas the plasmid containing the sequence of -70/-41 showed a slight but significant transcriptional activation by TPA. The plasmid containing the sequence of -114/-47 showed remarkable increase in basal transcription and TPA induced transcription of luciferase gene. Gel shift assay revealed that the oligonucleotides spanning -108/-79 and -70/-41 bound to c-Jun, whereas the oligonucleotides spanning -40/1, 1/30, 31/60, 61/84 did not bind. The oligonucleotide of -70/-41 bound to c-Jun with higher affinity compared to that of -108/-79. The one base pair mutant of -70/-41(deletion of C from the middle of TGACCTCA) bound to c-Jun with higher affinity, whereas the one base pair replaced mutant(C to G) bound with lower affinity compared to the wild type oligonucleotide. These results suggest that the rat TRH gene expression is stimulated by TPA to a smaller degree compared to that of other genes, and the two elements act cooperatively as TRE. The downstream TRE variant is mainly responsible for TPA response and c-Jun binding, and the upstream variant play a permissive role for transcriptional activation. The addition of one nucleotide C in the downstream element may be responsible for the relatively lower response of the rat TRH gene to TPA.
Identification of TPA - Response Element (TRE) in the Rat Thyrotropin - Releasing Hormone (TRH) Gene.
Woon Won Jung, Young Kil Choi, In Myung Yang, Kwang Sik Seo, Jeong Taek Woo, Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Young Kil Choi, Seung Joon Park
J Korean Endocr Soc. 1994;10(3):200-213.   Published online November 6, 2019
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AbstractAbstract PDF
There are two potential imperfect copies of the TRE consensus sequence between -47 and -113bp position on 5' upstream of the rat TRH gene. The upstream element(5'-TGcCgTCA-3') is located between -101 bp and -94 bp, and the downstream element(5'-TGAcCTCA-3') is positioned between -59bp and -52bp relative to the stranscription start site. The downstream variant differs from the consensus sequence of TRE(AP-1)(5'-TGACTCA-3'), by addition of one nucleotide. As there is no direct evidence that TPA stimulates the transcription of rat TRH gene, and there is no study to define TRE of the rat TRH gene, we performed Northern blot assay, transient gene expression study and gel shift assay to identify TRE. TRH mRNA expression of CA77 cells was increased about 2-2.5 fold 30 min after TPA stimulation. When PC12 cells were stimulated by TPA after transfection of the plasmids containing serially deleted 5'upstream of the rat TRH gene ligated to luciferase gene, the transcription of luciferase gene was increased more than 3.2 fold with the plasmid pTRH(-600/84)Luc and pTRH(-113/84)Luc. However, the transcriptional activation was remarkably decreased less than 1.6 fold with pTRH(-77/84)Luc, pTRH(-47/84)Luc, and pTRH(6/84)Luc. The plasmid containing the sequence of -108/-79 did not show any significant activation in both of basal and TPA-stimulated transcription, whereas the plasmid containing the sequence of -70/-41 showed a slight but significant transcriptional activation by TPA. The plasmid containing the sequence of -114/-47 showed remarkable increase in basal transcription and TPA induced transcription of luciferase gene. Gel shift assay revealed that the oligonucleotides spanning -108/-79 and -70/-41 bound to c-Jun, whereas the oligonucleotides spanning -40/1, 1/30, 31/60, 61/84 did not bind. The oligonucleotide of -70/-41 bound to c-Jun with higher affinity compared to that of -108/-79. The one base pair mutant of -70/-41(deletion of C from the middle of TGACCTCA) bound to c-Jun with higher affinity, whereas the one base pair replaced mutant(C to G) bound with lower affinity compared to the wild type oligonucleotide. These results suggest that the rat TRH gene expression is stimulated by TPA to a smaller degree compared to that of other genes, and the two elements act cooperatively as TRE. The downstream TRE variant is mainly responsible for TPA response and c-Jun binding, and the upstream variant play a permissive role for transcriptional activation. The addition of one nucleotide C in the downstream element may be responsible for the relatively lower response of the rat TRH gene to TPA.
Changes of Bone Turnover Markers after Treatment with Growth Hormone Therapy in Children with Growth Retardation.
In Myung Yang, Jeong Taek Woo, Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Young Kil Choi, Ki Oak han, Duk Yoon Kim, Hyung In Yang
J Korean Endocr Soc. 1994;9(4):344-349.   Published online November 6, 2019
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The effects of growth hormone(GH) deficiency and recombinant human GH replacement(0.5IU/kg per week) on bone mineral metabolism in 21GH-deficiency children were studied. All children had significantly reduction of bone density(Z score;-1.4+-0.71). After 1 month of therapy, the levels of serum insulin-like growth factor 1(IGF-1), osteocalcin(OC) and carboxyterminal propeptede of type 1 procollagen(PICP) were significantly elevated. But IGFBP-3 were not shown to change significantly. The changes in serum levels of PICP during the first month of recombinant human GH treatment were positively related to growth velocity, whereas the changes in IGF-1 and OC during the first month of therapy were not. We conclude that the recombinant human GH treatment caused significant modifications of mineral metablism and that the measurement of the changes of biochemical markers of bone metablism espacially PICP may be a useful tool in prediction improved growth velocity during long term GH replacement therpy.
The Responses of Pituitary Hormones to the Combined Pituitary Stimulation Test in Hypogonadotropic Hypogonadism.
In Myung Yang, Jeong Taek Woo, Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Young Kil Choi, Eun Kyung Park, Kyu Jeong Ahn
J Korean Endocr Soc. 1994;9(2):93-107.   Published online November 6, 2019
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To classify the causes of hypogonadotropic hypogonadism in Korean patients, and to improve the endocrinologic evaluation for the disease, we retrospectively studied the clinical findings and result of combined pituitary stimulation test in 35 patients with hypogonadotropic hypogonadism. The following results were obtained.1) The ratio of male to female was 1.3:1, and the 50% of male patients was under 20 years of age and the 20% of female patients in 30th decades. 2) The chief complaints of male patients on the admission were the failure of secondary sexual characteristics(95.0%) and loss of hair(5.0%), those of female patients were amenorrhea(46.7%), infertility(26.7%), failure of secondary characteristics(13.3%) and loss of hair(13.3%). 3) The causes of male hypogonadotropic hypogonadism were craniopharyngioma(35.0%), idiopathic(30.0%), Kallmann's syndrome(15.0%), pituitary adenoma(10.0%) and germinoma(5.0%), and those of female hypogonadotropic hypogonadism were prolactinoma(13.3%), Sheehan's syndrome(26.6%), pituitary adenoma(6.7%), tuberculous granuloma(6.7%), germinoma(6.7%), idiopathic hypogonadotropic hypogonadism(40.0%).4) The responses of LH and FSH to GnRH test were absent or markedly blunted in diffuse pituitary diseases such as pituitary tuberculous granuloma, pituitary macroadenomas, Sheehan's syndrome. However those were also absent or blunted in Cushing's disease and hypothalamic disease such as Kallmann's syndrome, germinoma, craniopharyngioma, idiopathic hypogonadotropic hypogonadism. 5) The responses of LH, FSH increased after repeated injection of GnRH in a patient with germinoma. 6) In diffuse destructive pituitary diseases such as Sheehan's syndrome, nonfunctioning macroadenomas, tuberculous granuloma, large prolactinoma, the combined deficiency of pituitary hormones other than gonadotropins was observed. 7) In many cases with hypothalamic diseases, the combined defects of pituitary hormone response were also seen.These data suggest that GnRH test is not always useful to localize the lesion between pituitary and hypothalamus, and combined pituitary stimulation test revealed defects of pituitary hormones other than gonadotropin in various hypothalamic diseases.Therefore repeated GnRH test would be useful for the differential diagnosis, and CRH test and GRH test would be necessary to demonstrate whether pituitary abnormality is present.
A case of multiple symmetric lipomatosis.
Seung Joon Oh, Jeong Taek Woo, Sung Woon Kim, Ihn Myung Yang, Jin Woo Kim, Young Seol Kim, Kwang Won Kim, Young Kil Choi
J Korean Endocr Soc. 1993;8(4):456-461.   Published online January 1, 2001
  • 840 View
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AbstractAbstract PDF
No abstract available.
Human IGF-I gene expression in normal and thyroid tumor tissues.
Sung Woon Kim, Hyun Ha Jang, Sang Mee Park, Deog Yoon Kim, Jeong Taek Woo, In Myung Yang, Jin Woo Kim, Young Seol Kim, Kwang Won Kim, Suck Hwan Koh, Sung Wha Hong, Young Kil Choi
J Korean Endocr Soc. 1993;8(4):414-421.   Published online January 1, 2001
  • 784 View
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AbstractAbstract PDF
No abstract available.
Effect of ipriflavone on the lumbodorsal pain in osteoporosis.
Jeong Taek Woo, Deok Yoon Kim, In Myung Yang, Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Kwang Won Kim, Young Kil Choi
J Korean Endocr Soc. 1993;8(3):340-346.   Published online January 1, 2001
  • 841 View
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AbstractAbstract PDF
No abstract available.
Expression of type 1?collagen mRNA of osteoblast like(MC3T3-E1) celss to sodium fluoride.
Jeong Taek Woo, Sung Woon Kim, In Myung Yang, Jin Woo Kim, Young Seol Kim, Kwang Won Kim, Young Kil Choi, Kwang Sik Seo, Kyu Rhim Chung, Jeung Bin Hwang
J Korean Endocr Soc. 1993;8(3):334-339.   Published online January 1, 2001
  • 752 View
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AbstractAbstract PDF
No abstract available.
A clinical study of thyrotoxic periodic paralysis.
Sung Yi Kang, Sung Hoon Kim, Duk Yoon Kim, Jeong Taek Woo, In Myung Yang, Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Kwang Won Kim, Young Kil Choi
J Korean Endocr Soc. 1993;8(1):19-26.   Published online January 1, 2001
  • 929 View
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AbstractAbstract PDF
No abstract available.
Thrombolytic effect of esterase on the cerebral thrombosis.
Deog Yoon Kim, Jeong Tack Woo, Jin Woo Kim, Young Seol Kim, Kwang Won Kim, Young Kil Choi
J Korean Endocr Soc. 1992;7(4):379-383.   Published online January 1, 2001
  • 897 View
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AbstractAbstract PDF
No abstract available.
Effect of cilostazol in diabetic patients with vascular complication .
Kyu Nam Lee, Jeong Tack Woo, Duck Yoon Kim, Sung Woon Kim, In Myung Yang, Jin Woo Kim, Young Seol Kim, Kwang Won Kim, Young Kil Choi
J Korean Endocr Soc. 1992;7(4):373-378.   Published online January 1, 2001
  • 876 View
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AbstractAbstract PDF
No abstract available.
Effects of human growth hormone treatment in healthy older female.
Jeong Tack Woo, Deog Yoon Kim, Sung Woon Kim, In Myung Yang, Jin Woo Kim, Young Seol Kim, Kwang Won Kim, Young Kil Choi, Jong Eun Park
J Korean Endocr Soc. 1992;7(4):352-357.   Published online January 1, 2001
  • 834 View
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AbstractAbstract PDF
No abstract available.
Apolipoprotein E genotypes in patients with diabetes, cerebrovascul- ar accident, and acute myocardial infarction.
Sung Yi Kang, Jeong Tack Woo, Sung Woon Kim, in Myung Yang, Jin Woo Kim, Young Seol Kim, Ke\wang Won Kim, Young Kil Choi, Jung Ryung Paeng
J Korean Endocr Soc. 1992;7(3):273-279.   Published online January 1, 2001
  • 751 View
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AbstractAbstract PDF
No abstract available.
Review of clinical characteristics of primary hyperparathyroidism.
Hyung Keun Chung, Deog Yoon Kim, Jeong Taek Woo, Sang Woon Kim, In Myung Yang, Jin Woo Kim, Young Seol Kim, Kwang Won Kim, Young Kil Choi
J Korean Endocr Soc. 1992;7(3):234-242.   Published online January 1, 2001
  • 935 View
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AbstractAbstract PDF
No abstract available.
Expression of apolipoprotein C-II mRNA in cultured HepG2 cell.
Myung Jae Park, Dong Hee Seo, Kwang Sik Seo, Jeong Taek Woo, Jin Woo Kim, Young Seol Kim, Kwang Won Kim, Young Kil Choi
J Korean Endocr Soc. 1992;7(2):127-135.   Published online January 1, 2001
  • 754 View
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AbstractAbstract PDF
No abstract available.
Increase of bone mineral density after surgical treatment of primary hyperparathyroidism.
Hyun Duck Son, Jeong Taek Woo, Sung Woon Kim, Ihn Myung Yang, Jin Woo Kim, Young Seol Kim, Kwang Won Kim, Young Kil Choi
J Korean Endocr Soc. 1992;7(1):76-79.   Published online January 1, 2001
  • 886 View
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AbstractAbstract PDF
No abstract available.
A case of true precocious puberty successfully treated with LHRH analogue.
Hyun Suck Son, Jeong Taek Woo, Sung Woon Kim, Ihn Myung Yang, Jin Woo Kim, Young Seol Kim, Kwang Won Kim, Young Kil Choi
J Korean Endocr Soc. 1992;7(1):71-75.   Published online January 1, 2001
  • 779 View
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AbstractAbstract PDF
No abstract available.
Expression of c-erb A mRNA according to thyroid function status.
Young Sil Ju, Jeong Taek Woo, Sung Woon Kim, In Myung Yang, Jin Woo Kim, Young Seol Kim, Kwang Won Kim, Young Kil Choi, Sang Mi Park
J Korean Endocr Soc. 1992;7(1):24-30.   Published online January 1, 2001
  • 883 View
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AbstractAbstract PDF
No abstract available.
Role of hepatitis B infection in pathogenesis of autoimmune thyroid disease.
Hyung In Yang, Jeong Taek Woo, Seong Wun Kim, In Myung Yang, Jin Woo Kim, Young Seol Kim, Kwang Won Kim, Young Kil Choi
J Korean Endocr Soc. 1991;6(4):348-352.   Published online January 1, 2001
  • 860 View
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AbstractAbstract PDF
No abstract available.
Serum lipoprotein(a) as an independent risk factor for cerebral infarction in Korea.
Yi Sook Hwang, Jeong Tack Woo, Jin Woo Kim, Young Seol Kim, Kwang Won Kim, Young Kil Choi
J Korean Endocr Soc. 1991;6(3):232-237.   Published online January 1, 2001
  • 732 View
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AbstractAbstract PDF
No abstract available.
Effect of fluoride and vandate on the osteoblast MC3T3-E1 function.
Jung Taek Woo, Hyun Koo Yoon, Young Seol Kim, Sung Woon Kim, In Myung Yang, Jin Woo Kim, Kwang Won Kim, Young Kil Choi, Kwang Sik Seo
J Korean Endocr Soc. 1991;6(2):157-162.   Published online January 1, 2001
  • 807 View
  • 16 Download
AbstractAbstract PDF
No abstract available.
A case of bilateral adrenal cortical hyperplasia.
Jung Hee Kim, Jin Woo Kim, Young Seol Kim, Kwang Won Kim, Young Kil Choi
J Korean Endocr Soc. 1991;6(1):97-99.   Published online January 1, 2001
  • 946 View
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AbstractAbstract PDF
No abstract available.
A clinical study on 79 cases of lymphocytic thyroiditis by fine needle aspiration.
Kyung Jin Kim, Jeong Taek Woo, Sung Woon Kim, In Myung Yang, Jin Woo Kim, Young Seol Kim, Kwang Won Kim, Young Kil Choi
J Korean Endocr Soc. 1991;6(1):38-44.   Published online January 1, 2001
  • 794 View
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AbstractAbstract PDF
No abstract available.

Endocrinol Metab : Endocrinology and Metabolism