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중증 비갑상선 질환에서 혈청 Angiotensin - Converting enzyme 활성도의 변화에 관한 연구
심재두(Jae Doo Shim),최성근(Seong Gun Choi),남연호(Yeun Ho Nam),김성운(Sung Woon Kim),양인명(In Myung Yang),김진우(Jin Woo Kim),김영설(Young Seoul Kim),최영길(Young Kil Choi) 대한내과학회 1987 대한내과학회지 Vol.33 No.2
N/A To examine the hypothesis that the serum ACE activity was decreased in proportion to decrement of the thyroid hormone concentration in patients with severe nonthyroidal illness, we measured serum T₃, T₄, free TTSH and serum ACE activity of 20 patients with nonthyroidal illness and 12 normal controls, 1) The mean serum T₃, concentration (57.6±25.1ng/dl) in patients with severe nonthyroidal illness was significantly different from that (100.9±10.5) of normal controls. (P<0.005). 2) The mean serum free T₃, concentration (1.39±0.79 pg/ml) in patients with severe nonthyroidal illness was signi fiantly different from that (2.47±0.50 pg/ml) of normal controls. (P <0.005). 3) There were no significant differences in the mean serum T₄, and TSH concentrations between two groups. 4) There was no significant difference in the mean serum ACE activity between patients with severe nonthyroidal illness (6.1±2.4 unit) and normal controls (6.9±2.2). 5) In 8 patients with severe nonthyroidal illness which could increase the serum ACE activity, the mean serum ACE activity was relatively high as compared to low mean serum free T₃, concentration and in other 6 patients with servere nonthyroidal illness, the decrease in serum ACE activity was associated with a parallel decrease in the serum T₃, concentration and there was significant correlation between serum free T, concentration and ACE activity (r=0.84). These dnta suggest that serum ACE activity can be an useful index of thyroid function in patients with severe nonthyroidal illness, but one should exclude the diseases which can increase serum ACE activity before interpretation.
동석호(Seok Ho Dong),오동환(Dong Hwan Oh),김성운(Sung Woon Kim),김영설(Young Seol Kim),최영길(Young Kil Choi),김진우(Jin Woo Kim),양인명(In Myung Yang) 대한내과학회 1988 대한내과학회지 Vol.35 No.4
N/A Serum lipid levels and lipoprotein profiles were studied in 64 normal Koreans and 73 Korean diabetics to observe the relationship among complications, serum lipid levels, lipoprotein patterns and clinical characteristics. The results are summarized as follows: 1) The concentrations of total lipid, cholesterol, trig-lyceride, lipoprotein, LDL and VLDL were significantly higher in diabetics than in the controls. 2) There were significant differences in the profiles of serum lipid and lipoprotein according to body weight, degree of glucose control and complication. 3) The frequency of neuropathy was 2.7 times higher in the group with hyperlipidemia, 2.5 times higher in hyperchole-sterolemia, 2.6 times higher in hypertrig-yceridemia, 2.9 times higher in high beta-lipoproteinemia and 2.8 times higher in high VLDL than in the control group. 4) The frequency of nephropathy was 4.2 times higher in the group with hyperlipidemia, 5.4 times higher in hyperchole-sterolemia, 3.4 times higher in high beta-lipoproteinemia and 2.6 times higher in high VLDL then in the control group. 5) The frequency of retinopathy was not significantly different among the above groups. We concluded that diabetic nephropathy had the closest relationship to a disorder in lipid metabolism, especially in cholesterol, and that the ratios of cholesterol,HDL and LDL.HDL could not predict the risk of diabetic complication.
임신성 당뇨병 환자에서 글루코키나제 유전자의 췌도 B 세포 특이 프로모터 -30bp 부위의 변화
김진우(Jin Woo Kim),양인명(In Myung Yang),김성운(Sung Woon Kim),김영설(Young Seol Kim),최영길(Young Kil Choi),우정택(Jung Taek Woo),김세윤(Se Yoon Kim),오승준(Seung Joon Oh),팽정령(Jeon Ryung Paeng),장학철(Hak Chul Chang) 대한내과학회 1999 대한내과학회지 Vol.57 No.5
Glucokinase is expressed only in both liver and pancreatic beta cells and has a key role in the regulation of glucose metabolism in these tissues. A number of gene defects associated with glucokinase gene and the cause of non-insulin-dependent diabetes mellitus are known, and the defects along the -30bp promoter site in particular are thought to be related to diabetes and glucose intolerance. To research on gene study related to diabetes, we looked into the relationship between the variation at -30bp of pancreatic beta cell specific glucokinase gene promoter and gestational diabetes mellitus(GDM) in Korea. Methods : Forty patients with GDM and 62 normal controls were studied. Genomic DNA was extracted from peripheral leukocyte of patients with GDM and normal controls. The nucleotide variation at -30 bp of pancreatic beta cell specific glucokinase gene promoter was analyzed by PCR-SSCP methods. The sequences of amplified DNA were confirmed with direct sequencing method. The clinical features and the response of insulin secretion to oral glucose were analyzed between patients with GDM according to genotypes. Results: Allelic frequency of position -30 bp of pancreatic beta cell specific glucokinase gene promoter did not differ between patients with GDM and normal subjects. However the frequency of G/A and A/A genotypes seemed to show a higher tendency in patients with GDM compare to the normal subjects. Clinical features, insulin response to oral glucose did not differ according to the type of variation at -30bp of pancreatic beta cell specific glucokinase gene promoter. Conclusion : These data suggested that the variation at -30 bp of pancreatic beta cell specific glucokinase gene promoter in patients with GDM are unlikely to be one of the possibilities of the genetic factors in the development of GDM. Therefore more sophisticated studies will be needed to elucidate the role of variation at -30bp of pancreatic beta cell specific glucokinase gene promoter in the insulin secretion to oral glucose. (Korean. J. Med 57:916-924, 1999)
인슐린 비의존형 당뇨병에서 글류코키나제 유전자 변이에 대한 연구
오승준(Seung Joon Oh),우정택(Jeong Taek Woo),김덕윤(Deok Yoon Kim),양인명(In Myung Yang),김성운(Sung Woon Kim),김진우(Jin Woo Kim),김영설(Young Seol Kim),최영길(Young Kil Choi),팽정령(Jeong Ryung Paeng) 대한내과학회 1996 대한내과학회지 Vol.50 No.3
Objectives : Considerable evidences suggest that genetic factors are of crucial importance in the pathogenesis of NIDDM. As glucokinase is a major enzyme of glucose homeostasis, the glucokinase gene has been proposed as one of candidate genes that confer genetic susceptibility to NIDDM. Although recent studies suggest that mutations of the glucokinase gene related to MODY, a possible relationship between this gene mutation and other subtypes of N1DDM has not investigated. Methods: To investigate the possible relationship between the mutations and NIDDM in Koreans, we screened mutation over all 12 exons of glucokinase gene in 30 normal controls (group 1) and 103 NIDDM patients, 34 patients without family history (group 2) and 69 patients with family history (group 3), by PCR-SSCP (polymerase chain reaction-single strand conformation polymorphism). Results : Eighteen of 133 subjects (13.5%) had mutations which were found in exon 10β, 1L, 1V, and 5, Four different types of polymorphisms were found in exon 10β, 3 types in exon 1L, 1 in both exon 1V and exon 5. Seventeen of 103 NIDDM patients (16.5%) and 1 of 30 normal control (3.3%) had mutations, which suggests that the mutations are related to NIDDM. The frequency of mutations was not different between group 2 and 3. However, the frequency of mutations was higher in the patients with low 24 hour urine C-peptide excretion than those who not. Serum glucose concentration was significantly higher and serum insulin level tended to decrease at 60 min after oral glucose loading in the patients with mutations. Conclusion: These data suggest that the mutations of glucokinase gene are related to NIDDM in Koreans, especially who have low insulin secretory capacity. Further studies are needed to clarify how the mutations relate to NIDDM.
당뇨병 백서의 간세포에서 Glucokinase 활성도 및 유전자 발현에 대한 인슐린의 영향
강성이(Sung Yi Kang),서광식(Kwang Sik Seo),팽정령(Jeong Ryung Paeng),우정택(Jeong Taek Woo),김성운(Sung Woon Kim),양인명(In Myung Yang),김진우(Jin Woo Kim),김영설(Young Seol Kim),김광원(Kwang Won Kim),최영길(Young Kil Choi) 대한내과학회 1994 대한내과학회지 Vol.47 No.2
Introduction: The liver-specific hexokinase isoenzyme, referred to as glucokinase, is thought to play a key reglulatory role in hepatic glucose metabolism. The glucokinase gene is, therefore, of interest both because of its tissue-specific expression and because of the several regulatory processes that can be analyzed. The level of hepatic glucokinase activity appers to be determined essentially by regulation of the rate of enzyme sythesis, with insulin playing a leading role as an inducer. We investigated the role of insulin for the induction of glucokinase in the liver of diabetic rats. Methods: Experimental diabetes was induced by injection of streptozotocin 7 days before the experiment. Regular insulin was given by three days intraperitoneal injection at 8-h interval. The glucokinase mRNA in the liver was estimated by Nothern blot assay, as well as by fluorometric enzyme activity assay. Results: Glucokinase activity was not reduced in the liver of normal fasting rats as compared to normal fed rats. But glucokinase activity was recuced in the liver of daibetic rats as compared to normal rats. In diabetic rats treated with insulin, glucokinase enzyme activity were increased. But glucokinase mRNA expression was only increased in normogycemic diabetic rat with treated with insulin as compared to hyperglycemic rat. Conclusion: These data indicate that insulin stimulates hepatic glucokinase enzyme activity and mRNA expression. But other hormonal or metabolic factors may be contribute to regulation of glucokinase mRNA expressiom.
당뇨유발 마우스에서의 hollow fiber 로 캡슐화한 췌장소도의 이종이식
이무열(Moo Yeol Lee),우정택(Jeong Taek Woo),김성운(Sung Woon Kim),양인명(In Myung Yang),김진우(Jin Woo Kim),김영설(Young Seol Kim),김광원(Kwang Won Kim),최영길(Young Kil Choi),서광식(Kwang Sik Suh) 대한내과학회 1994 대한내과학회지 Vol.46 No.3
Background: We have investigated whether xenograft of the pancreatic islets encapsulated in hollow fiber (Amicon, H1P 30~43 type) could normalize blood glucose levels and could secrete insulin normally in perifusion system. Method: Mice (ICR) made diabetic with 180 mg/kg streptozotocin were intraperitoneally transplanted with encapsulated rat pancreatic islets, Hollow fibers (Amicon, H1P30~43 type, nominal cutoff MW; 30,000) have been used for encapsulation of rat islet cells. Result: Rat islets in the hollow fibers secreted insulin normaly in perifusion system. Xenograft of rat islets in the hollow fibers produced and maintained temporarily normoglycemia in the recipient mice. Conclusion: These results suggest that xenograft of rat islets in the hollow fibers need further study for biocompatability, transplantation site, and islet cell counts.
HIT 세포에서의 Dexmethasone 이 글루코키나제와 글루코기나제 mRNA 발현에 미치는 영향
안규정(Kyu Jeong Ahn),김덕윤(Deok Yoon Kim),우정택(Jeong Taek Woo),김성운(Sung Woon Kim),양인명(In Myung Yang),김진우(Jin Woo Kim),김영설(Young Seol Kim),김광원(Kwang Won Kim),최영길(Young Kil Choi) 대한내과학회 1994 대한내과학회지 Vol.46 No.4
Objectives: The glucokinase-glucose sensor concept of physiological glucose recognition by pancreatic beta- cells has developed progressively since the presence of this enzyme in beta-cells was first reported in 1968. It is well known that HIT cells have glucokinase activity and then insulin secretory response according to glucose stimulation, but there are few data about the effect of hormone on insulin secretion and glucokinase in HIT cells. Therefore, we studied the effect of dexamethasone on glucokinase activity, mRNA expression and insulin secretion in HIT cells. Methods: HIT cells were cultured for 24 hours in medium containing 0, 50, or 500 nM dexamethasone, and then the activities of glucokinase was quantitiated using pyridine uncleotide-dependent fluorometric assays. Northern blot analysis of glucokinase mRNS was done. Results: 1) The Vmax and Km of glucokinase in HIT cells were 3.5 μ mol/min/mg protein, 0.77 mM in HIT cells exposed to 7 mM glucose, respectively and the Vmax and Km of hexokinase in HIT cells were 2.64 μmol/ min/mg protein, 0.06 mM, respectively. 2) 24 hours after incubation of HIT cell with dexamethasone 0, 50, 500 mM, the glucokinase activity and insulin secretion were observed: the glucokinase activities were 1.4±0.45(control), 0.87±0.43(50nmol dexarnethasone), 0.13±0.52 uU/mg protein(500 nmol dexamethasone), and insulin secretion were 44.57±4.1(control), 35.50±1.72(50 nmol dexamethasone), 31.62±1.07 ng/mg protein(500 nmol dexamethasone), respectively. 3) Northern analysis revealed that dexamethaxone increase glucokinase mRNA expression according to dexamethasone concentrations 24 hours after incubation of HIT cells with dexamethasone 50 or 500 nM. Conclusion: Our data showed that dexamethasone tended to increase glucokinase mRNS expression, but decrease glucokinase activity and insulin secretion in HIT cells. Thease data suggested that dexamethasone may have an variable effect on transcriptional or posttranslational levels of glucokinase.
인슐린 비의존성 당뇨병에서 제 4 형 당수송체 유전자의 제한효소분절 길이 다양성
김영설(Young Seol Kim),최성근(Sung Keun Choi),김성운(Sung Woon Kim),양인명(In Myung Yang),김진우(Jin Woo Kim),김광원(Kwang Won Kim),최영길(Young Kil Choi) 대한내과학회 1992 대한내과학회지 Vol.43 No.4
Background: Non-insulin-dependent mellitus (NIDDM) is a heterogenous pathophysiologic disorder with a strong genetic background in the development of disease state and the pathogenesis is characterized by insulin resistance and defective insulin secretion. Regarding to these abnormalities diabetes susceptibility genes may be involved, and one of these candidate genes is the insulin regulatable glucose transporter (GLUT4) expressed predominantly in the skeletal muscle and adipocytes. Recent isolation of genes encoding GLUT4 provides a means to assess the role of possible defect that might contribute to the genetic susceptibility in NIDDM. Methods; We evaluated the RFLP analysis of GLUT4 gene in Korean NIDDM patients with a radioabled GLUT4 cDNA as a probe to define the GLUT4 gene polymorphism as a genetic marker, Results; After digestion with restriction enzyme Kpn I, two band in size 6.5kb and 5.8kb ane noted with polymyphim on 5.8kb. In digestion with Bam HI 25kb and 9kb band. The allele frequency of GLUT 4/Kpn I in NIDDM was lower than that of control (0.29 vs 0.37 P= 0.021). In case of Bam HI the frequency of polymorphic band was not different between NIDDM and control. Conclusion; The GLUT 4 gene RFLP to Kpn I may be considered as a genetic marker of NIDDM in this population. But further studies will be required for its precise nature of gene.
김효종(Hyo Jong Kim),남연호(Yeon Ho Nam),김성운(Sung Woon Kim),양인명(In Myung Yang),김진우(Jin Woo Kim),김영설(Young Seol Kim),김광원(Kwang Won Kim),최영길(Young Kil Choi) 대한내과학회 1988 대한내과학회지 Vol.35 No.2
N/A Growth is an inherent property of life, The integrated function of many of the hormone, metabolic, and other growth factors is necessary for normal somatic growth, Because there are many causes of growth retardation and a vast number of laboratory determinations avail- able to exclude them, it is essential that the physician exercise restraint and select laboratory test on the basis of insights gained from the knowlege of the classification and the causes of growth retardation. Authors performed a etiologic classification and endocrinologic study of 54 patients with growth retardation to classify the categories and the causes of growth retardation and to observe the concentration of somatomedin-C in each category. The results were summarized as follows; 1) Intrinstic shortness was the most common causes of growth retardation coccuring 74% of the cases, followed by arrested growth (13%) and delayed growth (13%). 2) Chromosomal abnormalities were found in only 18 % of the patients with intrinsic shortness. 3) Definite causes were found in all the patients with arrested growth. 4) Definite causes were found in 43% of the patients with delayed growth. 5) Somatomedin-C concentration was within the normal range in all the patients with intrinsic shortness, but below the normal range in those patients with delayed growth in spite of normal GH responses. In conclusion, further studies will be required for the unkonwn causes of intrinsic shortness and dealyed growth and the measurement of somatomedin-C may be useful for the differential diagnosis of intrinsic shortness from the other categories.