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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.
고중성지방혈증 및 비만에서 미토콘드리아 DNA D - loop 영역 ( 16289 - 16547 ) 의 다형성
김주성(Ju Sung Kim),여성문(Sung Moon Yoe),오승준(Seung Joon Oh),김성운(Seong Woon Kim),양인명(In Myung Yang),김진우(Jin Woo Kim),김영설(Young Seol Kim),최영길(Young Kil Choi),팽정령(Jeong Ryung Paeng),박혜순(Hae Soon Park) 한국지질동맥경화학회(구 한국지질학회) 2000 韓國脂質學會誌 Vol.10 No.2
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당뇨병 백서의 간세포에서 Glucokinase 활성도 및 유전자 발현에 대한 인슐린의 영향
강성이,팽정령,서광식,안규정,우정택,김성운,양인명,김진우,김영설,김광원,최영길 경희대학교 유전공학연구소 1993 遺傳工學論文集 Vol.5 No.-
목적 당대사의 조절 상태에 따른 생체 변화를 분자 수준에서 이해하고자 식이 조건을 달리한 정상 백서와 화학적으로 유도된 당뇨병 백서의 간조직에서 혈당수준과 인슐린치료 정도에 따라 나타나는 글루코키나제 활성도 및 유전자 발현을 분석하였다. 방법 스트렙토조토신 정맥투여 후 당뇨병의 유발을 확인하고, 인슐린을 1일 3회 3일간 복강내로 투여하여 상태를 안정시킨 후, 인슐린 투여군은 인슐린 투여 6시간이내에 그리고 인슐린 비투여군은 24시간 후 단두하여 채혈하고 복강을 열어 간조직을 채취하였다. 채취한 간조직에서 글루코키나제 활성도는 인산화된 포도당에서 NADH의 형성을 형광분광계로 측정하였으며, 글루코키나제 유전자 mRNA발현은 Northern 분석법을 이용하였다. 성적 정상 백서에서 공복상태와 식이를 섭취한 경우에 간조직의 글루코키나제 효소의 활성은 차이가 없었으나, 글루코키나제 유전자 mRNA 발현은 증가되었다. 당뇨병이 유발된 백서의 간조직에서 글루코키나제 효소의 활성 및 글루코키나제 유전자의 mRNA 발현은 정상 백서에 비하여 낮았다. 인슐린 투쳐 후 글루코키나제 효소의 활성 및 글루코키나제 유전자의 mRNA 발현이 증가되었고, 특히 혈당이 정상화된 경우에서 글루코키나제 유전자의 mRNA 발현이 증가도었다. 결론 인슐린에 의한 간조직에서 글루코키나제 효소의 활성 및 글루코키나제 유전자의 mRNA을 증가를 볼수 있었다. 당뇨병 백서에서 인슐린 투여 후에 혈당조절이 안된 경우 간조직의 글루코키나제 유전자의 mRNA 발현이 증가가 없는 것으로 보아 글루코키나제 mRNA의 발현에는 인슐린 이외의 다른 요소가 관여할 것으로 생각된다. 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 appears to be determined essentially by regulation of the rate of enzyme synthesis, 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. 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. Glucokinase activity was not reduced in the liver of normal fasting rats as compared to normal fed rats. And glucokinase activity was reduced in the liver of diabetic 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 normoglycemic diabetic rat with treated with insulin as compared to hyperglycemic rat. 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 expression.
Graves병 환자의 HLA-DQ 유전자의 제한효소 분절 길이의 다형성
김진우,팽정령,최영길,김영설,김광원,양인명,김성운 대한내분비학회 1990 Endocrinology and metabolism Vol.5 No.1
The distributions of HLA-DR and DQ antigen were compared between 40 patients with Graves' disease and 24 normal controls. The frequency of HLA-DR 7 among 16 types of HLA-DR was significantly lower in the patient group. And the frequency of HLA-DQw4 among 6 types of HLA-DQ was significantly higher in the patients group.We compared the restriction fragments of HLA-DQ DNA digested with Bam HI and Taq I and hybridized with DQ cDNA between 10 patients and 10 normal controls who were homozygotes of HLA-DQw1 or DQw6. There was no band showing significant difference in the frequency. These data suggest that the pattern of linkage between HLA class II antigens and the disease susceptibility in Korean is different from that in Caucacian, and a gene responsible for disease suceptibility is not located on DQ gene (J. Kor Soc Endocrinol 5:29~36, 1990).
당뇨병, 뇌졸중 및 급성심근경색증에서의 아포리포단백질 E의 유전자형 분포
김진우,팽정령,최영길,김영설,김광원,양인명,김성운,우정택,강성이 대한내분비학회 1992 Endocrinology and metabolism Vol.7 No.3
We tested apolipoprotein E genotypes in 79 patients with hyperlipidemic diabetes, 44 patients with cerebrovascular accident and acute myocardial infaction, and normal subjects with normolipidemia. We distinguished four different apolipoprotein E genotypes by polymerase chain reaction (PCR) and polyacrylamide gel electrophoresis (PAGE) and determined genotypes and allele frequencies. 1) The frequencies of apo E genotype E3/E4 was higher in the patients with hyperlipidemic diabetes (20.2%) than in the normal subjects with normolipidemia(4.1%) (0.01$lt;P$lt;0.025, X2=10.8). 2) The frequencies of the apo E4 allele was signficantly higher in the hyperlipidemic diabetic patients (12.7%) than in the normal subjects(6.1%) (0.005$lt;P$lt;0.01, X2=12.7). 3) In patients with CVA and acute MI the frequencies of apo E genotype E3E4 and E4 allele tended to be higher in the hypercholesterolemia (40.0%, 20.0%) than in the normocholesterolemia(3.8%, 2.0%) P$lt;0.002, X2=14.7). These data suggest that Apo E genotype E3/E4 and E4 allele are one of predisposing factors to hypercholesterolemia in patients with diabetes, cerebrovascular accident, and acute myocardial infarction.(J Kor Soc Endocrinol 7:273~279, 1992)
인슐린 비의존형 당뇨병 환자의 지방대사에서 저밀도 지단백 수용체 유전자 다형성의 의의
김진우,이연태,팽정령,최영길,김영설,김광원,양인명,김성운 대한내분비학회 1989 Endocrinology and metabolism Vol.4 No.1
The restriction fragment length polymorphism (RFLP) of low density lipoprotein (LDL) gene was investigated to observe the possibility that a genetic defect of LDL receptor may contribute to hyperlipidemia patients with non-insulin dependent diabetes mellitus (NIDDM). Southern blottings were performed in 52 NIDDM patients and 36 controls by using the restriction enzyme Pvu II and the various fragments of human LDL receptor cDNA as probes. The results were as followings: 1) The hybridization of LDL binding domain probe (probe 1: 1.03 kb, Pst I site) to human DNA always only showed two bands of 2.7 and 2.5 kb without RFLP. 2) The autoradiography of three domains of LDL receptor cDNA (EGF precursor homology, glycosylation, membrane spanning domain) probe (probe 2: 1.39 kb, Pvu II-Xho I fragments) revealed five bands, 16.5, 14, 2.4, 1.6 and 1.4 kb, but RFLP was found only on 14 kb band. 3) The single domain of EGF precursor homology site (probe 3: 0.78 kb, Pst I fragment) showed 4 bands 16.5, 14, 8.2 and 2.4 kb and RFLP was found on 14 kb band. 4) Probe 4 (Pst I-Xho I site, 0.39 kb) was consist of glycosylation and membrane spanning domain and 2 (2.6, 2.4 kb) bands, but no RFLP was found. 5) Probe 5 (Bam HI site, 1.90 kb) containing all sequences of LDL receptor gene exept binding domain revealed RFLP on 16.5 kb band and 3.4 kb band. 6) The gene frequency of polymorphic band (B allele, 14 kb) was 0.14 and 0.07 in NIDDM and control groups each. 7) In NIDDM patients, high triglyceride (200 mg/dl$lt;) group showed significant higher polymorhic frequency than those of low triglyceride group. (p$lt;0.005) These data suggest that a genetic defect of LDL receptor, probably in EGF precursor homology domain gene, may contribute to hypertriglyceridemia in NIDDM. (J Kor Soc Endocrinol 4: 9-20, 1989)
최영길,배정환,팽정령,오승준,신현대,김영설,정인경 WHO COLLABORATING CENTRE FOR TRADITIONAL MEDICINE 1999 東西醫學硏究所 論文集 Vol.1999 No.-
Obesity can be defined as a metabolic disease due to an increased state of fat tissues caused by an imbalance of calorie intake and use. Recently, in Korea by irnprovernent and westernization of food intake, along with decrease in excercise activities, the prevalence of obesity has increased greatly. Our objectives were to study the stability and effects of decrease in body fat by administering red ginseng compound preparation (known to have body fat decreasing effects in laboratory animals) to obese patients on low calorie diets. Changes in weight and body fat were measured while earring out calorie-restricted diets on patients for 4 weeks, then administering red ginseng compound preparation for another 4 weeks. The number of patients was 20 whose BMI were 25kg/m²or over and whose percent body fat was also 30% or over when tested by bioelectrical conductivity. 1) Changes in weight were from 70.04 kg (base line) to 67.43 kg (after taking red ginseng compound preparation). 2) In similar sense, BMI decreased from 27.12 kg/m²(base line) to 26.56 kg/m²(after dieting), and further to 26.01 kg/m²(after taking red ginseng compound preparation). The BMI seemed decrease significantly compared to the baseline after the use of red ginseng compound. 3) Waist hip ratio was unchanged. 4) The percent body fat was 35.16% (base line ) 33,87% (after dieting), and 31.68% (after taking red ginseng compound preparation). 5) Complete blood cell count and blood chemistry remained unaffected by the administration. 6) In concern to endocrinologic studies,T₃decreased from 118.7 to 98.2 ng/dL, and T₄increased form 8.8 to 9.2 ㎍/dL, Epinephrine showed a tendency to decrease from 0.27 to 0.25 ng/mL, and norepinephrine increased from 0.39 to 0.44ng/mL. In conclusion, loss of weight without significant side effects was observed during low calorie diet and red ginseng compound preparation administration. This is thought to be in relation to sympathetic nerve system rather than adrenal gland. Also, further long term studies should be required, since the oberved results were based on short term changes in weight.