翁建平
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- 姓名:翁建平
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翁建平 男, 教授/主任医师 博士研究生导师 1965年8月出生 出生地:江苏省常熟市 专业:内科内分泌代谢病中华医学会糖尿病学会副主任委员广东省医学会糖尿病学分会主任委员亚洲分子糖尿病学会理事(委员)中华医学会《中华糖尿病杂志》编委中华医学会《中华全科医师杂志》编委欧洲糖尿病学(Diabetologia)杂志特约审稿人国家科学技术进步奖评审专家工作和教育经历:1980-1985年东南大学医学院(原南京铁道医学院),获医学学士。1988-1991年中山大学(原中山医科大学)获临床医学硕士学位.毕业后留校历任住院医生、住院总医生、主治医师。1993-1996年中山医科大学(博士研究生),获医学博士学位.1997年5月破格晋升副教授、副主任医师。1997.12-2000.3留学于欧洲最大和历史最悠久大学之一瑞典LUND大学,从事博士后研究。博士后期间完成3项研究,发表学术论文8篇,第一作者4篇。2000年7月任中山大学附属第一医院内分泌科科主任。2001年11月当选为亚洲分子糖尿病学会理事(委员)。2001年12月通过中山医科大学学术委员会评审,破格晋升教授/主任医师。2002年7月出任广东省医学会糖尿病学分会主任委员。2003年十月当选为中华医学会第四届糖尿病学分会(全国)副主任委员
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翁建平, JIANPINGWENG, MD, PHD JINHUA YAN, MD ZHIMIN HUANG, MD YI SUI, MD LINGLING XIU, PHD
DIABETES CARE, VOLUME 26, NUMBER 10, OCTOBER 2003,-0001,():
-1年11月30日
Type 2 diabetes is both a phenotypically and geneotypically heterogeneous disease. It is caused by defective insulin secretion and action. Protein tyrosine phosphatases (PTPases) play important roles in insulin cascade signal transduction and have been suggested to be related to insulin resistance (1,2). PTP-1B, a member of the PTP family, is expressed widely in many tissues, acting as a negative regulator in the insulin receptor signal transduction pathway (3-5). The PTP-1B gene is located on the long arm of human chromosome 20, in the region of q13.1-q13.2, which has been linked to quantitative trait loci of obesity and insulin (6,7). A recent study by Echwald S.M. et al. (8) demonstrated that a Pro387Leu variation of the PTP-1B gene, which resulted in the impairment of the serine phosphorylation of the PTP-1B peptide (in vitro experiment), was associated with type 2 diabetes in a Danish Caucasian population with a genotype relative risk of 3.7 (CI 1.26~10.93, P=0.02). Since studies involving the association between the genetic variations and type 2 diabetes are often controversial and inconsistent in different ethnic populations, we tested the association between the Pro387Leu variation of PTP-1B gene with type 2 diabetes in a Chinese Han population for the first time. The Pro387Leu variation of PTP-1B gene was detected usingPCRand restriction ragment–length polymorphism in 589 subjects chosen from the Han population living in southern China, including 329 type 2 diabetic patients (men/women 143/186, age 59.4±9.9 years, BMI 23.9±3.5kg/m2) and 238 control subjects (men/women 100/138, age 57.5±8.3 years, BMI 23.8±3.1kg/m2). The control subjects underwent a 75-g oral glucose tolerance test and were diagnosed with normal glucose tolerance (NGT) in accordance with the 1997 American Diabetes Association criteria. The study was approved by the ethnics committee of our institution. All the subjects gave informed consent. In our study, only two subjects heterozygous for the mutation were found in the NGT control group, with genotype and allele frequencies of 0.008 and 0.004, respectively. We found another two heterozygotes in the diabetic patient group; the genotype and allele frequencies were 0.006 and 0.003, respectively. The differences did not reach statistical significance between groups (P= 0.05 for both). The distribution was consistent with Hardy-Weinberg equilibrium. We then examined the impacts of the mutation on metabolic and anthropometric parameters in both groups. Among NGT control subjects, there were no significant differences in age, fasting plasma glucose (FPG), or lipid profile between the two subgroups with or without the Leu387 mutation (P=0.05), while BMI was significantly higher in subjects with the Leu387 allele (23.74±3.05 vs. 28.55±2.19 kg/m2, P=0.027). In the diabetic patient group, no differences were observed in age, BMI, FPG, HbA1c, Cpeptide, or lipid profile (P=0.05). Since the mutation rate was quite low in the examined Chinese Han population and at the same time there were 31 subjects with a BMI>27kg/m2 in the subgroup without the Leu387 mutation, the difference found in BMI between the mutation carriers and noncarriers in the control group was likely attributed to individual variance rather than the true difference caused by the presence of the mutation. In conclusion, our data indicated that the mutation of Pro387Leu in PTP-1B gene was present in the Chinese Han population examined, but this variation wa
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翁建平, YANBING LI, WEN XU, ZHIHONG LIAO, BIN YAO, XIAHUA CHEN, ZHIMIN HUANG, GUOLIANG HU, JIANPINGWENG,
Diabetes Care 27: 2597-2602, 2004,-0001,():
-1年11月30日
OBJECTIVE—To investigate whether long-term optimal glycemic control can be achieved without medication by transient continuous subcutaneous insulin infusion (CSII) and the possible mechanisms responsible for this remission. RESEARCH DESIGN AND METHODS—Newly diagnosed type 2 diabetic patients (n=138, fasting glucose>11.1mmol/l) were hospitalized and treated with CSII for 2 weeks. Intravenous glucose tolerance tests (IVGTTs) were performed, and blood glucose, HbA1c, lipid profiles, proinsulin, insulin, and C-peptide were measured before and after CSII. Patients were followed longitudinally on diet alone after withdrawal of insulin. RESULTS-Optimal glycemic control was achieved within 6.3±3.9 days by CSII in 126 patients. The remission rates (percentages maintaining near euglycemia) at the third, sixth, twelfth, and twenty-fourth month were 72.6, 67.0, 47.1, and 42.3%, respectively. Patients who maintained glycemic control 12 months (remission group) had greater recovery of β-cell function than those who did not (nonremission group) when assessed immediately after CSII. Homeostasis model assessment of β-cell function (HOMA-B) and the area under the curve (AUC) of insulin during IVGTT were higher in the remission group (145.4±89.6 vs. 78.5±68.5, P=0.002, and 1,423.4±523.2 vs. 1,159.5±476.8 pmol-l•min-1, P=0.044). Change in acute insulin response was also greater in the remission group than that in the nonremission group (621.8±430.4 vs. 387.3±428.8pmol-l•min-1, P=0.033). CONCLUSIONS—Short-term intensive insulin therapy can induce long-term glycemic control in newly diagnosed type 2 diabetic patients with severe hyperglycemia. The improvement of β-cell function, especially the restoration of first-phase insulin secretion, could be responsible for the remission.
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翁建平, XUDONG HUANG, ALLAN VAAG, MONA HANSSON, JIANPING WENG, ESA LAURILA, AND LEIF GROOP
The Journal of Clinical Endocrinology & Metabolism Vol. 85, No.4,-0001,():
-1年11月30日
To examine whether defective muscle glycogen synthase (GYS1) expression is associated with impaired glycogen synthesis in type 2 diabetes and whether the defect is inherited or acquired, we measured GYS1 gene expression and enzyme activity in muscle biopsies taken before and after an insulin clamp in 12 monozygotic twin pairs discordant for type 2 diabetes and in 12 matched control subjects. The effect of insulin on GYS1 fractional activity, when expressed as the increment over the basal values, was significantly impaired in diabetic (15.7±3.3%; P<0.01), but not in nondiabetic (23.7±1.8%; P =NS) twins compared with that in control subjects (28.1±2.3%). Insulin increased GYS1 messenger ribonucleic acid (mRNA) expression in control subjects (from 0.14±0.02 to 1.74±0.10 relative units; P, 0.01) and in nondiabetic (from 0.24±0.05 to 1.81±0.16 relative units; P<0.01) and diabetic (from 0.20±0.07 to 1.08±0.14 relative units; P<0.01) twins. The effect of insulin on GYS1 expression was, however, significantly reduced in the diabetic (P, 0.003), but not in the nondiabetic, twins compared with that in control subjects. The postclamp GYS1 mRNA levels correlated strongly with the hemoglobin A1c levels (r=-0.61; P<0.001). Despite the decrease in postclamp GYS1 mRNA levels, the GYS1 protein levels were not decreased in the diabetic twins compared with those in the control subjects (2.10±0.46 vs. 2.10±0.34 relative units; P 5 NS). We conclude that 1) insulin stimulates GYS1 mRNA expression; and 2) impaired stimulation of GYS1 gene expression by insulin in patients with type 2 diabetes is acquired and most likely is secondary to chronic hyperglycemia.
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翁建平, M. Lehto, C. Wipemo, S.-A. Ivarsson, C. Lindgren, M. Lipsanen-Nyman, J.Weng, L. Wibell, E. Wid
Diabetologia (1999) 42: 1131-1137,-0001,():
-1年11月30日
115 Finnish and Swedish patients with early-onset (≤40 years) diabetes using the single strand conformation polymorphism (SSCP) technique and direct sequencing. Allele frequencies were compared with 118 patients with onset of diabetes Type II (non-insulin-dependent) diabetes mellitus after the age of 40 and 92 non±diabetic control subjects without a family history of diabetes. Results. In total 52 sequence variants were found in the HNF-1a, HNF-4a and glucokinase genes, 12 of which were considered as MODY mutations. Three families had the A3243G mutation in the mitochondrial tRNALeu gene, which resulted in an overall prevalence of these mutations of 13%. Conclusion/interpretation. Among 115 Scandinavian families, mutations in the HNF-1a gene represented the most common cause of familial early-onset (≤40 years) diabetes: MODY3 (5.2%) more than MODY2 (3.5%) more than MIDD (2.6%) more than MODY1 (1.7%). [Diabetologia (1999) 42: 1131-1137]
Glucokinase,, HNF-1,, HNF-4,, MODY,, MIDD,, genetics.,
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翁建平
Diabetologia (2000) 43: 131-134,-0001,():
-1年11月30日
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翁建平, J. Weng*, W. M. Macfarlane*, M. Lehto, H. F. Gu, L. M. Shepherd, S.A. Ivarsson, L. Wibell, T. Smith, L. C. Groop
Diabetologia (2001) 44: 249-258,-0001,():
-1年11月30日
Aims/hypothesis. The aim of this study was to examine the putative role of mutations in the insulin promoter 1 (IPF1) gene in early-onset diabetes. Methods. We carried out mutation screening of the IPF1 gene in 115 Scandinavian families with at least two members with onset of diabetes younger than 40 years. The allele frequencies were also tested in 183 unrelated patients with late-onset Type II (non-insulin-dependent) diabetes mellitus and in 92 nondiabetic control subjects. Results. Two novel IPF1 variants (G212R and P239Q) and one previously reported (D76N) IPF1 variant were identified in the 115 families (3.5%). The D76N variant was found in one MODY3 family (S315fsinsA of HNFla) and also in two families with late-onset Type II diabetes. The P239Q variant was identified in two families with early-onset diabetes in cluding one with MODY3 (R272C of HNF 1 α) and in three families with late-onset Type II diabetes. Despite the fact that the variants did not segregate completely with diabetes, the non-diabetic carriers of the IPF1 variants had increased blood glucose concentrations (p<0.05) and reduced insulin:glucose ratios (p<0.05) during an oral glucose tolerance test compared with non-diabetic family members without these variants. In addition, when the G212R and P239Q variants were expressed in cells without IPF1 i.e.. Nes2 y cells, both variants showed about a 50% reduction in their ability to activate insulin gene transcription compared to wild-type IPF1, as measured by reporter gene assay. Conclusion/interpretation. Although mutations in the IPF-1 gene are rare in early-(3.5%) and late-onset (2.7%) Type H diabetes, they are functionally important and occur also in families with other MODY mutations. [Diabetologia (2001) 44: 249-258]
Insulin promoter factor 1,, Type II diabetes,, maturity-onset diabetes of the young (, MODY), ,, gene expression,, insulin gene.,
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翁建平, Cecilia M. Lindgren, Elisabeth Widen, Tiinamaija Tuomi, , Haiyan Li, Peter Almgren, Timo Kanninen, Olle Melander, Jianping Weng, Markku Lehto, and Leif C. Groop
harbor novel genes that contribute to EOD. Diabetes 51: 1609-1617, 2002,-0001,():
-1年11月30日
In an attempt to identify novel susceptibility genes predisposing to early-onset diabetes (EOD), we performed a genome-wide scan using 433 markers in 222 individuals (119 with diabetes) from 29 Scandinavian families with≥2 members with onset of diabetes≤45 years. The highest nonparametric linkage (NPL) score, 2.7 (P<0.01), was observed on chromosome 1p (D1S473/D1S438). Six other regions on chromosomes 3p, 7q, 11q, 18q, 20q, and 21q showed a nominal P value<0.05. Of the EOD subjects in these 29 families, 20% were GAD antibody positive and 68% displayed type 1 diabetes HLA risk alleles (DQB*02 or 0302). Mutations in maturity-onset diabetes of the young (MODY) 1-5 genes and the A3243G mitochondrial DNA mutation were detected by single-strand conformation polymorphism and direct sequencing. To increase homogeneity, we analyzed a subsample of five families with autosomal dominant inheritance of EOD (greater than or equal to two members with age at diagnosis≤35years). The highest NPL scores were found on chromosome 1p (D1S438-D1S1665; NPL 3.0; P<0.01) and 16q (D16S419; NPL 2.9; P<0.01). After exclusion of three families with MODY1, MODY3, and mitochondrial mutations, the highest NPL scores were observed on chromosomes 1p (D1S438; NPL 2.6; P<0.01), 3p (D3S1620; NPL 2.2; P<0.03), 5q (D5S1465; NPL 2.1; P<0.03), 7q (D7S820; NPL 2.0; P<0.03), 18q (D18S535; NPL 1.9; P<0.04), 20q (D20S195; NPL 2.5; P<0.02), and 21q (D21S1446; NPL 2.2; P<0.03). We conclude that considerable heterogeneity exists in Scandinavian subjects with EOD; 24% had MODY or maternally inherited diabetes and deafness, and ~60% were GAD antibody positive or had type 1 diabetes-associated HLA genotypes. Our data also point at putative chromosomal regions, which could families that fulfill MODY criteria do not have mutations in known MODY genes (MODYX) (3,8,17-20). To evaluate the relative contribution of known and unknown susceptibility genes in families with EOD, we screened 222 subjects from 29 families with EOD for type 1 diabetes-associated HLA genotypes, GAD antibody (GADA), known MODY mutations, and the A3243G mitochondrial DNA mutation and subjected them to a genome wide scan.
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翁建平, WENG Jianping, Markku Lehto, Anna Berglund and Leif C. Groop
Chinses Medical Journal 2001; 114 (11): 1147-ll50,-0001,():
-1年11月30日
Objective To develope a high throughput mutational detection method by mutiple fluorescence-labeled polyrnerase chain reaction (PCR) products. Methods A total of 27 known mutations including 22 substitutions, 3 iosertions (1, 2 and 7 bp) and 2 deletions (t and 2 bp) in the hepateeyte nuclear factor (HNF)-4a, glucokinase and HNF-la genes were tested. During nested PCR, amplified fragments were labeled with three fluorescent dyes. PCR products were visualized with an ABI-3T/ fluorescence sequencer using 5% glycerol or 10% sucrose in nondenaturing gel conditions. Results Twenty-five of 27 variants (93%) could be detected by combining 5% gtycerol and 10% sucrose gel matrix conditions. Twenty-two of 27 (82%) and 18 of 27 (67%) variants were identified using 5% glycerol and 10% sucrose conditions, respectively. Conclusion This fluorescence-based PCR single strand conformation polymorphism technique represents a simple, non-hazardous, time-savino and sensitive method for hiah throuahout mutation detection.
genetics
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翁建平, HAIYAN LI, LEIF GROOP, ANITA NILSSON, JIANPING WENG, AND TIINAMAIJA TUOMI
The Journal of Clinical Endocrinology & Metabolism 88 (6): 2767-2774,-0001,():
-1年11月30日
Our previous results have suggested that genes outside the human leukocyte antigen (HLA) class II locus may affect the phenotype of type 2 diabetic patients from families with both type 1 and type 2 diabetes (mixed type 1/2). To study whether the TNFα gene could be such a modifying gene, we studied TNFα promoter polymorphisms (G3A substitution at positions -308 and -238) in relation to HLA-DQB1 genotypes in type 2 patients from mixed type 1/2 families or common type 2 diabetes families as well as in patients with adult-onset type 1 diabetes and control subjects. The TNFα308 AA/AG genotype frequency was increased in adult onset type 1 patients (55%, 69 of 126), but it was similar in type 2 patients from type 1/2 families (35%, 33/93) or common type 2 families (31%, 122 of 395), compared with controls (33%, 95/284; P<0.0001 vs. type 1). The TNF 308 A and DQB1*02 alleles were in linkage disequilibrium in type 1 patients (Ds=0.81; P<0.001 vs. Ds=0.25 in controls) and type 2 patients from type 1/2 families (Ds=0.59, P<0.05 vs. controls) but not in common type 2 patients (Ds=0.39). The polymorphism was associated with an insulindeficient phenotype in the type 2 patients from type 1/2 families only together with DQB*02, whereas the common type 2 patients with AA/AG had lower waist to hip ratio [0.92 (0.12) vs. 0.94 (0.11), P=0.008] and lower fasting C-peptide concentration [0.48 (0.47) vs. 0.62 (0.46) nmol/liter, P=0.020] than those with GG, independently of the presence of DQB1*02. In conclusion, TNFα is unlikely to be the second gene in the HLA area responsible for our previous findings in type 1/2 patients. However, we could show an association between TNFα308 polymorphism and the phenotype of common type 2 diabetes.
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翁建平, 许雯, 廖志红, 李延兵, 胡国亮
中国糖尿病杂志,2003,11(2):88~91,-0001,():
-1年11月30日
目的 了解2型糖尿病患者体脂分布与胰岛素抵抗(IR)的关系,比较各种体脂评价方法。方法 41例2型糖尿病患者,以双能x线吸收法(DExA)测定全身脂肪百分比(BF%)及局部脂肪百分比,同时测定身高、体重,计算体重指数(BMI),测定腰围、臀围,并计算其比值(WHR),以生物电阻抗法体脂测定仪(TANITA仪)测定BF%,以空腹血糖与胰岛素乘积的倒数(取自然对数LnIAI)作为IR指标,分析体脂分布与IR的关系。评价TANITA仪测定的BF%与DEXA测定结果的相关性。结果 2型糖尿病患者腹型肥胖组LnIAI(-4.6±O.6)明显低于非腹型肥胖组(-4.2±O.7),腹型肥胖组中BMI与LnIAI相关(r=-O.488, P=O.021),而非腹型肥胖组中各指标与LnIAI均不相关。各种体脂指标经聚类分析后BMI与腰围、WHR归为一类。TANITA与DEXA测定的BF%显著相关(r=O.839)。结论 2型糖尿病患者存在腹型肥胖,则胰岛素抵抗明显。在2型糖尿病患者中,BMI仍是反映胰岛素抵抗的较佳指标。TANITA仪与DExA测定的BF%显著相关。
2型糖尿病, 胰岛素抗药性, 肥胖症,, 糖尿病性
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