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【进展】Diabetes 2005年第7期摘要征译者 [精华]

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Diabetes杂志2004年影响因子8.848分，近年来稳定上升。

本期中有6篇文章第一作者似华人。但无任何一篇的作者单位是中国？中国人笨？缺研究基金？中国人不勤奋？科研体制不行？语言障碍？......................?

Diabetes杂志 2005年第7期已出版。内分泌版现面向全球招聘摘要译者。战友可选择自己感兴趣的摘要进行翻译，每位战友最多领取两篇。为提高效率，战友可直接翻译后跟贴，不必再PM领取。一般以每篇摘要加1分（每篇摘要有三处用词不规范或翻译不准确将不予加分）。

注意：
1 翻译后请注明篇号。
2 请认真校对，尽量使用规范词，规范词的使用以《中华内分泌代谢杂志》的规定为准。
3 本期翻译版主将不提供摘要，请自行下载：
http://diabetes.diabetesjournals.org/content/vol54/issue7/?etoc

已完成 1 Perspectives in Diabetes:
Nutritional Epigenomics of Metabolic Syndrome: New Perspective Against the Epidemic
Catherine Gallou-Kabani and Claudine Junien
Diabetes 2005 54: 1899-1906. [Abstract] [Full Text] [PDF]

已完成 2 Metabolism:
Effect of Fructose Overfeeding and Fish Oil Administration on Hepatic De Novo Lipogenesis and Insulin Sensitivity in Healthy Men
David Faeh, Kaori Minehira, Jean-Marc Schwarz, Raj Periasami, Park Seongsu, and Luc Tappy
Diabetes 2005 54: 1907-1913. [Abstract] [Full Text] [PDF]

已完成 3 Assessing the Predictive Accuracy of QUICKI as a Surrogate Index for Insulin Sensitivity Using a Calibration Model
Hui Chen, Gail Sullivan, and Michael J. Quon
Diabetes 2005 54: 1914-1925. [Abstract] [Full Text] [PDF]

已完成 4 A High-Fat Diet Coordinately Downregulates Genes Required for Mitochondrial Oxidative Phosphorylation in Skeletal Muscle
Lauren M. Sparks, Hui Xie, Robert A. Koza, Randall Mynatt, Matthew W. Hulver, George A. Bray, and Steven R. Smith
Diabetes 2005 54: 1926-1933. [Abstract] [Full Text] [PDF] Online-Only Appendix

5 A Multicompartmental Model of In Vivo Adipose Tissue Glycerol Kinetics and Capillary Permeability in Lean and Obese Humans
Simon W. Coppack, David L. Chinkes, John M. Miles, Bruce W. Patterson, and Samuel Klein
Diabetes 2005 54: 1934-1941. [Abstract] [Full Text] [PDF]

已完成 6 Obesity and Type 2 Diabetes Impair Insulin-Induced Suppression of Glycogenolysis as Well as Gluconeogenesis
Rita Basu, Visvanathan Chandramouli, Betty Dicke, Bernard Landau, and Robert Rizza
Diabetes 2005 54: 1942-1948. [Abstract] [Full Text] [PDF]

已完成 7 Dual Role of Phosphofructokinase-2/Fructose Bisphosphatase-2 in Regulating the Compartmentation and Expression of Glucokinase in Hepatocytes
Victoria A. Payne, Catherine Arden, Chaodong Wu, Alex J. Lange, and Loranne Agius
Diabetes 2005 54: 1949-1957. [Abstract] [Full Text] [PDF]

8 Signal Transduction:
Impact of the Liver-Specific Expression of SHIP2 (SH2-Containing Inositol 5'-Phosphatase 2) on Insulin Signaling and Glucose Metabolism in Mice
Kazuhito Fukui, Tsutomu Wada, Syota Kagawa, Kiyofumi Nagira, Mariko Ikubo, Hajime Ishihara, Masashi Kobayashi, and Toshiyasu Sasaoka
Diabetes 2005 54: 1958-1967. [Abstract] [Full Text] [PDF]

已完成 9 The Regulation of Fatty Acid Synthase by STAT5A
Jessica C. Hogan and Jacqueline M. Stephens
Diabetes 2005 54: 1968-1975. [Abstract] [Full Text] [PDF]

已完成 10 Role of Upstream Stimulatory Factors in Regulation of Renal Transforming Growth Factor-ß1
Yanqing Zhu, Marta Casado, Sophie Vaulont, and Kumar Sharma
Diabetes 2005 54: 1976-1984. [Abstract] [Full Text] [PDF]

11 Obesity Studies:
Distinct Forebrain and Caudal Brainstem Contributions to the Neuropeptide Y Mediation of Ghrelin Hyperphagia
Lucy F. Faulconbridge, Harvey J. Grill, and Joel M. Kaplan
Diabetes 2005 54: 1985-1993. [Abstract] [Full Text] [PDF]

已完成 12Long-Term Efficacy of Leptin Replacement in Patients With Generalized Lipodystrophy
Edward D. Javor, Elaine K. Cochran, Carla Musso, Janice Ryan Young, Alex M. DePaoli, and Phillip Gorden
Diabetes 2005 54: 1994-2002. [Abstract] [Full Text] [PDF]

已完成13 Autocrine Action of Adiponectin on Human Fat Cells Prevents the Release of Insulin Resistance-Inducing Factors
Daniela Dietze-Schroeder, Henrike Sell, Mathias Uhlig, Marlis Koenen, and Jürgen Eckel
Diabetes 2005 54: 2003-2011. [Abstract] [Full Text] [PDF]

已完成 14 Role of Selective Leptin Resistance in Diet-Induced Obesity Hypertension
Kamal Rahmouni, Donald A. Morgan, Gina M. Morgan, Allyn L. Mark, and William G. Haynes
Diabetes 2005 54: 2012-2018. [Abstract] [Full Text] [PDF]

已完成 15 NOD B-cells Are Insufficient to Incite T-Cell-Mediated Anti-islet Autoimmunity
Daniel J. Moore, Hooman Noorchashm, Tina H. Lin, Siri A. Greeley, and Ali Naji
Diabetes 2005 54: 2019-2025. [Abstract] [Full Text] [PDF]

已完成 16 Immunology and Transplantation:
Maternal Factors in a Model of Type 1 Diabetes Differentially Affect the Development of Insulitis and Overt Diabetes in Offspring
Yukiko Kagohashi, Jun Udagawa, Norio Abiru, Masakazu Kobayashi, Kenji Moriyama, and Hiroki Otani
Diabetes 2005 54: 2026-2031. [Abstract] [Full Text] [PDF]

已完成 17 The Influence of the Major Histocompatibility Complex on Development of Autoimmune Diabetes in RIP-B7.1 Mice
F. Susan Wong, Wei Du, Ian J. Thomas, and Li Wen
Diabetes 2005 54: 2032-2040. [Abstract] [Full Text] [PDF]

18 Immune Cell Infiltration, Cytokine Expression, and ß-Cell Apoptosis During the Development of Type 1 Diabetes in the Spontaneously Diabetic LEW.1AR1/Ztm-iddm Rat
Anne Jörns, Armin Günther, Hans-Jürgen Hedrich, Dirk Wedekind, Markus Tiedge, and Sigurd Lenzen
Diabetes 2005 54: 2041-2052. [Abstract] [Full Text] [PDF]

19 Identification of Naturally Processed HLA-A2—Restricted Proinsulin Epitopes by Reverse Immunology
Yousra Hassainya, Francisco Garcia-Pons, Roland Kratzer, Vivian Lindo, Fiona Greer, François A. Lemonnier, Gabriele Niedermann, and Peter M. van Endert
Diabetes 2005 54: 2053-2059. [Abstract] [Full Text] [PDF]

已完成20 Five-Year Follow-Up After Clinical Islet Transplantation
Edmond A. Ryan, Breay W. Paty, Peter A. Senior, David Bigam, Eman Alfadhli, Norman M. Kneteman, Jonathan R.T. Lakey, and A.M. James Shapiro
Diabetes 2005 54: 2060-2069. [Abstract] [Full Text] [PDF]

已完成21 Islet Studies:
Saturated and cis/trans Unsaturated Acyl CoA Esters Differentially Regulate Wild-Type and Polymorphic ß-Cell ATP-Sensitive K+ Channels
Michael J. Riedel and Peter E. Light
Diabetes 2005 54: 2070-2079. [Abstract] [Full Text] [PDF]

22 Role for ß1 Integrin and Its Associated 3, 5, and 6 Subunits in Development of the Human Fetal Pancreas
Rennian Wang, Jinming Li, Kristina Lyte, Nina K. Yashpal, Fraser Fellows, and Cynthia G. Goodyer
Diabetes 2005 54: 2080-2089. [Abstract] [Full Text] [PDF]

23 Targeted Inactivation of Hepatocyte Growth Factor Receptor c-met in ß-Cells Leads to Defective Insulin Secretion and GLUT-2 Downregulation Without Alteration of ß-Cell Mass
Jennifer Roccisana, Vasumathi Reddy, Rupangi C. Vasavada, Jose A. Gonzalez-Pertusa, Mark A. Magnuson, and Adolfo Garcia-Ocaña
Diabetes 2005 54: 2090-2102. [Abstract] [Full Text] [PDF]

已完成 24 Peptide-Mediated Targeting of the Islets of Langerhans
Kausar N. Samli, Michael J. McGuire, Christopher B. Newgard, Stephen Albert Johnston, and Kathlynn C. Brown
Diabetes 2005 54: 2103-2108. [Abstract] [Full Text] [PDF] Online-Only Appendix

25 Overexpression of Glutathione Peroxidase With Two Isoforms of Superoxide Dismutase Protects Mouse Islets From Oxidative Injury and Improves Islet Graft Function
Tharun B. Mysore, Trixie A. Shinkel, James Collins, Evelyn J. Salvaris, Nella Fisicaro, Lisa J. Murray-Segal, Lucinda E.A. Johnson, Diana A. Lepore, Stacey N. Walters, Rebecca Stokes, Abhilash P. Chandra, Philip J. O’Connell, Anthony J.F. d’Apice, and Peter J. Cowan
Diabetes 2005 54: 2109-2116. [Abstract] [Full Text] [PDF]

26 Aberrant Processing of Human Proislet Amyloid Polypeptide Results in Increased Amyloid Formation
Johan F. Paulsson and Gunilla T. Westermark
Diabetes 2005 54: 2117-2125. [Abstract] [Full Text] [PDF]

27 Inhibition of Purinoceptors Amplifies Glucose-Stimulated Insulin Release With Removal of its Pulsatility
Albert Salehi, Saleem S. Quader, Eva Grapengiesser, and Bo Hellman
Diabetes 2005 54: 2126-2131. [Abstract] [Full Text] [PDF]

已完成 28 Redox Control of Exocytosis: Regulatory Role of NADPH, Thioredoxin, and Glutaredoxin
Rosita Ivarsson, Roel Quintens, Sandra Dejonghe, Katsura Tsukamoto, Peter in ’t Veld, Erik Renström, and Frans C. Schuit
Diabetes 2005 54: 2132-2142. [Abstract] [Full Text] [PDF]

已完成 29 Complications:
Tissue Factor as a Link Between Wounding and Tissue Repair
Jiang Chen, Michael Kasper, Tobias Heck, Katsumi Nakagawa, Per M. Humpert, Ling Bai, Gang Wu, Youming Zhang, Thomas Luther, Martin Andrassy, Stephan Schiekofer, Andreas Hamann, Michael Morcos, Baoshen Chen, David M. Stern, Peter P. Nawroth, and Angelika Bierhaus
Diabetes 2005 54: 2143-2154. [Abstract] [Full Text] [PDF]

已完成 30 Impaired Arachidonic Acid–Mediated Activation of Large-Conductance Ca2+-Activated K+ Channels in Coronary Arterial Smooth Muscle Cells in Zucker Diabetic Fatty Rats
Tong Lu, Xiao-Li Wang, Tongrong He, Wei Zhou, Terry L. Kaduce, Zvonimir S. Katusic, Arthur A. Spector, and Hon-Chi Lee
Diabetes 2005 54: 2155-2163. [Abstract] [Full Text] [PDF]

已完成 31 The Early Natural History of Nephropathy in Type 1 Diabetes: III. Predictors of 5-Year Urinary Albumin Excretion Rate Patterns in Initially Normoalbuminuric Patients
Julia M. Steinke, Alan R. Sinaiko, Michael S. Kramer, Samy Suissa, Blanche M. Chavers, Michael Mauer for the International Diabetic Nephropathy Study Group
Diabetes 2005 54: 2164-2171. [Abstract] [Full Text] [PDF]

已完成 32 Heparanase-1 Gene Expression and Regulation by High Glucose in Renal Epithelial Cells: A Potential Role in the Pathogenesis of Proteinuria in Diabetic Patients
Justin B. Maxhimer, Michael Somenek, Geetha Rao, Catherine E. Pesce, David Baldwin, Jr., Paolo Gattuso, Melvin M. Schwartz, Edmund J. Lewis, Richard A. Prinz, and Xiulong Xu
Diabetes 2005 54: 2172-2178. [Abstract] [Full Text] [PDF]

已完成 33 Metformin Prevents High-Glucose–Induced Endothelial Cell Death Through a Mitochondrial Permeability Transition-Dependent Process
Dominique Detaille, Bruno Guigas, Christiane Chauvin, Cécile Batandier, Eric Fontaine, Nicolas Wiernsperger, and Xavier Leverve
Diabetes 2005 54: 2179-2187. [Abstract] [Full Text] [PDF]

34 The Effect of Ruboxistaurin on Visual Loss in Patients With Moderately Severe to Very Severe Nonproliferative Diabetic Retinopathy: Initial Results of the Protein Kinase C ß Inhibitor Diabetic Retinopathy Study (PKC-DRS) Multicenter Randomized Clinical Trial
The PKC-DRS Study Group
Diabetes 2005 54: 2188-2197. [Abstract] [Full Text] [PDF]

已完成 35 Advanced Glycation End Product Precursors Impair ABCA1-Dependent Cholesterol Removal From Cells
Marisa Passarelli, Chongren Tang, Thomas O. McDonald, Kevin D. O’Brien, Ross G. Gerrity, Jay W. Heinecke, and John F. Oram
Diabetes 2005 54: 2198-2205. [Abstract] [Full Text] [PDF]

已完成 36 Rosiglitazone Improves Glomerular Hyperfiltration, Renal Endothelial Dysfunction, and Microalbuminuria of Incipient Diabetic Nephropathy in Patients
Frank Pistrosch, Kay Herbrig, Beate Kindel, Jens Passauer, Sabine Fischer, and Peter Gross
Diabetes 2005 54: 2206-2211. [Abstract] [Full Text] [PDF]

已完成 37 Pharmacology and Therapeutics:
Erythromycin Antagonizes the Deceleration of Gastric Emptying by Glucagon-Like Peptide 1 and Unmasks Its Insulinotropic Effect in Healthy Subjects
Juris J. Meier, Guido Kemmeries, Jens J. Holst, and Michael A. Nauck
Diabetes 2005 54: 2212-2218. [Abstract] [Full Text] [PDF]

已完成 38 Tempol Reduces Oxidative Stress, Improves Insulin Sensitivity, Decreases Renal Dopamine D1 Receptor Hyperphosphorylation, and Restores D1 Receptor–G-Protein Coupling and Function in Obese Zucker Rats
Anees Ahmad Banday, Aditi Marwaha, Lakshmi S. Tallam, and Mustafa F. Lokhandwala
Diabetes 2005 54: 2219-2226. [Abstract] [Full Text] [PDF]

已完成 39 Signaling Pathways Involved in Human Vascular Smooth Muscle Cell Proliferation and Matrix Metalloproteinase-2 Expression Induced by Leptin: Inhibitory Effect of Metformin
Ling Li, Jean-Claude Mamputu, Nicolas Wiernsperger, and Geneviève Renier
Diabetes 2005 54: 2227-2234. [Abstract] [Full Text] [PDF]

已完成 40 Long-Term Treatment With Rosiglitazone and Metformin Reduces the Extent of, but Does Not Prevent, Islet Amyloid Deposition in Mice Expressing the Gene for Human Islet Amyloid Polypeptide
Rebecca L. Hull, Zhen-Ping Shen, Melissah R. Watts, Keiichi Kodama, Darcy B. Carr, Kristina M. Utzschneider, Sakeneh Zraika, Feng Wang, and Steven E. Kahn
Diabetes 2005 54: 2235-2244. [Abstract] [Full Text] [PDF]

已完成 41 Brief Genetics Reports:
Genetic Variation in Adiponectin Receptor 1 and Adiponectin Receptor 2 Is Associated With Type 2 Diabetes in the Old Order Amish
Coleen M. Damcott, Sandra H. Ott, Toni I. Pollin, Laurie J. Reinhart, Jian Wang, Jeffrey R. O’Connell, Braxton D. Mitchell, and Alan R. Shuldiner
Diabetes 2005 54: 2245-2250. [Abstract] [Full Text] [PDF] Online-Only Appendix

已完成 42 Hepatic Lipase Gene Variant –514C>T Is Associated With Lipoprotein and Insulin Sensitivity Response to Regular Exercise: The HERITAGE Family Study
Margarita Teran-Garcia, Nicola Santoro, Tuomo Rankinen, Jean Bergeron, Treva Rice, Arthur S. Leon, D.C. Rao, James S. Skinner, Richard N. Bergman, Jean-Pierre Després, and Claude Bouchard
Diabetes 2005 54: 2251-2255. [Abstract] [Full Text] [PDF]

已完成 43 Polymorphisms in the SLC2A2 (GLUT2) Gene Are Associated With the Conversion From Impaired Glucose Tolerance to Type 2 Diabetes: The Finnish Diabetes Prevention Study
Olli Laukkanen, Jaana Lindström, Johan Eriksson, Timo T. Valle, Helena Hämäläinen, Pirjo Ilanne-Parikka, Sirkka Keinänen-Kiukaanniemi, Jaakko Tuomilehto, Matti Uusitupa, and Markku Laakso
Diabetes 2005 54: 2256-2260. [Abstract] [Full Text] [PDF]

已完成 44 Evidence of an Association Between the Arg72 Allele of the Peptide YY and Increased Risk of Type 2 Diabetes
Signe S. Torekov, Lesli H. Larsen, Charlotte Glümer, Knut Borch-Johnsen, Torben Jørgensen, Jens J. Holst, Ole D. Madsen, Torben Hansen, and Oluf Pedersen
Diabetes 2005 54: 2261-2265. [Abstract] [Full Text] [PDF]

45 Retraction:
Retraction
Franz M. Matschinsky
Diabetes 2005 54: 2266. [Extract] [Full Text] [PDF]

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2005-06-29 14:04 浏览 : 3595 回复 : 31

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knewmans 编辑于 2005-07-26 18:23

• 世卫组织称新冠病毒变异速度比流感慢

hsy3982

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第40和44篇摘要
40

Long-Term Treatment With Rosiglitazone and Metformin Reduces the Extent of, but Does Not Prevent, Islet Amyloid Deposition in Mice Expressing the Gene for Human Islet Amyloid Polypeptide
Rebecca L. Hull, Zhen-Ping Shen, Melissah R. Watts, Keiichi Kodama, Darcy B. Carr, Kristina M. Utzschneider, Sakeneh Zraika, Feng Wang, and Steven E. Kahn
Diabetes 2005 54: 2235-2244. [Abstract] [Full Text] [PDF]
长期罗格列酮与二甲双胍治疗能降低表达人胰岛淀粉样多肽小鼠基因的胰岛淀粉样沉积物形成程度但不能预防其发生
2型糖尿病胰岛淀粉样沉积物与ß细胞群有关。因此，能减少胰岛淀粉样沉积物形成的干预措施可能有助于保护2型糖尿病的ß细胞群。罗格列酮和二甲双胍通过两种不同的机制提高胰岛素敏感性，他们可以减少ß细胞分泌需求，这将导致胰岛素分泌和胰岛淀粉样多肽(IAPP)（IAPP是胰岛淀粉样沉积物的唯一成分）减少。我们假设降低ß细胞分泌需求可以减少胰岛淀粉样物质的生成。人IAPP (hIAPP)转基因小鼠是胰岛淀粉样物质的模型。分别给予hIAPP转基因小鼠罗格列酮(1.5 mg · kg–1 · day–1, n = 19)、二甲双胍(1 g · kg–1 · day–1, n = 18)12个月，对照组例数为17。试验结束时，检测胰岛淀粉样发生率（产生淀粉样物质胰岛所占的百分率）、胰岛重量、ß细胞群和胰岛素分泌。用罗格列酮和二甲双胍治疗后，胰岛淀粉样发生率（对照为44 ± 8%，二甲双胍治疗组为13 ± 4%，罗格列酮治疗组为11 ± 3%）和严重度（对照为9.2 ± 3.0%，二甲双胍治疗组为0.22 ± 0.11%，罗格列酮治疗组为0.10 ± 0.05%）明显降低（两种治疗方法两个指标均P<0.001）。这两种治疗方法均与胰岛素释放降低有关（胰岛素释放降低是静脉注射葡萄糖后的急性胰岛素反应。对照组、二甲双胍治疗组、罗格列酮治疗组小鼠胰岛素分别为2,189 ± 857, 621 ± 256, 14 ± 158 pmol/l；二甲双胍组与对照相比P < 0.05，洛格列酮组与对照相比P < 0.005）,该结果与分泌需求降低一致。与此相似，胰岛重量（对照组、二甲双胍治疗组、罗格列酮治疗组小鼠胰岛重量分别为33.4 ± 7.0 mg, 16.6 ± 3.6 mg, and 12.2 ± 2.1 mg）不随二甲双胍治疗变化(与对照组相比P = 0.06)，但随着罗格列酮治疗显著降低 (与对照组相比P < 0.05)。总之，罗格列酮和二甲双胍可以保护ß细胞免受胰岛淀粉样物质的有害作用，该作用可能有助于这两种药物减轻2型糖尿病ß细胞重量和功能的渐进性降低。

44
Evidence of an Association Between the Arg72 Allele of the Peptide YY and Increased Risk of Type 2 Diabetes
Signe S. Torekov, Lesli H. Larsen, Charlotte Glümer, Knut Borch-Johnsen, Torben Jørgensen, Jens J. Holst, Ole D. Madsen, Torben Hansen, and Oluf Pedersen
Diabetes 2005 54: 2261-2265. [Abstract] [Full Text] [PDF]
多肽YY激素Arg72等位基因与2型糖尿病危险性增高之间关联的证据

我们验证了编码前多肽原YY(PYY)基因的变异与2型糖尿病和/或肥胖关联的假说。对84名患有肥胖和家族性2型糖尿病的患者进行DNA突变分析后发现，PYY有两个基因多态性（即IVS3 + 68C>T和Arg72Thr）和一个罕见的变异即+151C>A。常见的Arg72Thr等位基因型与2型糖尿病有关， 4639名能耐受葡萄糖的研究对象中Arg等位基因的等位基因率为0.667(95% 可信区间为0.658–0.677)，1326名伴有超重(25 < BMI < 30 kg/m2)的2型糖尿病患者精氨酸等位基因率为0.692 (0.674–0.710) (P = 0.005, 优势比为1.19 [95%可信区间 1.05–1.35])。Arg72Thr等位基因型与超重(25 BMI < 30 kg/m2)有关(P = 0.018, 1.15 [1.02–1.28])。对6022名研究对象进行数量特征分析，Arg等位基因与葡萄糖耐量试验(OGTT)后2小时血糖水平增高有关(P = 0.03),与葡萄糖耐量试验后血糖曲线下面积升高有关(P = 0.03)，还与低胰岛素源性指数有关(P = 0.01)。总之，PYY 常见Arg等位基因型Arg72Thr很可能与2型糖尿病以及2型糖尿病相关数量特征有关。

2005-06-29 21:35

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hsy3982 编辑于 2005-06-30 15:53

• 教育部：今年国家定向培养免费医学生，你会报考吗？——回帖

yuc018

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1.Perspectives in Diabetes

Nutritional Epigenomics of Metabolic Syndrome
New Perspective Against the Epidemic
Catherine Gallou-Kabani, and Claudine Junien
Institut National de la Santé et de la Recherche Médicale (INSERM) Unit 383, Clinique Maurice Lamy, Hôpital Necker-Enfants Malades, Paris, France

Human epidemiological studies and appropriately designed dietary interventions in animal models have provided considerable evidence to suggest that maternal nutritional imbalance and metabolic disturbances, during critical time windows of development, may have a persistent effect on the health of the offspring and may even be transmitted to the next generation. We now need to explain the mechanisms involved in generating such responses. The idea that epigenetic changes associated with chromatin remodeling and regulation of gene expression underlie the developmental programming of metabolic syndrome is gaining acceptance. Epigenetic alterations have been known to be of importance in cancer for 2 decades. This has made it possible to decipher epigenetic codes and machinery and has led to the development of a new generation of drugs now in clinical trials. Although less conspicuous, epigenetic alterations have also been progressively shown to be relevant to common diseases such as atherosclerosis and type 2 diabetes. Imprinted genes, with their key roles in controlling feto-placental nutrient supply and demand and their epigenetic lability in response to nutrients, may play an important role in adaptation/evolution. The combination of these various lines of research on epigenetic programming processes has highlighted new possibilities for the prevention and treatment of metabolic syndrome.

Address correspondence and reprint requests to Claudine Junien Pharm D, PhD, INSERM Unit 383, Clinique Maurice Lamy, porte 15, Hôpital Necker-Enfants Malades, 149 rue de Sèvres, 75743 Paris, France. E-mail: junien@necker.fr

________________________________________________
代谢综合征的营养性表基因组学研究——对该流行病的新观察

在多种人类流行病学研究及在科学设计的动物模型饮食干预试验中，已得到大量证据，表明在胎儿发育关键时期的母体营养失衡和各种代谢紊乱,会对子代的健康有持续稳固的影响，这种影响作用甚至还会进一步传递。本文中，我们要解释产生这种现象的机制。伴随染色质重构和基因表达调整的表遗传改变，是代谢综合征起病的基础，这一观点正得到越来越多的支持。表遗传改变在癌症中的重要性的认识已经有二十余年，表遗传密码及其体系已能加以解释，据此开发的一类新一代药物现已进入临床研究。虽然不很明显，表遗传改变与常见病如动脉硬化及2型糖尿病有相关性正不断地得到揭示。有印记的基因、这种基因在控制胎儿胎盘营养供给和需求中的重要作用及其对营养响应的表遗传易变性，在适应环境和进化过程中可能起重要作用。综合上述表遗传计划行动研究的各种信息，明确了代谢综合征防治的新的可能性。

2005-06-30 01:33

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yuc018 编辑于 2005-06-30 01:42

• 调查：你们医院发年终奖吗？

paulinexu

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33
Metformin Prevents High-Glucose–Induced Endothelial Cell Death Through a Mitochondrial Permeability Transition-Dependent Process
二甲双胍通过线粒体通透性转运依赖程序预防高血糖诱导的内皮细胞死亡

Hyperglycemia-induced oxidative stress is detrimental for endothelial cells, contributing to the vascular complications of diabetes.
高血糖诱导的氧化应激对内皮细胞是有害的, 并由此导致糖尿病血管并发症.

The mitochondrial permeability transition pore (PTP) is an oxidative stress–sensitive channel involved in cell death;
线粒体通透性转运孔(PTP)是参于细胞死亡的氧化应激敏感通道.

therefore, we have examined its potential role in endothelial cells exposed to oxidative stress or high glucose level.
所以, 我们检测了它在内皮细胞暴露于氧化应激或高糖水平时可能的作用.

Metformin, an antihyperglycemic agent used in type 2 diabetes, was also investigated because it inhibits PTP opening in transformed cell lines.
二甲双胍是用于治疗2型糖尿病的降糖药, 能够抑制转化细胞系PTP的开放, 所以我们对其进行调查.

Cyclosporin A (CsA), the reference PTP inhibitor, and a therapeutic dose of metformin (100 µmol/l) led to PTP inhibition in permeabilized human microvascular endothelial cells (HMEC-1).
环胞霉素 A (CsA, PTP抑制剂) , 和治疗剂量的二甲双胍(100 µmol/l) 抑制了具有渗透性的人微血管内皮细胞(HMEC-1)的PTP.

Furthermore, exposure of intact HMEC-1 or primary endothelial cells from either human umbilical vein or bovine aorta to the oxidizing agent tert-butylhydroperoxide or to 30 mmol/l glucose triggered PTP opening, cytochrome c decompartmentalization, and cell death.
另外, 将人脐静脉或小牛动脉的未经处理的HMEC-1或原始的内皮细胞暴露在氧化剂过氧化叔丁醇或30mmol/l葡萄糖中, 触发PTP的开放, 细胞色素c 的失分隔作用, 及细胞死亡.

CsA or metformin prevented all of these effects. The antioxidant N-acetyl-L-cysteine also prevented hyperglycemia-induced apoptosis.
CsA或二甲双胍预防了上述效应. 抗氧化剂N-乙酰基-L-半胱氨酸也能够防止高血糖诱导的细胞凋亡.

We conclude that 1) elevated glucose concentration leads to an oxidative stress that favors PTP opening and subsequent cell death in several endothelial cell types and 2) metformin prevents this PTP opening–related cell death. We propose that metformin improves diabetes-associated vascular disease both by lowering blood glucose and by its effect on PTP regulation.
我们认为, 1) 在几种内皮细胞中, 血糖水平升高产生氧化应激, PTP开放, 结果导致细胞死亡. 2) 二甲双胍预防了PTP开放相关的细胞死亡. 我们认为二甲双胍改善糖尿病相关的血管疾病是通过降糖及调节PTP效应的双重作用而实现的.

Diabetes 54:2179-2187, 2005

2005-06-30 13:40

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paulinexu 编辑于 2005-07-01 14:17

• 综合医院全科门诊中乏力患者特征及就诊原因分析

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