请进 http://thelancet.cn/dnn1201/tabid/65/ArticleID/726/cid/707/Default.aspx 中文标题: 在稳定型冠心病伴左室收缩功能障碍的患者中应用伊伐布雷定（BEAUTIFUL）：一项随机、双盲、安慰剂对照试验 英文标题: Ivabradine for patients with stable coronary artery disease and left-ventricular systolic dysfunction (BEAUTIFUL): a randomised, double-blind, placebo-controlled trial 作者: Kim Fox, Ian Ford, P Gabriel Steg, Michal Tendera, Roberto Ferrari, on behalf of the BEAUTIFUL Investigators*
请进 http://thelancet.cn/dnn1201/tabid/65/ArticleID/40/cid/707/Default.aspx 中文标题: 心率作为冠心病与左室收缩障碍患者的预后危险因素（BEAUTIFUL）：一项随机、对照试验的一个亚组分析 英文标题: Heart rate as a prognostic risk factor in patients with coronary artery disease and left-ventricular systolic dysfunction (BEAUTIFUL): a subgroup analysis of a randomised controlled trial 作者: Kim Fox, Ian Ford, P Gabriel Steg, Michal Tendera, Michele Robertson, Roberto Ferrari, on behalf of the BEAUTIFUL investigators
国内文献分析结果 1 脂肪类 7 41.1765% 2 动脉硬化 6 35.2941% 3 冠状动脉疾病 5 29.4118% 4 脂细胞 4 23.5294% 5 糖尿病, 2型 3 17.6471% 6 代谢综合征X 2 11.7647% 7 胞间信号肽类和蛋白质类 2 11.7647% 8 肿瘤坏死因子 2 11.7647% 9 肥胖症 2 11.7647% 10 细胞因子类 2 11.7647% 1 曾鸿毅 2 11.7647% 2 常志文 2 11.7647% 3 阎鸿 1 5.8824% 4 张玮 1 5.8824% 5 谢谦 1 5.8824% 6 王巍 1 5.8824% 7 罗敏 1 5.8824% 8 王卉 1 5.8824% 9 柴若楠 1 5.8824% 10 姜德健 1 5.8824% 1 河北省唐山市妇幼保健院妇产科, 063000 1 5.8824% 2 上海市糖尿病研究所上海市糖尿病临床医学中心上海交通大学附属第六人民医院, 200233 1 5.8824% 3 (2)中南大学湘雅三医院超声科 1 5.8824% 4 (4)沈阳医学院环境教研室,沈阳110031 1 5.8824% 5 (1)青海大学医学院 1 5.8824% 6 (1)中南大学湘雅三医院心内科,长沙410013 1 5.8824% 7 上海交通大学医学院附属瑞金医院,上海市内分泌代谢病研究所, 200025 1 5.8824% 8 (2)四川大学华西医院心血管疾病研究室 1 5.8824% 9 (3)中南大学药学院 1 5.8824% 10 广西医科大学第五附属医院核医学科,柳州 545001 1 5.8824% 1 中华医学杂志 1 5.8824% 2 青海医学院学报 1 5.8824% 3 临床心血管病杂志 1 5.8824% 4 热带医学杂志 1 5.8824% 5 放射免疫学杂志 1 5.8824% 6 第三军医大学学报 1 5.8824% 7 中国医药导刊 1 5.8824% 8 中国慢性病预防与控制 1 5.8824% 9 北京医学 1 5.8824% 10 河北医药 1 5.8824% 1. 【分类号】:R322.74;R344.2;R543.5;R589;*R589.2;R977.6 【标题】:内脂素与代谢综合征关系的研究进展 【作者】:王桢(综述);张薇(审校) 【作者单位】:教育部和卫生部心血管重构和功能研究重点实验室:山东大学齐鲁医院心内科,山东济南 250012 【摘要】:内脂素是新近发现的由内脏脂肪细胞分泌的一种脂肪因子,与前B细胞克隆增强因子结构相同,具有胰岛素样作用、能促进脂肪的积聚和合成、参与动脉粥样硬化的形成、调节血管平滑肌的成熟,因此内脂素可能是联系糖脂代谢紊乱以及心血管疾病的新纽带,这为代谢综合征的防治提供了新的方向。但目前的研究方法尚不完善,研究结论不统一,尚有大量工作需要去做。 【出处】:心血管病学进展 2009;30(2) 226-229 【关键词】:内脂素;内脏脂肪;糖尿病;动脉粥样硬化;代谢综合征 【主题词】:B淋巴细胞;*代谢综合征X;*动脉硬化;*肌, 平滑, 血管;内脏;糖脂类/代谢;心血管疾病;*脂肪类;综述 【特征词】:人类 2. 【分类号】:R322;R322.12;R344.2;R543.5;*R544.2;R977.6 【标题】:内脏脂肪素与动脉粥样硬化及血管内皮功能相关性的研究 【作者】:曹宇(1);肖丽(2);肖坚(3);姜德健(3) 【作者单位】:(1)中南大学湘雅三医院心内科,长沙410013; (2)中南大学湘雅三医院超声科; (3)中南大学药学院 【摘要】:目的:通过测定不同动脉粥样硬化(AS)程度受试者的血浆内脏脂肪素(Visfatin)水平并评估内皮功能状态,探讨血浆Visfatin在AS发生发展及血管内皮功能紊乱中的意义。方法:62例接受冠状动脉造影和颈总动脉、肱动脉超声检测的患者,采用Gensini积分系统和测定颈总动脉内-中膜厚度(IMT)评价AS严重程度后分为对照组、早期AS组、严重AS组。采用超声检测肱动脉血流介导的血管扩张(FMD)评估各组血管内皮功能。同时检测各组血浆Visfatin水平,并将其与颈总动脉IMT、冠状动脉Gensini积分及肱动脉FMD进行相关性分析。结果:①与对照组比较,AS组血浆Visfatin水平显著升高,且严重AS组高于早期AS组(PO.01);②血浆Visfatin水平与颈总动脉IMT呈正相关(r=0.475;P0.01);③血浆Visfatin水平与冠状动脉Gensini积分呈正相关(r=0.359;P0.01);④血浆Visfatin水平与肱动脉FMD呈负相关(r=-0.488;P0.01)。结论:血浆Visfatin水平与AS的发生和发展密切相关。AS患者血浆Visfatin水平的高低能初步反映血管内皮功能受损的状况和As的严重程度,提示血浆Visfatin水平可能是一个新的心血管疾病预测因子。 【出处】:临床心血管病杂志 2009;25(3) 212-215 【关键词】:内脏脂肪素;动脉粥样硬化;血管内皮功能 【主题词】:*动脉硬化;冠状血管;颈总动脉;内皮;*内皮, 血管;*内脏;*脂肪类;肱动脉 【特征词】:人类 3. 【分类号】:*R341;R543.304;R587.1 【标题】:血清内脂素在2型糖尿病合并冠心病中的临床意义 【作者】:柴若楠(1);吕肖峰(1);张绍维(2);阎鸿(3);李鹏飞(4);刘静(5);王巍(2);罗晶(2);徐涤非(2);高伟(2) 【作者单位】:(1)北京军区总医院内分泌科,北京100000; (2)解放军202医院内分泌科,沈阳110005; (3)解放军202医院急诊科,沈阳110005; (4)沈阳医学院环境教研室,沈阳110031; (5)第三军医大学新桥医院检验科,重庆 400038 【摘要】:目的:分析血清内脂素在2型糖尿病及其合并冠心病中的变化,并探讨内脂素与糖尿病或/和冠心病的相关关系。方法:依据WHO的糖尿病诊断标准随机选择2型糖尿病(T2DM)患者61例,经心电图及冠脉造影检查分为:单纯T2DM组(DM)18例、T2DM合并冠心病(CHD)组(DC)43例以及正常对照组(NC)29例,其中DM组均为新诊断患者。经统计学分析3组间一般资料具有可比性。结果:DM组及DC组血清内脂素浓度水平显著高于健康人对照组(t=4.9921,P0.05;t=4.722,P0.05)。DC组患者血清内脂素水平与DM组对照组有显著下降(t=4.236,P0.05)。结论:2型糖尿病患者内脂素水平下降可能提示冠心病的发生或加重,在2型糖尿病合并冠心病诊断和治疗中可能具有一定的意义。 【出处】:第三军医大学学报 2009;31(5) 454-456 【关键词】:糖尿病;内脂素;2型糖尿病合并冠心病;降糖作用 【主题词】:冠状动脉疾病/*诊断;冠状血管造影术;世界卫生组织;*糖尿病;*糖尿病, 2型;统计学(主题);心电描记术 【特征词】:人类 4. 【分类号】:R446.112;*R541.4;R543.3;R816 【标题】:冠心病患者血浆内脂素水平的初步研究 【作者】:付华(1);祝烨(1);游桂英(1);刘小菁(2) 【作者单位】:(1)四川大学华西医院心内科,成都610041; (2)四川大学华西医院心血管疾病研究室 【摘要】:目的:比较冠心病患者和正常人血浆中内脂素(visfatin)水平,并评价血浆visfatin水平与冠脉病变程度的相关关系。方法:对48例冠心病患者(均接受冠脉造影确诊)及41例健康志愿者抽血测定血浆内脂素水平,并进行比较。同时记录冠心病患者冠脉病变支数及Gensini冠脉病变积分,与血浆内脂素水平进行相关性分析。结果:冠心病组血浆内脂素水平为(28.5814.53)ng/mL,对照组血浆内脂素水平为(16.016.09)ng/mL,冠心病组明显高于对照组,两组比较有统计学差异(PO.01)。血浆内脂素水平与冠脉病变支数呈正相关(r=0.762,P0.01);与Gensini冠脉病变积分呈显著正相关(r=0.906,P0.01)。结论:检测血浆内脂素水平有助于冠心病的早期诊断;血浆内脂素水平越高,冠脉病变程度越严重。 【出处】:四川大学学报医学版 2009;40(2) 322-324 【关键词】:冠心病;内脂素;Gensini评分 【主题词】:*冠状动脉疾病;*冠状血管造影术;统计学(主题);*血样采集;早期诊断;志愿工作者 【特征词】:人类 5. 【分类号】:*R587.1;R344.2;R345.57;R543.5;R977.3;R977.6 【标题】:内脂素与糖尿病及动脉粥样硬化的关系 【作者】:王卉;常志文 【作者单位】:首都医科大学附属北京同仁医院干部医疗科,北京 100730 【摘要】:近来大量研究表明脂肪组织是重要的内分泌器官,能够分泌多种脂肪因子,与肥胖、胰岛素抵抗、2型糖尿病(DM)、心血管疾病等密切相关。内脂素(Visfatin)是其中一种脂肪因子,与胰岛素受体结合并活化产生类胰岛素作用。本文就其目前国内外研究现状做一概述。 【出处】:中国医药导刊 2008;10(9) 1344-1346 【关键词】:动脉粥样硬化;内脂素;糖尿病 【主题词】:*动脉硬化;肥胖症;内分泌腺;*受体, 胰岛素;*糖尿病;心血管疾病;胰岛素;*脂肪类 6. 【分类号】:*R589;R-05;R319;R329.24;R347;R977.1 【标题】:内脂素与代谢综合征关系的研究进展 【作者】:张冰;苏胜偶 【作者单位】:河北医科大学第二医院内分泌科,河北石家庄 050000 【摘要】:脂肪组织不仅能储存能量,而且是人体最大的内分泌器官,已发现可分泌几十种具有生物活性的脂肪细胞因子:瘦素、脂联素、抵抗素、肿瘤坏死因子、内脂素等。这些因子形成具有一定层次、错综复杂的代谢一神经内分泌一免疫网络,以应对性质各异的代谢性问题。其中内脂素是新近发现的一种脂肪细胞因子,主要由内脏脂肪产生,具有类胰岛素活性,参与代谢综合征(MS)各组分如肥胖、2型糖尿病(T2DM)、脂肪肝等的发生,并直接作用于血管,促进动脉粥样硬化的发生发展。目前对内脂素与MS的关系尚有争议,现就此综述如下。 【出处】:临床荟萃 2008;23(24) 1807-1808 【关键词】:代谢综合征X;内脂素;信息研究 【主题词】:*代谢综合征X;动脉硬化;肥胖症;*激素类, 异位;*计算机通信网络;内分泌腺;内脏;*脂细胞;综述 7. 【分类号】:*R587.1;R543.3 【标题】:2型糖尿病伴冠心病及冠心病患者血清内脂素水平的研究 【作者】:曾鸿毅;邹劲涛 【作者单位】:广西医科大学第五附属医院核医学科,柳州 545001 【摘要】:目的:探讨血清内脂素在2型糖尿病伴冠心病及冠心病患者中的作用。方法:采用酶联免疫法(EusA)对临床上确诊为2型糖尿病伴冠心病患者64例,冠心病患者85例及健康对照组30例,进行血清内脂素水平的测定。结果:2型糖尿病伴冠心病组及冠心病组的血清内脂素水平明显高于正常对照组(P0.01),有统计学意义。结论:血清内脂素在2型糖尿病的发生和发展中具有一定的生理作用,并可能对冠心病的发生和发展中也具有一定的生理作用。 【出处】:热带医学杂志 2008;8(10) 1044-1045 【关键词】:2型糖尿病;冠心病;内脂素;糖尿病 【主题词】:*冠状动脉疾病;酶联免疫吸附测定;*糖尿病, 2型;统计学(主题) 【特征词】:人类 8. 【分类号】:R329.24;R341;R458.5;*R587.1;R915;R977.6 【标题】:脂肪细胞因子与胰岛素抵抗:共识与分歧 【作者】:贾伟平 【作者单位】:上海市糖尿病研究所上海市糖尿病临床医学中心上海交通大学附属第六人民医院, 200233 【摘要】:胰岛素抵抗不仅是糖尿病的病因之一,也是高血压、血脂异常及动脉粥样硬化的共同危险因素。已明确肥胖是导致胰岛素抵抗发生的重要原因之一。近年研究见到,肥胖发生胰岛素抵抗的机制不仅受底物代谢(游离脂肪酸)及神经内分泌调节的影响,更与脂肪细胞因子的变化有关。脂肪细胞因子是由脂肪组织所分泌的。研究报道与胰岛素抵抗有关的脂肪细胞因子主要有瘦素、脂联素、内脂素、 【出处】:中华医学杂志 2008;88(6) 363-364 【主题词】:*胰岛素抗药性;*脂细胞;*细胞因子类 9. 【分类号】:R329.24;R331.32;R341.3;R341.32;*R587.2;R977.6 【标题】:测定视黄醇结合蛋白-4的临床意义 【作者】:高璐;常志文 【作者单位】:首都医科大学附属北京同仁医院干部医疗科, 100730 【摘要】:脂肪组织一直被认为是惰性的能量储存器官.现在人们认识到脂肪组织还是个在机体能量代谢过程中起关键作用的内分泌器官。由脂肪细胞合成分泌的功能蛋白或多肽激素称为脂肪细胞因子.如脂联素、瘦素、抵抗素、内脂素、肿瘤坏死因子(TNF-)等,它们参与细胞凋亡、血管再生、神经免疫、炎症反应等生理和病理生理调节,影响血糖、血脂等代谢,并可直接作用于血管,促进动脉粥样硬化的发生、发展。 【出处】:北京医学 2008;30(9) 555-557 【主题词】:内分泌腺;能量代谢;神经免疫调节;*视黄醇结合蛋白质类;血管/*生理学;脂肪组织;*脂细胞;*肿瘤坏死因子;综述 【特征词】:人类 10. 【分类号】:R341;R341.32;R344.2;*R364.2;R543.5;R977.6 【标题】:脂联素-一种负性脂肪因子 【作者】:谢谦;张帆;胡小平 【作者单位】:北京大学深圳医院内分泌科,广东深圳 518036 【摘要】:脂肪组织能够以旁分泌、自分泌和远距分泌方式产生生物活性因子或因子样分子,称为脂肪因子。包括肿瘤坏死因子(TNF-)、酰化刺激蛋白、瘦素、纤溶酶原激活剂抑制因子1(PAI-1)、白细胞介素6(IL-6)、抵抗素(resistin)、脂联素(adiponectin,ADP)、人内脂素(visfatin)等多种因子,这些脂肪因子影响胰岛素敏感性、血压水平、内皮功能、纤溶活动及炎症反应,参与机体多种重要病理生理过程。在众多功能各异的脂肪细胞因子中,脂连素是迄今为止所发现的唯一与肥胖呈负相关的细胞因子,有降低三酰甘油和血糖水平、改善胰岛素抵抗、保护心血管内皮功能和抑制动脉粥样硬化形成等作用。 【出处】:临床和实验医学杂志 2008;7(8) 186,191 【主题词】:*胞间信号肽类和蛋白质类;*动脉硬化;肥胖症;激素类, 异位;内皮;瘦素;*脂肪类;*肿瘤坏死因子;综述 【特征词】:人类 11. 【分类号】:R322.121;R323.3;R543.5;*R587.1 【标题】:血浆Visfatin与2型糖尿病颈动脉粥样硬化的关系 【作者】:吴爱兵(1);卢承德(2);高继东(2);张惠莉(2);刘洪(1);曹越(1) 【作者单位】:(1)青海大学医学院; (2)青海大学附属医院内分泌科 【摘要】:目的:探讨血浆内脏脂肪素(visfatin)水平与2型糖尿病(T2DM)患者发生动脉粥样硬化的关系。方法:采用酶联免疫吸附法测定T2DM患者和正常人空腹血浆visfatin水平,并在伴或不伴颈动脉粥样硬化的T2DM患者及正常对照组之间比较。结果:T2DM组的空腹血浆visfatin水平均显著高于正常对照组(P均0.05);伴颈动脉粥样硬化T2DM组空腹血浆visfatin水平明显高于不伴颈动脉粥样硬化T2DM组(P0.05)。多元逐步回归分析表明:血浆visfatin水平升高主要受代谢综合征构成成份累积的影响而Logistic回归则显示动脉粥样硬化会受到代谢综合征的构成成分、C反应蛋白和visfatin的影响并且与颈动脉粥样硬化(AC)密切相关。结论:visfatin可能与T2DM颈动脉粥样硬化的发生和发展相关。 【出处】:青海医学院学报 2008;(1) 7-10 【关键词】:2型糖尿病;颈动脉粥样硬化;内脏脂肪素 【主题词】:代谢综合征X;*动脉硬化;多元分析;*腹部;*颈动脉;酶联免疫吸附测定;内脏;*糖尿病, 2型 【特征词】:人类 12. 【分类号】:R197.3;R329.24;R341;R344.2;*R71;R977.6 【标题】:脂联素在妇产科的研究进展 【作者】:刘丽俊;陈茜松;季淑英;张玮 【作者单位】:河北省唐山市妇幼保健院妇产科, 063000 【摘要】:随着众多脂肪细胞因子的不断发现,如瘦素、抵抗素、脂肪源性TNF-、Ⅰ型纤溶酶原激活剂抑制物1(PAI-1)、IL-6、内脏脂肪素和脂联素(adiponectin,APN)等,人们认识到脂肪组织不仅仅是一个贮能器官,而且它还具有丰富的分泌功能,从而成为众多学者研究的热点。APN是由脂肪细胞分泌的一种糖蛋白,参与机体葡萄糖的平衡调节及脂质代谢,对胰岛素敏感性调节、抗炎症发生及抗动脉粥样硬化的影响意义深远。近年研究发现APN对多囊卵巢综合征、妊娠期糖尿病和妊娠期高血压疾病等妇产科疾病的发生、发展有一定作用。 【出处】:河北医药 2008;30(5) 682-684 【主题词】:*胞间信号肽类和蛋白质类;*妇产科, 医院;肌肉骨骼平衡;内脏;葡萄糖;纤溶酶原激活物抑制物1;*脂肪类;*脂细胞;综述 【特征词】:女(雌)性;人类;妊娠 13. 【分类号】:R322.5;R329.52;R344.2;*R589.2;R977.6 【标题】:Visfatin研究进展 【作者】:林奉森;陈兆樵 【作者单位】:宁德市医院, 352100 【摘要】:肥胖症是一种以体脂的过度堆积和异常分布为特征的内分泌代谢疾病,是代谢综合征的重要因素之一。肥胖可以增加2型糖尿病、高血压和冠心病等相关疾病的危险性,已逐渐成为二十一世纪影响人们健康的主要问题之一。然而,并非每一种类型的肥胖都会威胁公众的健康,充分的流行病学证据显示内脏脂肪即环绕胃肠器官周围的脂肪组织的过度堆积较皮下脂肪堆积具有更大的危险性,因此体脂的分布可能比体脂的总量显得更为重要。但是,不同部位脂肪组织的过度膨胀导致糖尿病和心血管疾病危险性增加的确切机制尚不清楚,目前普遍认为与脂肪因子密切相关。 【出处】:福建医药杂志 2008;30(1) 102-103 【主题词】:代谢综合征X;*肥胖症;冠状动脉疾病;内分泌腺/*代谢;内脏;糖尿病, 2型;*脂肪类;*脂肪组织;综述 【特征词】:人类 14. 【分类号】:R543.3;*R587.1 【标题】:血清内脂素水平检测在2型糖尿病伴冠心病中的临床意义 【作者】:曾鸿毅 【作者单位】:广西医科大学第五附属医院核医学科, 545001 【摘要】:目的:探讨血清内脂素水平在2型糖尿病伴冠心病中的临床意义。方法:用酶联免疫法(ELISA)对临床上确诊为2型糖尿病伴冠心病患者33例,健康对照组30例,进行内脂素水平的测定。结果:2型糖尿病伴冠心病组的血清内脂素水平明显高于正常对照组(P0.01),有显著的差异性。结论:血清内脂素在2型糖尿病伴冠心病的病理生理机制中有一定的相关性。 【出处】:放射免疫学杂志 2008;21(1) 70-71 【主题词】:*冠状动脉疾病;酶联免疫吸附测定;糖尿病, 2型 【特征词】:人类 15. 【分类号】:R341;R344;R347;*R541.4;R543.302.5;R730.3;R977.1;R977.6 【标题】:内脂素与冠心病危险因素 【作者】:胡明磊;胡世红 【作者单位】:广西医科大学第五附属医院/柳州市人民医院心内科, 530021 【摘要】:最近研究发现脂肪组织可以分泌许多的细胞因子,如抵抗素(resistin)、瘦素(leptin)、脂联素(adiponectin)、肿瘤坏死因子(TNF-a)、纤溶酶原激活物抑制剂1(PAI-1)等,各自具有重要的生物学功能。最近研究发现内脂素具有调节糖、脂代谢、提高胰岛素敏感性及抗动脉粥样硬化等作用,与脂代谢、糖代谢、肥胖、炎症、斑块及代谢综合征等危险因素关系十分密切.本文就内脂素与冠心病危险因素相关性研究进展做一综述。 【出处】:医学研究杂志 2008;37(2) 8-10 【主题词】:冠状动脉疾病/*病因学;激素类, 异位;葡萄糖/代谢;生物学;*瘦素;纤溶酶原激活物抑制物1;脂类/*代谢;*肿瘤坏死因子类 16. 【分类号】:R329.24;R344.2;*R364.2;R364.5;R543.5;R977.6 【标题】:一个新识别出的脂肪因子Visfatin 【摘要】:Visfatin是一个新近确认的脂肪因子,由脂肪组织、骨髓、骨骼肌、肝产生。Dahl报道,它表达于颈动脉粥样斑硬化病变中的富含脂质的巨噬细胞。症状性病人颈动脉斑块表达增加。在功能的水平上,外周血的单核细胞中,它有强力的基质降解和炎症作用。有多篇报道反映它具有代谢作用,尤其可能与糖尿病及代谢综合征有关。Dahl的结果还提示,它是炎症的介质。局限于不稳定粥样硬化病变的泡沫细胞巨噬细胞可能在斑块不稳定中起一定作用。进一步强调了动脉粥样硬化形成中脂质积聚与炎症的关系。 【出处】:中国慢性病预防与控制 2007;15(2) 149 【主题词】:*动脉硬化;骨髓;肌, 骨骼;颈动脉;*巨噬细胞;*炎症;*脂肪类;脂类 【特征词】:人类 17. 【分类号】:R341;*R364.2;R589.2;R977.6 【标题】:内脏素又一新的脂肪因子 【作者】:徐伟斌;俞璐;罗敏 【作者单位】:上海交通大学医学院附属瑞金医院,上海市内分泌代谢病研究所, 200025 【摘要】:近年来的研究表明,脂肪组织不仅是机体储存能量的场所,还是功能活跃的内分泌器官,分泌多种生物活性分子,如瘦素、脂联素、抵抗素等,统称脂肪因子。目前认为,肥胖导致脂肪因子分泌失调,参与了多种肥胖相关性疾病的发生,如胰岛素抵抗、代谢综合征、2型糖尿病、动脉粥样硬化等。最近,Fukuhara等利用DD-PCR技术发现了又一新的脂肪因子,命名为内脏素,序列分析显示内脏素即为前B细胞克隆增强因子(PBEF)。本文就内脏素的相关研究作一综述。 【出处】:中国糖尿病杂志 2006;14(2) 153-154,157 【主题词】:肥胖症/*代谢;聚合酶链反应;*细胞因子类;综述 外文文献计量分析结果 16 documents semantically analyzed Top Years Publications 2009 7 2008 6 2007 2 2006 1 Top Countries Publications China 3 USA 3 Poland 2 Serbia 1 Germany 1 Turkey 1 South Korea 1 Taiwan 1 India 1 Norway 1 United Kingdom 1 Top Cities Publications Bia?ystok 2 Nanjing 1 Belgrade 1 Nashville 1 Chengdu 1 Beijing 1 Mainz 1 Louisville 1 Seoul 1 Newark 1 Chennai 1 Oslo 1 London 1 Top Journals Publications Int Urol Nephrol 1 Clin Chim Acta 1 Med Pregl 1 Lupus 1 Sichuan Da Xue Xue Bao Yi Xue Ban 1 Transplant P 1 Clin Endocrinol (oxf) 1 Clin Lab 1 Int J Cardiol 1 J Ky Med Assoc 1 Eur J Endocrinol 1 Biol Chem 1 Int J Obes (lond) 1 Metabolism 1 Circulation 1 Hum Mol Genet 1 1 2 3 ... 16 Top Terms Publications Nicotinamide Phosphoribosyltransferase 16 Coronary Disease 15 Adipokines 13 Coronary Artery Disease 12 visfatin 12 Humans 12 Coronary Vessels 11 Patients 11 Arteries 11 Middle Aged 8 Adiposity 7 Inflammation 7 Obesity 7 Insulin 7 receptor binding 7 insulin 7 Atherosclerosis 7 Heart Diseases 6 Case-Control Studies 6 adiponectin binding 6 1 2 3 ... 16 1 2 3 4 5 Top Authors Publications Huang J 1 Yan J 1 Tang N 1 Tang J 1 Jia E 1 Wang M 1 Wang Q 1 Zhu J 1 Yang Z 1 Wang L 1 Stein C 1 Chung C 1 Long A 1 Solus J 1 Rho Y 1 Oeser A 1 Raggi P 1 Liu X 1 Fu H 1 Zhu Y 1 1 2 3 4 5 相关研究论文 PMID- 19908160 OWN - NLM STAT- Publisher DA - 20091112 IS - 1573-2584 (Electronic) DP - 2009 Nov 12 TI - Type of arteriovenous fistula, NYHA class and apelin in hemodialyzed patients. AB - Apelin, a newly discovered adipocytokine, is produced by white adipose tissue and also expressed in kidney and heart. Increasing evidence suggests a role for apelin in the pathology of the cardiovascular system. It was demonstrated that apelin may contribute to the pathophysiology of human chronic heart failure. Apelin locates at the endothelium-a site of key functional importance in the kidney, and apelin has been shown to increase cardiac output. Cardiovascular disease is a major contributor to the mortality and morbidity of patients with chronic renal failure. We previously found that apelin was significantly lower in dialyzed patients with coronary artery disease and its level was predicted by cardiac function. Creation of a-v fistula might contribute to the development or worsening of chronic heart failure. The aim of this study was to assess associations between apelin, other adipocytokines, NYHA class and location of a-v fistula in hemodialyzed patients. This cross-sectional study was performed on a cohort of one hundred, clinically stable hemodialyzed patients. We investigated plasma apelin as well other adipocytokines: resistin, visfatin and von Willebrand factor (vWF)-a marker of endothelial cell injury. In patients with a-v fistula on the forearm (n = 77), apelin was significantly higher than in patients with a-v fistula on the arm (n = 23) (56.79 +/- 23.56 vs. 43.12 +/- 23.19 pg/ml). Patients with forearm a-v fistula had lower left ventricular internal end-diastolic dimension (LVIDd) (P 0.05), left ventricular internal end-systolic dimension (LVISd) (P 0.05), NYHA class (P 0.05), hsCRP (P 0.01), plasma vWF (P 0.01), and plasma resistin (P 0.05), whereas the ejection fraction was higher than in patients with arm a-v fistula (P 0.05), as well as hemoglobin (P 0.05), hematocrit (P 0.01), prevalence of diabetes (n 0.05), prevalence of coronary heart disease (P 0.05), serum pH (P 0.05), serum bicarbonate (P 0.05). Apelin was related to echocardiographic parameters, presence of diabetes, coronary artery disease, chronic heart failure, NYHA class and serum lipids (total cholesterol, LDL, triglycerides), hsCRP, vWF, residual renal function, and Kt/V. In multiple logistic regression analysis, apelin was significantly associated with ejection fraction (beta value was -0.51, P = 0.007), the presence of diabetes (beta value 0.39, P = 0.049), a-v fistula arm location (beta value 0.42, P = 0.047). Multiple adjusted r (2) for variables in the equation = 0.45, F = 1.75, P = 0.04, SE of estimate = 20.85. Apelin level in dialyzed patients is predicted by cardiac function, presence of diabetes and location of a-v fistula. Apelin might be involved in the pathophysiology of cardiovascular disease in chronic renal failure. The arm location of the fistula might contribute to the development or the worsening of chronic heart failure in hemodialyzed patients. AD - Department of Nephrology and Transplantology, Medical University, 14 Zurawia, Bialystok, 15-540, Poland, jolmal@poczta.onet.pl . AU - Malyszko J AU - Kozminski P AU - Malyszko J AU - Mysliwiec M LA - ENG PT - JOURNAL ARTICLE DEP - 20091112 TA - Int Urol Nephrol JT - International urology and nephrology JID - 0262521 EDAT- 2009/11/13 06:00 MHDA- 2009/11/13 06:00 CRDT- 2009/11/13 06:00 PHST- 2009/02/22 PHST- 2009/10/17 PHST- 2009/11/12 AID - 10.1007/s11255-009-9667-1 PST - aheadofprint SO - Int Urol Nephrol. 2009 Nov 12. PMID- 19804767 OWN - NLM STAT- Publisher DA - 20091019 IS - 1873-3492 (Electronic) DP - 2009 Oct 3 TI - Genetic variant in visfatin gene promoter is associated with decreased risk of coronary artery disease in a Chinese population. AB - BACKGROUND: Visfatin is a newly identified pro-inflammatory adipokine expressed predominantly in visceral fat. Previous studies have suggested a role for visfatin in low-grade inflammation and regulation of lipid metabolism. Most recently, a genetic polymorphism -1535CT located in the visfatin gene promoter has been identified, and suggested to be associated with the regulation of visfatin expression, lipid levels. However, it is unclear whether this polymorphism has a linkage with CAD. METHODS: We conducted a hospital-based case-control study with 257 CAD patients and 292 controls to examine the potential association of the Visfatin -1535CT polymorphism with CAD. RESULTS: The frequencies of the CC, CT, and TT genotypes in cases were significantly different from those of controls (chi(2)=6.223, P=0.045). Subjects with the variant genotypes (CT+TT) had a 40% decreased risk of CAD relative to CC carriers (adjusted OR=0.60, 95%CI=0.40-0.89). Furthermore, the adjusted OR of a TT genotype for CAD was 0.52 (95%CI=0.31-0.87). There was a significant association between Visfatin -1535CT polymorphism and triglyceride levels in both CAD patients and controls (P=0.003, 0.018, respectively). In stratified analyses, the T allele was significantly associated with reduced risk of CAD in males, subjects with age 59years, and non-smokers. Moreover, a borderline statistical significance (P=0.058 for trend) was observed between the variant genotypes and severity of CAD. CONCLUSION: Our results suggested that Visfatin -1535CT polymorphism might be associated with reduced risk of CAD in a Chinese population. AD - Department of Cardiology, First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210029, Jiangsu Province, China. AU - Yan JJ AU - Tang NP AU - Tang JJ AU - Jia EZ AU - Wang MW AU - Wang QM AU - Zhu J AU - Yang ZJ AU - Wang LS AU - Huang J LA - ENG PT - JOURNAL ARTICLE DEP - 20091003 TA - Clin Chim Acta JT - Clinica chimica acta; international journal of clinical chemistry JID - 1302422 EDAT- 2009/10/07 06:00 MHDA- 2009/10/07 06:00 CRDT- 2009/10/07 06:00 PHST- 2009/03/28 PHST- 2009/09/27 PHST- 2009/09/29 AID - S0009-8981(09)00519-1 AID - 10.1016/j.cca.2009.09.033 PST - aheadofprint SO - Clin Chim Acta. 2009 Oct 3. PMID- 19702115 OWN - NLM STAT- MEDLINE DA - 20090825 DCOM- 20091001 LR - 20091109 IS - 0025-8105 (Print) VI - 62 Suppl 3 DP - 2009 TI - PG - 43-6 AB - The epidemic of obesity and overweight leads to many diseases including cardiovascular disease. Having an influence on function and heart structure, obesity and overweight are in connection with coronary heart disease, heart failure and sudden heart death. Cardiomyopathy in obesity (adipositas cordis) appears due to accumulation of adipose tissue between the heart muscle fibers and degeneration of myocites. The degeneration of myocardial could be due to lipotoxicity of free fatty acids in adipose tissue. The left ventricle hypertrophy, diastolic dysfunction, increasing blood volume, ejection fraction lead to heart failure. Obesity is low inflammation state with increased adipocitokine production from truncal adipose tissue which causes endothelial dysfunction and insulin resistance. Adipocitokines include leptin, adiponectin, resistin, visfatin, RBP 4 (retinol binding protein), angiotenzinogen, TNF alpha (tumor necrosis factor), PAI 1 (plazminogen activator inhibitor), fatty acids, sex steroids and different growth factors. Adipocitokines act synergistically or competitively with insulin, that explaining their impact on insulin resistance. Inflammatory citokines from adipose tissue could have influence on blood vessels endothelial function without their increase in plasma concentrations. AD - Klinicki centar Srbije, Beograd, Institut za endokrinologiju, dijabetes i bolesti metabolizma. FAU - Micic, Dragan AU - Micic D FAU - Polovina, Snezana AU - Polovina S LA - srp PT - English Abstract PT - Journal Article PT - Review PL - Serbia TA - Med Pregl JT - Medicinski pregled JID - 2985249R RN - 0 (Adipokines) SB - IM MH - Adipokines/*physiology MH - Atherosclerosis/etiology/*physiopathology MH - Humans MH - Insulin Resistance MH - Obesity/complications/*physiopathology RF - 36 EDAT- 2009/08/26 09:00 MHDA- 2009/10/02 06:00 CRDT- 2009/08/26 09:00 PST - ppublish SO - Med Pregl. 2009;62 Suppl 3:43-6. PMID- 19578104 OWN - NLM STAT- MEDLINE DA - 20090706 DCOM- 20091022 IS - 0961-2033 (Print) VI - 18 IP - 9 DP - 2009 Aug TI - Adipocytokines in systemic lupus erythematosus: relationship to inflammation, insulin resistance and coronary atherosclerosis. PG - 799-806 AB - We tested the hypothesis that concentrations of adipocytokines are altered in SLE and associated with coronary atherosclerosis, insulin resistance and inflammation. Concentrations of resistin, leptin, adiponectin and visfatin were measured in 109 patients with SLE and 78 control subjects. Coronary calcification was measured using electron beam-computed tomography, and insulin resistance was defined by the homeostasis model assessment index. Concentrations of adiponectin (28.7 +/- 17.9 vs 22.0 +/- 15.3 microg/mL, P = 0.003), leptin (41.1 +/- 49.9 vs 19.8 +/- 24.6 ng/mL, P 0.001) and visfatin (7.5 +/- 10.5 vs 4.5 +/- 2.8 ng/mL, P 0.001) were higher in patients with SLE than in controls. These differences remained significant after adjustment for age, race, sex and body mass index (BMI; all P values 0.02). Concentrations of resistin (10.7 +/- 7.6 vs 9.1 +/- 5.1 ng/mL, P = 0.41) did not differ in patients and controls. In patients with SLE, leptin was positively associated with BMI (rho = 0.80, P 0.001), insulin resistance (rho = 0.46, P 0.001) and C-reactive protein (CRP) (rho = 0.30, P = 0.002), whereas adiponectin was negatively associated with the same factors (rho = -0.40, P 0.001; rho = -0.38, P 0.001; rho = -0.22, P = 0.02, respectively). None of the adipocytokines were associated with coronary atherosclerosis in SLE. In conclusion, patients with SLE have increased concentrations of adiponectin, leptin and visfatin. Lower concentrations of adiponectin and higher concentrations of leptin are associated with insulin resistance, BMI and CRP in patients with SLE. AD - Department of Medicine, Vanderbilt University, Nashville, Tennessee 37232-6602, USA. FAU - Chung, C P AU - Chung CP FAU - Long, A G AU - Long AG FAU - Solus, J F AU - Solus JF FAU - Rho, Y H AU - Rho YH FAU - Oeser, A AU - Oeser A FAU - Raggi, P AU - Raggi P FAU - Stein, C Michael AU - Stein CM LA - eng GR - 1UL1RR-024975/RR/NCRR NIH HHS/United States GR - GM5M01-RR00095/GM/NIGMS NIH HHS/United States GR - HL65082/HL/NHLBI NIH HHS/United States GR - P60AR056116/AR/NIAMS NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PL - England TA - Lupus JT - Lupus JID - 9204265 RN - 0 (Adipokines) RN - 0 (Adiponectin) RN - 0 (Leptin) RN - 0 (Resistin) RN - 9007-41-4 (C-Reactive Protein) RN - EC 2.4.2.12 (Nicotinamide Phosphoribosyltransferase) SB - IM MH - Adipokines/*blood MH - Adiponectin/blood MH - Adult MH - Body Mass Index MH - C-Reactive Protein/metabolism MH - Case-Control Studies MH - Coronary Artery Disease/*blood/*epidemiology MH - Cross-Sectional Studies MH - Female MH - Humans MH - Inflammation/*blood/*epidemiology MH - Insulin Resistance/*physiology MH - Leptin/blood MH - Lupus Erythematosus, Systemic/*blood/complications/physiopathology MH - Male MH - Metabolic Syndrome X/blood/epidemiology MH - Middle Aged MH - Nicotinamide Phosphoribosyltransferase/blood MH - Resistin/blood MH - Risk Factors PMC - PMC2707942 MID - NIHMS92696 OID - NLM: NIHMS92696 OID - NLM: PMC2707942 EDAT- 2009/07/07 09:00 MHDA- 2009/10/23 06:00 CRDT- 2009/07/07 09:00 PMCR- 2010/01/01 AID - 18/9/799 AID - 10.1177/0961203309103582 PST - ppublish SO - Lupus. 2009 Aug;18(9):799-806. PMID- 19462918 OWN - NLM STAT- In-Process DA - 20090525 IS - 1672-173X (Print) VI - 40 IP - 2 DP - 2009 Mar TI - PG - 322-4 AB - OBJECTIVE: To study the plasma visfatin level in patients with coronary artery disease (CAD) and evaluate the correlation between plasma visfatin level and coronary lesion severity. METHODS: The level of plasma visfatin of 48 patients with CAD (proved by angiography) and 41 normal controls were detected and compared. Plasma visfatin was determined by an enzyme immunoassay. The lesion severity of coronary arteries was assessed by Gensini coronary scoring system, and the correlation between plasma visfatin level and coronary lesion severity was evaluated. RESULTS: Plasma visfatin level in the CAD group was significantly higher than that in the control group . A significant positive correlation was found between coronary lesion severity score and Plasma visfatin level (r = 0.906, P 0.01). CONCLUSION: Plasma visfatin level may be related to the pathogenesis of CAD. Detection of plasma visfatin might be helpful for early diagnosis of CAD, and patients with higher Plasma visfatin level may have more severe coronary lesion. AD - Laboratory of Cardiovascular Diseases, West China Hospital, Sichuan University, Chengdu 610041, China. FAU - Fu, Hua AU - Fu H FAU - Zhu, Ye AU - Zhu Y FAU - You, Gui-ying AU - You GY FAU - Liu, Xiao-jing AU - Liu XJ LA - chi PT - English Abstract PT - Journal Article PL - China TA - Sichuan Da Xue Xue Bao Yi Xue Ban JT - Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition JID - 101162609 SB - IM EDAT- 2009/05/26 09:00 MHDA- 2009/05/26 09:00 CRDT- 2009/05/26 09:00 PST - ppublish SO - Sichuan Da Xue Xue Bao Yi Xue Ban. 2009 Mar;40(2):322-4. PMID- 19249500 OWN - NLM STAT- MEDLINE DA - 20090302 DCOM- 20090427 IS - 0041-1345 (Print) VI - 41 IP - 1 DP - 2009 Jan-Feb TI - Visfatin, a new adipocytokine, is predominantly related to inflammation/endothelial damage in kidney allograft recipients. PG - 150-3 AB - Visfatin, a ubiquitous adipokine, was first described in 2005. It was found to be selectively up-regulated in the adipose tissue and to have insulin-mimetic effects. It has been reported that visfatin is associated with endothelial damage in chronic kidney disease. We investigated plasma visfatin levels (using commercially available kits) in 100 clinically stable kidney allograft recipients. We assessed visfatin markers of coagulation: thrombin-antithrombin complexes, prothrombin fragments 1 + 2; fibrinolysis: tissue plasminogen activator, plasminogen activator inhibitor, plasmin-antiplasmin complexes; endothelial function/injury: von Willebrand factor, thrombomodulin, intracellular adhesion molecule, vascular cell adhesion molecule (VCAM); inflammation: hsCRP and interleukin-6. Visfatin was significantly higher in kidney allograft recipients than in healthy volunteers. Visfatin did not differ significantly between diabetic and nondiabetics, hypertensives and normotensives, patients with and without coronary artery disease, and between male and female subjects. Type of immunosuppressive regimen (mycophenolate mofetil vs azathioprine) did not affect visfatin levels. On univariate analysis, visfatin correlated positively with prothrombin fragments 1 + 2, VCAM, creatinine, high-sensitivity C-reactive protein, and negatively with albumin. In multivariate analysis, only VCAM was associated with visfatin in kidney allograft recipients. Visfatin, which is related to markers of inflammation, may represent a novel link between inflammation and adipocytokines among long-term kidney transplant recipients. AD - Department of Nephrology and Transplantology, Medical University, Bialystok, Poland. jolmal@poczta.onet.pl FAU - Malyszko, J AU - Malyszko J FAU - Malyszko, J S AU - Malyszko JS FAU - Mysliwiec, M AU - Mysliwiec M LA - eng PT - Journal Article PL - United States TA - Transplant Proc JT - Transplantation proceedings JID - 0243532 RN - 0 (Biological Markers) RN - 0 (Cytokines) RN - 0 (Immunosuppressive Agents) RN - EC 2.4.2.12 (Nicotinamide Phosphoribosyltransferase) RN - EC 2.4.2.12 (nicotinamide phosphoribosyltransferase, human) SB - IM MH - Adult MH - Aged MH - Biological Markers/blood MH - Blood Coagulation MH - Cytokines/*metabolism MH - Diabetic Nephropathies/enzymology/surgery MH - Endothelium, Vascular/enzymology/*pathology MH - Female MH - Fibrinolysis MH - Humans MH - Immunosuppressive Agents/therapeutic use MH - Inflammation/enzymology/*pathology MH - Kidney Transplantation/immunology/*pathology MH - Male MH - Middle Aged MH - Nicotinamide Phosphoribosyltransferase/*metabolism MH - Reference Values MH - Transplantation, Homologous EDAT- 2009/03/03 09:00 MHDA- 2009/04/28 09:00 CRDT- 2009/03/03 09:00 PHST- 2008/06/30 PHST- 2008/08/21 PHST- 2008/10/15 AID - S0041-1345(08)01614-X AID - 10.1016/j.transproceed.2008.10.086 PST - ppublish SO - Transplant Proc. 2009 Jan-Feb;41(1):150-3. PMID- 19178507 OWN - NLM STAT- MEDLINE DA - 20090715 DCOM- 20090928 IS - 1365-2265 (Electronic) VI - 71 IP - 2 DP - 2009 Aug TI - Association of plasma visfatin levels with inflammation, atherosclerosis and acute coronary syndromes (ACS) in humans. PG - 202-7 AB - OBJECTIVES: Visfatin is a new cytokine that act as an insulin analogue on the insulin receptor and may link obesity and insulin resistance. It was recently shown that visfatin plays a role in plaque destabilization. However, the role of visfatin in atherosclerosis remains to be elucidated. We sought to assess whether plasma visfatin level is independently associated with inflammation, atherosclerosis and acute coronary syndromes (ACS). DESIGN AND PATIENTS: Two hundred and fifty-three patients undergoing coronary angiography were divided into three subgroups: chronic coronary artery disease (CAD) (n = 102), ACS (n = 100) and control patients (n = 51). The plasma samples were thawed and analysed for circulating visfatin, monocyte chemoattractant protein 1 (MCP-1), interleukin-6 (IL-6), high sensitivity C-reactive protein (hs-CRP). The association of visfatin with risk factors, inflammation, atherosclerosis, and ACS was determined. RESULTS: Plasma visfatin levels were significantly higher in chronic CAD and ACS compared with control patients. Multiple regression analysis demonstrated that plasma visfatin levels correlated with inflammatory factors and were associated with chronic CAD (odds ratio , for second, third and fourth quartiles were 1.74 , 1.54 and 1.84 , respectively) and ACS (ORs for second, third and fourth quartiles were 2.56 , 4.61 and 6.52 , respectively) following adjustment for established risk factors and other inflammatory factors. CONCLUSIONS: Plasma visfatin levels are significantly associated with CAD, particularly ACS, independent of well-known CAD risk factors. AD - Department of Cardiology, Cardiovascular Institute and Fuwai Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China. FAU - Liu, Sheng Wen AU - Liu SW FAU - Qiao, Shu Bin AU - Qiao SB FAU - Yuan, Jian Song AU - Yuan JS FAU - Liu, Dong Qin AU - Liu DQ LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20081020 PL - England TA - Clin Endocrinol (Oxf) JT - Clinical endocrinology JID - 0346653 RN - EC 2.4.2.12 (Nicotinamide Phosphoribosyltransferase) SB - IM MH - Acute Coronary Syndrome/*blood/immunology MH - Aged MH - Atherosclerosis/*blood/immunology MH - Case-Control Studies MH - Female MH - Humans MH - Inflammation/*blood/immunology MH - Male MH - Middle Aged MH - Nicotinamide Phosphoribosyltransferase/*blood EDAT- 2009/01/31 09:00 MHDA- 2009/09/29 06:00 CRDT- 2009/01/31 09:00 PHST- 2008/10/20 AID - CEN3453 AID - 10.1111/j.1365-2265.2008.03453.x PST - ppublish SO - Clin Endocrinol (Oxf). 2009 Aug;71(2):202-7. Epub 2008 Oct 20. PMID- 18942491 OWN - NLM STAT- MEDLINE DA - 20081023 DCOM- 20081104 IS - 1433-6510 (Print) VI - 54 IP - 7-8 DP - 2008 TI - Impact of rosiglitazone on visfatin and adiponectin plasma concentrations in patients with type 2 diabetes and coronary artery disease. PG - 237-41 AB - Visfatin is a recently described new adipokine that is considered to bind to the insulin receptor and induce insulin action via signal transduction pathways distinct from those of insulin. This study investigated whether circulating plasma visfatin levels may be influenced by PPARy activation, as shown for adiponectin and other adipokines. Samples from a prospective single-blinded placebo-controlled three-month intervention study with rosiglitazone were retrospectively analysed. The samples were derived from 39 patients with type 2 diabetes mellitus suffering from coronary artery disease as confirmed by angiography (rosiglitazone arm: 18 men, 1 woman, age (mean +/- STD): 65 +/- 9 years, disease duration: 4.8 +/- 4.0 years, HbA1c: 7.3 +/- 1.3%; Placebo: 19 men, 1 woman, age: 64 +/- 10 years, disease duration: 5.1 +/- 6.5 years, HbA1c: 7.5 +/- 1.5%). Laboratory measurements for lipids, adiponectin, and visfatin were performed with validated tests. The baseline values were comparable for all observation markers. After three months, a significant increase in the adiponectin concentrations could be observed only in the rosiglitazone group (from: 6.9 +/- 0.9 mg/l to 16.5 +/- 1.5 mg/l, (p 0.001) vs placebo: 7.8 +/- 6.3 mg/l to 8.0 +/- 0.8 mg/l, (n.s.), p 0.001 between the groups at endpoint). No changes were seen in both treatment arms for the other observation parameters. In particular, no influence of rosiglitazone was seen on the visfatin concentrations (25.9 +/- 2.3 ng/ml to 25.8 +/- 1.9 ng/ml; Placbo: 26.9 +/- 5.4 ng/ml to 27.2 +/- 4.9 ng/ml, n.s.). Our investigation demonstrates that rosiglitazone has different effects on circulating concentrations of adiponectin and visfatin. Visfatin secretion is not regulated by PPARgamma and further research is required to investigate its role in insulin resistance. AD - IKFE Institute for Clinical Research and Development Mainz, Germany. AndreasP@IKFE.de FAU - Pfutzner, A AU - Pfutzner A FAU - Marx, N AU - Marx N FAU - Walcher, D AU - Walcher D FAU - Lobig, M AU - Lobig M FAU - Seidel, D AU - Seidel D FAU - Forst, T AU - Forst T LA - eng PT - Journal Article PL - Germany TA - Clin Lab JT - Clinical laboratory JID - 9705611 RN - 0 (Adiponectin) RN - 0 (Cytokines) RN - 0 (Hypoglycemic Agents) RN - 0 (PPAR gamma) RN - 0 (Thiazolidinediones) RN - 0 (adiponectin, human) RN - 122320-73-4 (rosiglitazone) RN - EC 2.4.2.12 (Nicotinamide Phosphoribosyltransferase) RN - EC 2.4.2.12 (nicotinamide phosphoribosyltransferase, human) SB - IM MH - Adiponectin/blood MH - Aged MH - Coronary Artery Disease/*blood MH - Cytokines/*blood MH - Diabetes Mellitus, Type 2/*blood MH - Female MH - Humans MH - Hypoglycemic Agents/*pharmacology MH - Male MH - Middle Aged MH - Nicotinamide Phosphoribosyltransferase/*blood MH - PPAR gamma/agonists/metabolism MH - Retrospective Studies MH - Thiazolidinediones/*pharmacology EDAT- 2008/10/24 09:00 MHDA- 2008/11/05 09:00 CRDT- 2008/10/24 09:00 PST - ppublish SO - Clin Lab. 2008;54(7-8):237-41. PMID- 18723235 OWN - NLM STAT- Publisher DA - 20080825 IS - 1874-1754 (Electronic) DP - 2008 Aug 22 TI - A new frame in thromboembolic cardiovascular disease: Adipocytokine. AB - Recent researches have shown that adipocytokines secreted by adipose tissue play an important role in inflammation which is considered to be a crucial step in the pathogenesis of atherosclerosis. Leptin, one of the earlier adipocytokines, is known to play a major role in cardiovascular disease and recent observations suggest that leptin is an independent risk factor for coronary heart disease. Resistin, another recently discovered adipocytokine, has been related to risk factors of atherosclerosis, and in diabetic individuals serum resistin levels correlate well with inflammatory markers and are predictive for the development of cardiovascular disease. Adiponectin, another adipocytokine of interest in recent years, seems to be the most promising one studied to date. In contrast to leptin and resistin, adiponectin seems to be beneficial for health and it is a protective factor and decreased in obesity. However, many other factors derived from adipose tissue have also been discovered, such as interleukin-6, tumor necrosis factor alpha, monocyte chemoattractant protein 1, apelin, visfatin and probably others awaiting discovery in the near future. In this paper, we discussed the role of adipocytokines in the pathogenesis of atherosclerotic cardiovascular disease. AD - Department of Cardiology, Gulhane Military Medical School, Turkey. AU - Amasyali B AU - Kilic A AU - Celik T AU - Iyisoy A LA - ENG PT - JOURNAL ARTICLE DEP - 20080822 TA - Int J Cardiol JT - International journal of cardiology JID - 8200291 EDAT- 2008/08/30 09:00 MHDA- 2008/08/30 09:00 CRDT- 2008/08/30 09:00 PHST- 2008/04/22 PHST- 2008/06/28 AID - S0167-5273(08)00886-3 AID - 10.1016/j.ijcard.2008.06.082 PST - aheadofprint SO - Int J Cardiol. 2008 Aug 22. PMID- 18390031 OWN - NLM STAT- MEDLINE DA - 20080408 DCOM- 20080506 IS - 0023-0294 (Print) VI - 106 IP - 2 DP - 2008 Feb TI - The physiology of adiposity. PG - 53-62 AB - Normal energy homeostasis requires a balance between fat storage and energy utilization that is guaranteed by regulation of one billion fat cells which arguably constitute the body's largest endocrine unit. Such physiology is required to maintain normal adiposity which if depleted from under- or malnutrition results in lipodystrophy that causes hormonal, reproductive, and developmental abnormalities. Conversely, excess adiposity provides inflammatory secretagogues, particularly from central visceral fat depots that enhance insulin resistance, excessive fatty acids with lipotoxicity and hypertension that escalate atherosclerosis including coronary artery disease. This review describes normal adiposity for maintenance of normal body mass and the roles of adipocyte hormones and adipokines for normal regulation of energy storage and its utilization. Therefore, in this context, the roles of leptin, insulin, adiponectin, and lesser known acylation-stimulating protein, visfatin, and apelin are outlined. Further, adipocyte inflammatory secretagogues are outlined that affect diabetes mellitus 2 with insulin resistance,fatty acid lipotoxicity, dyslipidemia, and hypertension that contribute to the metabolic syndrome. These effects are opposed by adipocyte hormones adiponectin, acylation-stimulating protein, visfatin, and apelin that help maintain normal energy utilization. AD - Department of Medicine, University of Louisville, Kentucky 40292, USA. FAU - Redinger, Richard N AU - Redinger RN LA - eng PT - Case Reports PT - Journal Article PT - Review PL - United States TA - J Ky Med Assoc JT - The Journal of the Kentucky Medical Association JID - 7505615 RN - 0 (Adipokines) SB - IM MH - Adipokines/physiology MH - Adiposity/*physiology MH - Adult MH - Energy Metabolism/physiology MH - Female MH - Humans MH - Obesity/*complications/*physiopathology RF - 74 EDAT- 2008/04/09 09:00 MHDA- 2008/05/07 09:00 CRDT- 2008/04/09 09:00 PST - ppublish SO - J Ky Med Assoc. 2008 Feb;106(2):53-62. PMID- 18230827 OWN - NLM STAT- MEDLINE DA - 20080130 DCOM- 20080207 IS - 1479-683X (Electronic) VI - 158 IP - 2 DP - 2008 Feb TI - Implication of lipocalin-2 and visfatin levels in patients with coronary heart disease. PG - 203-7 AB - OBJECTIVES: Visfatin and lipocalin-2 are novel adipokines associated with insulin resistance (IR) and obesity-related metabolic disorders. We compared lipocalin-2 and visfatin concentrations between patients with coronary heart disease (CHD) and control subjects and evaluated their association with cardiovascular risk factors. METHODS: We examined serum visfatin, lipocalin-2 levels, and cardiovascular risk factors in 91 subjects (49 patients with angiographically confirmed CHD versus 42 age- and gender-matched control participants). RESULTS: Circulating lipocalin-2 levels were significantly higher in patients with CHD compared with the control subjects (82.6+/-38.7 ng/ml versus 43.8+/-27.8 ng/ml; P0.001). However, visfatin levels were not significantly different between patients with CHD and control subjects. Serum lipocalin-2 levels were positively associated with weight (r=0.26; P=0.036), fasting insulin (r=0.36; P=0.003), and IR (r=0.33; P=0.007), whereas these levels showed a negative correlation with high-density lipoprotein (HDL) cholesterol (r=-0.30; P=0.016) after adjustment for gender and body mass index. However, visfatin levels were not associated with any variables of the metabolic syndrome. The multiple regression analysis showed that lipocalin-2 levels were independently associated with HDL cholesterol and IR (R2=0.199). Furthermore, the multiple logistic regression analysis showed that systolic blood pressure, IR, and lipocalin-2 levels were independently associated with CHD. CONCLUSIONS: Serum lipocalin-2 levels were significantly elevated in patients with CHD and were independently associated with CHD. The present findings suggest that the measurement of serum lipocalin-2 levels may be useful for assessing CHD risk. AD - Division of Endocrinology and Metabolism, Department of Internal Medicine, Korea University College of Medicine, Seoul 152-050, South Korea. FAU - Choi, K M AU - Choi KM FAU - Lee, J S AU - Lee JS FAU - Kim, E J AU - Kim EJ FAU - Baik, S H AU - Baik SH FAU - Seo, H S AU - Seo HS FAU - Choi, D S AU - Choi DS FAU - Oh, D J AU - Oh DJ FAU - Park, C G AU - Park CG LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - England TA - Eur J Endocrinol JT - European journal of endocrinology / European Federation of Endocrine Societies JID - 9423848 RN - 0 (Acute-Phase Proteins) RN - 0 (Biological Markers) RN - 0 (LCN2 protein, human) RN - 0 (Lipocalins) RN - 0 (Proto-Oncogene Proteins) RN - 11061-68-0 (Insulin) RN - EC 2.4.2.12 (Nicotinamide Phosphoribosyltransferase) SB - IM MH - Acute-Phase Proteins MH - Aged MH - Biological Markers/blood MH - Body Weight MH - Case-Control Studies MH - Coronary Disease/*blood/enzymology MH - Female MH - Humans MH - Insulin/blood MH - Insulin Resistance MH - Lipocalins/*blood MH - Logistic Models MH - Male MH - Middle Aged MH - Nicotinamide Phosphoribosyltransferase/*blood MH - Proto-Oncogene Proteins/*blood MH - Risk Factors EDAT- 2008/01/31 09:00 MHDA- 2008/02/08 09:00 CRDT- 2008/01/31 09:00 AID - 158/2/203 AID - 10.1530/EJE-07-0633 PST - ppublish SO - Eur J Endocrinol. 2008 Feb;158(2):203-7. PMID- 18208353 OWN - NLM STAT- MEDLINE DA - 20080304 DCOM- 20080418 IS - 1431-6730 (Print) VI - 389 IP - 3 DP - 2008 Mar TI - Sirt1 protects the heart from aging and stress. PG - 221-31 AB - The prevalence of heart diseases, such as coronary artery disease and congestive heart failure, increases with age. Optimal therapeutic interventions that antagonize aging may reduce the occurrence and mortality of adult heart diseases. We discuss here how molecular mechanisms mediating life span extension affect aging of the heart and its resistance to pathological insults. In particular, we review our recent findings obtained from transgenic mice with cardiac-specific overexpression of Sirt1, which demonstrated delayed aging and protection against oxidative stress in the heart. We propose that activation of known longevity mechanisms in the heart may represent a novel cardioprotection strategy against aging and certain types of cardiac stress, such as oxidative stress. AD - Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark, NJ 07103, USA. FAU - Hsu, Chiao-Po AU - Hsu CP FAU - Odewale, Ibrahim AU - Odewale I FAU - Alcendor, Ralph R AU - Alcendor RR FAU - Sadoshima, Junichi AU - Sadoshima J LA - eng GR - AG23039/AG/NIA NIH HHS/United States GR - AG28787/AG/NIA NIH HHS/United States GR - HL 59139/HL/NHLBI NIH HHS/United States GR - HL67724/HL/NHLBI NIH HHS/United States GR - HL69020/HL/NHLBI NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't PT - Review PL - Germany TA - Biol Chem JT - Biological chemistry JID - 9700112 RN - 0 (Stilbenes) RN - 501-36-0 (resveratrol) RN - EC 2.4.2.12 (Nicotinamide Phosphoribosyltransferase) RN - EC 3.5.1.- (SIRT1 protein, human) RN - EC 3.5.1.- (Sirtuins) SB - IM MH - Aging/*drug effects MH - Animals MH - Apoptosis/drug effects MH - Caloric Restriction MH - Heart/*drug effects/*physiology MH - Heart Diseases/*prevention control MH - Heart Failure/drug therapy MH - Humans MH - Longevity/physiology MH - Mice MH - Nicotinamide Phosphoribosyltransferase/metabolism MH - Oxidative Stress/drug effects MH - Saccharomyces cerevisiae/drug effects MH - Sirtuins/*physiology MH - Stilbenes/pharmacology MH - Up-Regulation RF - 140 EDAT- 2008/01/23 09:00 MHDA- 2008/04/19 09:00 CRDT- 2008/01/23 09:00 AID - 10.1515/BC.2008.032 PST - ppublish SO - Biol Chem. 2008 Mar;389(3):221-31. PMID- 17878891 OWN - NLM STAT- MEDLINE DA - 20080218 DCOM- 20080804 LR - 20090915 IS - 1476-5497 (Electronic) VI - 32 IP - 2 DP - 2008 Feb TI - Adipocytokines and proinflammatory mediators from abdominal and epicardial adipose tissue in patients with coronary artery disease. PG - 268-74 AB - OBJECTIVE: Epicardial and abdominal adipose tissues have recently been demonstrated to play inflammatory roles in coronary atherosclerosis. We sought to compare tissue adipocytokine levels of these two anatomically distinct adipose stores in patients with and without coronary artery diseases (CAD). DESIGN: Samples of abdominal and epicardial fat tissues were harvested to detect the levels of adipocytokines and proinflammatory mediators. SUBJECTS: Forty-six patients with CAD who underwent coronary artery bypass surgery and 12 non-CAD control subjects who underwent other types of open-heart surgery. MEASUREMENTS: Tissue levels of adipocytokines (adiponectin, leptin and visfatin) and proinflammatory mediators (tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6)) were determined by enzyme-linked immunosorbent assay. RESULTS: Tissue levels of TNF-alpha, IL-6, leptin and visfatin were significantly higher in CAD patients relative to control subjects. In addition, significantly higher tissue levels of these four cytokines from abdominal fat depots were found compared to those from epicardial fat in CAD patients. Conversely, in comparison with control subjects, tissue levels of adiponectin were significantly reduced in CAD patients with a significantly lower tissue levels of abdominal than epicardial fat depots demonstrated. CONCLUSION: Abdominal adiposity may play more significant role than epicardial fat in the pathogenesis of coronary atherosclerosis. AD - Department of Cardiology, Kaohsiung Municipal Hsiao-Kang Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan. FAU - Cheng, K-H AU - Cheng KH FAU - Chu, C-S AU - Chu CS FAU - Lee, K-T AU - Lee KT FAU - Lin, T-H AU - Lin TH FAU - Hsieh, C-C AU - Hsieh CC FAU - Chiu, C-C AU - Chiu CC FAU - Voon, W-C AU - Voon WC FAU - Sheu, S-H AU - Sheu SH FAU - Lai, W-T AU - Lai WT LA - eng PT - Comparative Study PT - Journal Article DEP - 20070918 PL - England TA - Int J Obes (Lond) JT - International journal of obesity (2005) JID - 101256108 RN - 0 (Adipokines) RN - 0 (Inflammation Mediators) SB - IM MH - Adipokines/*metabolism MH - Adipose Tissue/*metabolism MH - Adolescent MH - Adult MH - Aged MH - Aged, 80 and over MH - Case-Control Studies MH - Coronary Artery Disease/etiology/*metabolism MH - Enzyme-Linked Immunosorbent Assay MH - Female MH - Humans MH - Inflammation Mediators/*metabolism MH - Male MH - Middle Aged MH - Obesity/complications/metabolism EDAT- 2007/09/20 09:00 MHDA- 2008/08/05 09:00 CRDT- 2007/09/20 09:00 PHST- 2007/09/18 AID - 0803726 AID - 10.1038/sj.ijo.0803726 PST - ppublish SO - Int J Obes (Lond). 2008 Feb;32(2):268-74. Epub 2007 Sep 18. PMID- 17379018 OWN - NLM STAT- MEDLINE DA - 20070323 DCOM- 20070424 LR - 20071115 IS - 0026-0495 (Print) VI - 56 IP - 4 DP - 2007 Apr TI - Serum visfatin in relation to visceral fat, obesity, and type 2 diabetes mellitus in Asian Indians. PG - 565-70 AB - To investigate the role of the novel adipokine visfatin in type 2 diabetes mellitus and obesity and to examine its association with visceral and subcutaneous fat in Asian Indians, who have increased susceptibility to type 2 diabetes mellitus and coronary artery disease, 150 subjects with type 2 diabetes mellitus (75 men, 75 women) and 150 age- and sex-matched subjects with normal glucose tolerance were recruited from the Chennai Urban Rural Epidemiology Study, a population-based study done in Chennai, southern India. Anthropometric and biochemical measurements were done by using standardized techniques. Fasting serum visfatin levels were measured by enzyme-linked immunosorbent assay. Visceral and subcutaneous fat were measured by computerized tomography in a subset of 130 individuals. Serum visfatin levels were significantly higher in diabetic subjects compared with nondiabetic subjects (11.4+/-5.9 vs 9.8+/-4.3 ng/mL, P=.008). However, this association was lost when adjusted for body mass index (odds ratio , 1.048; 95% confidence interval , 0.997-1.101; P=.067) or waist circumference (OR, 1.050; 95% CI, 0.999-1.104; P=.057). Serum visfatin showed a significant association with obesity even after adjusting for age, sex, and type 2 diabetes mellitus (OR, 1.060; 95% CI, 1.005-1.119; P=.033). Visceral fat, but not subcutaneous fat, was significantly associated with serum visfatin levels even after adjusting for age, sex, type 2 diabetes mellitus, and body mass index (P=.002). In Asian Indians, serum visfatin levels are associated with obesity and visceral fat but not with subcutaneous fat. Although visfatin levels are increased in type 2 diabetes mellitus, the association seems to be primarily through obesity. AD - Madras Diabetes Research Foundation Dr Mohan's Diabetes Specialities Centre, Gopalapuram, Chennai 600 086, India. FAU - Sandeep, Sreedharan AU - Sandeep S FAU - Velmurugan, Kaliyaperumal AU - Velmurugan K FAU - Deepa, Raj AU - Deepa R FAU - Mohan, Viswanathan AU - Mohan V LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - United States TA - Metabolism JT - Metabolism: clinical and experimental JID - 0375267 RN - 0 (Cytokines) RN - EC 2.4.2.12 (Nicotinamide Phosphoribosyltransferase) RN - EC 2.4.2.12 (nicotinamide phosphoribosyltransferase, human) SB - IM MH - Adult MH - Body Mass Index MH - Case-Control Studies MH - Cytokines/*blood MH - Diabetes Mellitus, Type 2/*blood/complications/radiography MH - Female MH - Humans MH - India MH - *Intra-Abdominal Fat/radiography MH - Male MH - Middle Aged MH - Nicotinamide Phosphoribosyltransferase MH - Obesity/*blood/complications/radiography MH - Tomography, X-Ray Computed EDAT- 2007/03/24 09:00 MHDA- 2007/04/25 09:00 CRDT- 2007/03/24 09:00 PHST- 2006/06/16 PHST- 2006/12/18 AID - S0026-0495(07)00021-2 AID - 10.1016/j.metabol.2006.12.005 PST - ppublish SO - Metabolism. 2007 Apr;56(4):565-70. PMID- 17283255 OWN - NLM STAT- MEDLINE DA - 20070227 DCOM- 20070312 LR - 20071115 IS - 1524-4539 (Electronic) VI - 115 IP - 8 DP - 2007 Feb 27 TI - Increased expression of visfatin in macrophages of human unstable carotid and coronary atherosclerosis: possible role in inflammation and plaque destabilization. PG - 972-80 AB - BACKGROUND: Although the participation of inflammation in atherogenesis is widely recognized, the identification of the different components has not been clarified. In particular, the role of inflammation in plaque destabilization is not fully understood. METHODS AND RESULTS: Our main findings were as follows: (1) In a microarray experiment, we identified visfatin, one of the most recently identified adipokines, as a gene that was markedly enhanced in carotid plaques from symptomatic compared with plaques from asymptomatic individuals. This finding was confirmed when carotid plaques from 7 patients with asymptomatic and 14 patients with symptomatic lesions were examined with real-time reverse transcription polymerase chain reaction. (2) Immunohistochemistry showed that visfatin was localized in areas that were rich in lipid-loaded macrophages. (3) The relationship between visfatin and unstable lesions was also found in patients with coronary artery disease, demonstrating a strong visfatin immunostaining in lipid-rich regions within the material obtained at the site of plaque rupture in patients with acute myocardial infarction. (4) Both oxidized low-density lipoprotein and tumor necrosis factor-alpha increased visfatin expression in THP-1 monocytes, with a particularly enhancing effect when these stimuli were combined. (5) Visfatin increased matrix metalloproteinase-9 activity in THP-1 monocytes and tumor necrosis factor-alpha and interleukin-8 levels in peripheral blood mononuclear cells. Both of these effects were abolished when insulin receptor signaling was blocked. CONCLUSIONS: Our findings suggest that visfatin should be regarded as an inflammatory mediator, localized to foam cell macrophages within unstable atherosclerotic lesions, that potentially plays a role in plaque destabilization. AD - Research Institute for Internal Medicine, Rikshospitalet-Radiumhospitalet Medical Center and University of Oslo, N-0027 Oslo, Norway. FAU - Dahl, Tuva B AU - Dahl TB FAU - Yndestad, Arne AU - Yndestad A FAU - Skjelland, Mona AU - Skjelland M FAU - Oie, Erik AU - Oie E FAU - Dahl, Arve AU - Dahl A FAU - Michelsen, Annika AU - Michelsen A FAU - Damas, Jan K AU - Damas JK FAU - Tunheim, Siv H AU - Tunheim SH FAU - Ueland, Thor AU - Ueland T FAU - Smith, Camilla AU - Smith C FAU - Bendz, Bjorn AU - Bendz B FAU - Tonstad, Serena AU - Tonstad S FAU - Gullestad, Lars AU - Gullestad L FAU - Froland, Stig S AU - Froland SS FAU - Krohg-Sorensen, Kirsten AU - Krohg-Sorensen K FAU - Russell, David AU - Russell D FAU - Aukrust, Pal AU - Aukrust P FAU - Halvorsen, Bente AU - Halvorsen B LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20070205 PL - United States TA - Circulation JT - Circulation JID - 0147763 RN - 0 (Cytokines) RN - 0 (Interleukin-8) RN - 0 (Tumor Necrosis Factor-alpha) RN - EC 2.4.2.12 (Nicotinamide Phosphoribosyltransferase) RN - EC 2.4.2.12 (nicotinamide phosphoribosyltransferase, human) RN - EC 3.4.24.35 (Matrix Metalloproteinase 9) SB - AIM SB - IM MH - Aged MH - Angina, Unstable/immunology MH - Atherosclerosis/*metabolism MH - Carotid Artery Diseases/*metabolism MH - Cell Line MH - Coronary Artery Disease/*metabolism MH - Cytokines/analysis/genetics/*physiology MH - Female MH - Gene Expression Regulation MH - Humans MH - Immunohistochemistry MH - Inflammation/*etiology MH - Interleukin-8/biosynthesis MH - Macrophages/*metabolism MH - Male MH - Matrix Metalloproteinase 9/genetics MH - Middle Aged MH - Monocytes/metabolism MH - Nicotinamide Phosphoribosyltransferase MH - Tumor Necrosis Factor-alpha/biosynthesis EDAT- 2007/02/07 09:00 MHDA- 2007/03/14 09:00 CRDT- 2007/02/07 09:00 PHST- 2007/02/05 AID - CIRCULATIONAHA.106.665893 AID - 10.1161/CIRCULATIONAHA.106.665893 PST - ppublish SO - Circulation. 2007 Feb 27;115(8):972-80. Epub 2007 Feb 5. PMID- 16987875 OWN - NLM STAT- MEDLINE DA - 20060921 DCOM- 20061120 LR - 20071115 IS - 0964-6906 (Print) VI - 15 Spec No 2 DP - 2006 Oct 15 TI - Genetics of obesity and the prediction of risk for health. PG - R124-30 AB - Obesity has always existed in human populations, but until very recently was comparatively rare. The availability of abundant, energy-rich processed foods in the last few decades has, however, resulted in a sharp rise in the prevalence of obesity in westernized countries. Although it is the obesogenic environment that has resulted in this major healthcare problem, it is acting by revealing a sub-population with a pre-existing genetic predisposition to excess adiposity. There is substantial evidence for the heritability of obesity, and research in both rare and common forms of obesity has identified genes with significant roles in its aetiology. Application of this understanding to patient care has been slower. Until very recently, the health risks of obesity were thought to be well understood, with a straightforward correlation between increasing obesity and increasing risk of health problems such as type 2 diabetes, coronary heart disease, hypertension, arthritis and cancer. It is becoming clear, however, that the location of fat deposition, variation in the secretion of adipokines and other factors govern whether a particular obese person develops such complications. Prediction of the health risks of obesity for individual patients is not straightforward, but continuing advances in understanding of genetic factors influencing obesity risk and improved diagnostic technologies mean that the future for such prediction is looking increasingly bright. AD - Section of Genomic Medicine, Division of Medicine, Imperial College London, Hammersmith Hospital, Du Cane Road, London W12 0NN, UK. a.walley@imperial.ac.uk FAU - Walley, Andrew J AU - Walley AJ FAU - Blakemore, Alexandra I F AU - Blakemore AI FAU - Froguel, Philippe AU - Froguel P LA - eng PT - Journal Article PT - Review PL - England TA - Hum Mol Genet JT - Human molecular genetics JID - 9208958 RN - 0 (Biological Markers) RN - 0 (Cytokines) RN - 0 (Ghrelin) RN - 0 (Isoenzymes) RN - 0 (Peptide Hormones) RN - EC 2.4.2.12 (Nicotinamide Phosphoribosyltransferase) RN - EC 2.4.2.12 (nicotinamide phosphoribosyltransferase, human) RN - EC 4.1.1.15 (Glutamate Decarboxylase) RN - EC 4.1.1.15 (glutamate decarboxylase 2) SB - IM MH - Bardet-Biedl Syndrome/genetics MH - Biological Markers MH - Cytokines/genetics MH - Epigenesis, Genetic MH - Ghrelin MH - Glutamate Decarboxylase/genetics MH - Humans MH - Isoenzymes/genetics MH - Nicotinamide Phosphoribosyltransferase MH - Obesity/complications/*genetics MH - Peptide Hormones/genetics MH - Quantitative Trait Loci MH - Risk Factors RF - 88 EDAT- 2006/09/22 09:00 MHDA- 2006/12/09 09:00 CRDT- 2006/09/22 09:00 AID - 15/suppl_2/R124 AID - 10.1093/hmg/ddl215 PST - ppublish SO - Hum Mol Genet. 2006 Oct 15;15 Spec No 2:R124-30.
崔略商 发表于 2009-06-03 15:21 阿司匹林于1899年进入临床使用，年龄比中国的云南白药还要大（云南白药创制于1902年），是名副其实的百年老药。除了最早发现的解热、消炎、镇痛作用外，它用于防治心脑血管疾病也有许多年的历史。它是所有医生最熟悉的药物之一，医生们对于它已经积累了相当丰富的经验。 但是，经验毕竟是主观的东西，会受到各种主客观混淆因素的影响，所以就需要严格设计的大规模临床试验来验证。又由于药物对于具有不同特点的患者人群会有不同的作用，所以，过去在某个患者人群中得出的研究结果不一定适用于其他人群。正因为如此，这种百年老药也还是有不断接受再评价的必要。 正如上文所说，人们已经知道阿司匹林可用于防治心脑血管疾病。对于曾经有过心脏病发作和中风史的患者，以及确诊的冠心病患者，服用阿司匹林治疗目前没有异议。但是对于没有心脏病和心脑血管事件发作史，却有此种风险的人群，是否应该常规服用阿司匹林，却是一直有着争议。这是因为阿司匹林虽然是好药，却也有着导致出血的副作用。 目前的心血管疾病防治指南推荐将阿司匹林用于中度冠心病风险人群的一级预防，就是推荐已知有一定冠心病风险但还没有患这个病的人通过吃阿司匹林来预防（这里简单介绍一下现代医学中三级预防的概念：一级预防就是没病防病；二级预防是指早期发现、早期诊断、早期治疗；三级预防是指疾病后期的治疗和康复）。但今年5月30日的《柳叶刀》杂志上发表的一篇研究论文指出，阿司匹林用于心脑血管疾病的一级预防时，可以使非致命性心肌梗死减少1/5，但不能显著降低中风的风险；而在不良反应方面，出血的风险却增加了1/3。因此，该论文的作者认为，对于无心脑血管疾病的患者，不应该推荐使用阿司匹林作为预防用药。 对此，美国心脏学会发言人，心血管病专家杰拉德弗莱彻（Gerald Fletcher）博士有不同意见。他认为指南是合理的，小剂量阿司匹林对出血风险小而又有心脏病发作风险的人群，带来的裨益大于风险。他认为这篇论文所分析的有的临床试验中使用的阿司匹林每日剂量高达500mg，这个剂量过大，小剂量更安全。当然，指南中也已经指出，不耐受阿司匹林的患者，或者有胃肠道出血，及出血性中风的患者，不应该服用阿司匹林。 鉴于这些不同意见的存在，对于每一个具体的患者，可能还是应该具体情况具体分析，由经治医生权衡利弊，来决定是否需要使用阿司匹林。 但无论是否赞同使用阿司匹林用于一级预防，两方面的专家都认为，预防心脑血管疾病，重点应放在控制血压和胆固醇上。对于胆固醇升高的人来说，首先要考虑的是使用他汀类降脂药，而不是急着用阿司匹林。 延伸阅读： Aspirin in the primary and secondary prevention of vascular disease: collaborative meta-analysis of individual participant data from randomised trials Debate Grows on Aspirin for Heart Risk Study Suggests Risks Outweigh Benefits of Taking Aspirin to Prevent Heart Attacks 图片来源：Image from soundentistry.com
标签: 冠心病
