2型糖尿病痰热互结证证候分布及生物学基础研究
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摘要
世界卫生组织统计,糖尿病患病率为6.3%。目前中国每年增加糖尿病病例100万,其中95%是2型糖尿病,积极开展2型糖尿病的防治工作已成为主要的社会公共卫生问题。运用中医药有效防治糖尿病是中医学界研究的重要任务。导师多年从事糖尿病的临床与科研工作,导师的临床实践和课题组既往研究表明痰热互结证是2型糖尿病的主要证型之一。本研究主要是对2型糖尿病痰热互结证证候进行理论探讨、临床流行病调查及生物学基础研究,以期阐明2型糖尿病痰热互结证证侯分布及生物学基础。
1.理论研究部分梳理了糖尿病中医病因病机与辨证分型研究文献,概述了2型糖尿病中医证型与微观指标关系研究进展,归纳总结了导师对2型糖尿病痰热互结证的认识及诊治心得。得出如下结论:长期的不良生活习惯伴随着现代人的精神压力、体质变化是糖尿病亦是其痰热互结证候形成的最重要的因素。2型糖尿病痰热互结证其形成多因过食肥甘、多坐少动、精神紧张等而致。2型糖尿病发病过程中痰热可互结共存、易与腑实胶结、易耗气伤阴、易痰热瘀互结等,致病具有复杂性,痰热互结可阻碍气机,壅遏血脉,变证丛生,致病具有广泛性,针对其致病广泛性、复杂性的特点,在临床中要引起高度重视,积极防治2型糖尿病痰热互结证。
2.临床研究部分采用随机、分层、整群抽样的前瞻性研究方法,对北京市宣武区、昌平区及平谷区的3个社区20岁以上长住社区居民5465人进行糖尿病流行病学和中医证型分布调查。得出如下结论:2型糖尿病与消渴病古今存在差异,无典型“三多一少”症状的肥胖患者为2型糖尿病的主体,痰热互结证是2型糖尿病的主要证型之一。正确认识它的作用和地位,对于2型糖尿病患者病情的控制具有重要意义。
3.基础研究部分以代谢状态异常为切入点,从人体测量学、血液代谢学、内分泌因子等三个层次研究2型糖尿病痰热互结证的生物学基础,得出如下结论:2型糖尿病痰热互结证组抵抗素分泌显著降低,与阴虚热盛证组组间差异有显著性意义,提示抵抗素可作为区分痰热互结证、阴虚热盛证不同证型的指标;脂联素的水平两证型组较对照组显著降低、瘦素、IL-6的水平两证型组较对照组显著升高。E-选择素、TNF-α、GLP-1、体重指数、腰臀比、糖代谢指标中空腹血糖、糖化血红蛋白、胰岛素、C-肽水平、脂代谢指标中胆固醇、甘油三酯、低密度脂蛋白、极低密度脂蛋白,尿肾功三项中尿白蛋白排泄率、糖蛋白和β_2-微球蛋白,血压、红细胞压积、纤维蛋白原、C反应蛋白指标中痰热互结证组较阴虚热盛证组虽无统计学差异,但皆有明显变化趋势,提示2型糖尿病痰热互结证与阴虚热盛证可能存在差异,还需进一步研究。
本研究的创新点在于1.开展了前瞻性2型糖尿病证型分布的流行病学调查,为2型糖尿病证型客观化研究提供思路与方法,资料证实了痰热互结证是现代2型糖尿病的主要证型之一。2.结合现代医学研究进展选择多个指标,对2型糖尿病痰热互结证的生物学基础进行了多角度、多层次的积极探索。
According toWorld Health Organization statistics,There is more than 170 million by 2025 which is expected to more than 300 million all over the world with diabetes,diabetes prevalence was 6.3%.China's current annual increase of one million cases of diabetes,of which 95 percent are type 2 diabetes, active prevention and treatment of type 2 diabetes has become a major public health problem in society.
The use of effective prevention and treatment of diabetes in Chinese medicine are important academic research mission.Instructor for many years engaged in diabetes clinical and research work,clinical practice and the instructor group study shows that previously Phlegm-heat syndrome are the main type of type 2 diabetes syndrome.The purpose of this study are of the type 2 diabetes Phlegm-heat syndrome explore theoretical,clinical epidemiological surveys and basic research in biology,with a view to clarify the type 2 diabetes Phlegm-heat syndrome distribution and basic biology.
1.Theoretical Study of some sort of diabetes etiology and pathogenesis of TCM Syndrome Types with the research literature,provides an overview of diabetes TCM Syndrome-and micro-target the relationship between research, summarized instructor of type 2 diabetes Phlegm-heat syndrome know and treatment experiences.Reached the following conclusion:long-term adverse living habits associated with modern mental stress,physical changes are diabetic it is also an inter-node heat syndromes formed the most important factor.Type 2 diabetes Phlegm-heat syndrome because of its formation have been many food,many sitting paucimobilis,mental tension due.Pathogenesis of type 2 diabetes during the heat can be inter-node co-exist easily with the internal organs is cemented, easily gas consumption and easy to heat,such as blood stasis Phlegm,pathogenic complexity,heat each node can block the gas machine,blood,variable permit proliferation with extensive disease,in view of its extensive disease,the complexity of the characteristics of clinical attach great importance to and actively control type 2 diabetes Phlegm-heat syndrome.
2.Part of clinical research using randomized,stratified,cluster sampling method A prospective study of Beijing Xuanwu District,Changping District, and Pinggu District 3 community over the age of 20 community residents to live a long 5465 for diabetes epidemiology and people TCM Syndrome Study investigate.
Draw the following conclusions:Type 2 Diabetes and Diabetes past differences, non-typical "one little more than three" symptoms of obese patients with type 2 diabetes as the main body of Phlegm-heat syndrome is type 2 diabetes,one of the main type.A correct understanding of its role and status,for patients with type 2 diabetes control the disease of great significance.
3.Part of basic research to abnormal metabolic status as the breakthrough point,from anthropometry,blood metabolism study,the three levels of endocrine factors such as type 2 diabetes study of Phlegm-heat syndrome each end of the biological basis of evidence,to draw the following conclusions:Phlegm-heat syndrome group resistin secretion was significantly higher,with the hot-Yin deficiency syndrome group permit difference between groups was significant, suggesting that resistin could be used as evidence to distinguish between Phlegm-heat,the hot-Yin deficiency Syndrome target different;adiponectin the level of pigment-type group than in the two permits a significant reduction in the control group,leptin,IL-6 level of the two syndrome group than in the control group significantly increased.E-selectin,TNF-α,GLP-1 level of each node Phlegm-heat syndrome group than in the hot Yin deficiency syndrome group and the control group no significant difference,but the trend has increased; body mass index,waist-hip ratio,sugar metabolism in the target fasting blood glucose,glycosylated hemoglobin insulin,C-peptide levels,lipid metabolism in the target cholesterol,triglyceride,low-density lipoprotein,very low density lipoprotein,three renal urinary albumin excretion rate in urine,sugar protein andβ2-microglobulin,blood pressure,hematocrit,fibrinogen, C-reactive protein in the target Phlegm-heat syndrome group than the hot-Yin deficiency syndrome group no significant difference between groups,but there is increase or decrease the Change trend,suggesting that there are differences between type 2 diabetes Phlegm-heat syndrom and the hot-Yin deficiency syndrome,and evidence of the possible differences need further study.
This study has two innovations:1.To carry out a prospective type 2 diabetes mellitus syndrom epidemiological survey distribution,evidence for Type 2 diabetes to provide an objective study of ideas and methods,data confirmed the evidence that type 2 diabetes Phlegm-heat syndrome was one of the main syndrom. 2.Combined withmodern medical research progress in a number of target selection, type 2 diabetes Phlegm-heat syndrome evidence for the basic biology of many ways to explore multi-level active.
1.理论研究部分梳理了糖尿病中医病因病机与辨证分型研究文献,概述了2型糖尿病中医证型与微观指标关系研究进展,归纳总结了导师对2型糖尿病痰热互结证的认识及诊治心得。得出如下结论:长期的不良生活习惯伴随着现代人的精神压力、体质变化是糖尿病亦是其痰热互结证候形成的最重要的因素。2型糖尿病痰热互结证其形成多因过食肥甘、多坐少动、精神紧张等而致。2型糖尿病发病过程中痰热可互结共存、易与腑实胶结、易耗气伤阴、易痰热瘀互结等,致病具有复杂性,痰热互结可阻碍气机,壅遏血脉,变证丛生,致病具有广泛性,针对其致病广泛性、复杂性的特点,在临床中要引起高度重视,积极防治2型糖尿病痰热互结证。
2.临床研究部分采用随机、分层、整群抽样的前瞻性研究方法,对北京市宣武区、昌平区及平谷区的3个社区20岁以上长住社区居民5465人进行糖尿病流行病学和中医证型分布调查。得出如下结论:2型糖尿病与消渴病古今存在差异,无典型“三多一少”症状的肥胖患者为2型糖尿病的主体,痰热互结证是2型糖尿病的主要证型之一。正确认识它的作用和地位,对于2型糖尿病患者病情的控制具有重要意义。
3.基础研究部分以代谢状态异常为切入点,从人体测量学、血液代谢学、内分泌因子等三个层次研究2型糖尿病痰热互结证的生物学基础,得出如下结论:2型糖尿病痰热互结证组抵抗素分泌显著降低,与阴虚热盛证组组间差异有显著性意义,提示抵抗素可作为区分痰热互结证、阴虚热盛证不同证型的指标;脂联素的水平两证型组较对照组显著降低、瘦素、IL-6的水平两证型组较对照组显著升高。E-选择素、TNF-α、GLP-1、体重指数、腰臀比、糖代谢指标中空腹血糖、糖化血红蛋白、胰岛素、C-肽水平、脂代谢指标中胆固醇、甘油三酯、低密度脂蛋白、极低密度脂蛋白,尿肾功三项中尿白蛋白排泄率、糖蛋白和β_2-微球蛋白,血压、红细胞压积、纤维蛋白原、C反应蛋白指标中痰热互结证组较阴虚热盛证组虽无统计学差异,但皆有明显变化趋势,提示2型糖尿病痰热互结证与阴虚热盛证可能存在差异,还需进一步研究。
本研究的创新点在于1.开展了前瞻性2型糖尿病证型分布的流行病学调查,为2型糖尿病证型客观化研究提供思路与方法,资料证实了痰热互结证是现代2型糖尿病的主要证型之一。2.结合现代医学研究进展选择多个指标,对2型糖尿病痰热互结证的生物学基础进行了多角度、多层次的积极探索。
According toWorld Health Organization statistics,There is more than 170 million by 2025 which is expected to more than 300 million all over the world with diabetes,diabetes prevalence was 6.3%.China's current annual increase of one million cases of diabetes,of which 95 percent are type 2 diabetes, active prevention and treatment of type 2 diabetes has become a major public health problem in society.
The use of effective prevention and treatment of diabetes in Chinese medicine are important academic research mission.Instructor for many years engaged in diabetes clinical and research work,clinical practice and the instructor group study shows that previously Phlegm-heat syndrome are the main type of type 2 diabetes syndrome.The purpose of this study are of the type 2 diabetes Phlegm-heat syndrome explore theoretical,clinical epidemiological surveys and basic research in biology,with a view to clarify the type 2 diabetes Phlegm-heat syndrome distribution and basic biology.
1.Theoretical Study of some sort of diabetes etiology and pathogenesis of TCM Syndrome Types with the research literature,provides an overview of diabetes TCM Syndrome-and micro-target the relationship between research, summarized instructor of type 2 diabetes Phlegm-heat syndrome know and treatment experiences.Reached the following conclusion:long-term adverse living habits associated with modern mental stress,physical changes are diabetic it is also an inter-node heat syndromes formed the most important factor.Type 2 diabetes Phlegm-heat syndrome because of its formation have been many food,many sitting paucimobilis,mental tension due.Pathogenesis of type 2 diabetes during the heat can be inter-node co-exist easily with the internal organs is cemented, easily gas consumption and easy to heat,such as blood stasis Phlegm,pathogenic complexity,heat each node can block the gas machine,blood,variable permit proliferation with extensive disease,in view of its extensive disease,the complexity of the characteristics of clinical attach great importance to and actively control type 2 diabetes Phlegm-heat syndrome.
2.Part of clinical research using randomized,stratified,cluster sampling method A prospective study of Beijing Xuanwu District,Changping District, and Pinggu District 3 community over the age of 20 community residents to live a long 5465 for diabetes epidemiology and people TCM Syndrome Study investigate.
Draw the following conclusions:Type 2 Diabetes and Diabetes past differences, non-typical "one little more than three" symptoms of obese patients with type 2 diabetes as the main body of Phlegm-heat syndrome is type 2 diabetes,one of the main type.A correct understanding of its role and status,for patients with type 2 diabetes control the disease of great significance.
3.Part of basic research to abnormal metabolic status as the breakthrough point,from anthropometry,blood metabolism study,the three levels of endocrine factors such as type 2 diabetes study of Phlegm-heat syndrome each end of the biological basis of evidence,to draw the following conclusions:Phlegm-heat syndrome group resistin secretion was significantly higher,with the hot-Yin deficiency syndrome group permit difference between groups was significant, suggesting that resistin could be used as evidence to distinguish between Phlegm-heat,the hot-Yin deficiency Syndrome target different;adiponectin the level of pigment-type group than in the two permits a significant reduction in the control group,leptin,IL-6 level of the two syndrome group than in the control group significantly increased.E-selectin,TNF-α,GLP-1 level of each node Phlegm-heat syndrome group than in the hot Yin deficiency syndrome group and the control group no significant difference,but the trend has increased; body mass index,waist-hip ratio,sugar metabolism in the target fasting blood glucose,glycosylated hemoglobin insulin,C-peptide levels,lipid metabolism in the target cholesterol,triglyceride,low-density lipoprotein,very low density lipoprotein,three renal urinary albumin excretion rate in urine,sugar protein andβ2-microglobulin,blood pressure,hematocrit,fibrinogen, C-reactive protein in the target Phlegm-heat syndrome group than the hot-Yin deficiency syndrome group no significant difference between groups,but there is increase or decrease the Change trend,suggesting that there are differences between type 2 diabetes Phlegm-heat syndrom and the hot-Yin deficiency syndrome,and evidence of the possible differences need further study.
This study has two innovations:1.To carry out a prospective type 2 diabetes mellitus syndrom epidemiological survey distribution,evidence for Type 2 diabetes to provide an objective study of ideas and methods,data confirmed the evidence that type 2 diabetes Phlegm-heat syndrome was one of the main syndrom. 2.Combined withmodern medical research progress in a number of target selection, type 2 diabetes Phlegm-heat syndrome evidence for the basic biology of many ways to explore multi-level active.
引文
[1]页:14熊曼琪.脾虚是消渴病的重要病机[J].广州中医学院学报,1991,(7):13-14.
[2]页:14庞铁良.脾升理论在治疗2型糖尿病中的地位.四川中医.2006,24(4):62-63.
[3]页:14王东,李敬林从“脾主运化”论治消渴.中国中医基础医学杂志.2002,8(12):43-44.
[4]页:14张凌志.试论糖尿病脾虚湿滞证.北京中医药大学学报.2002,25(3):71.
[5]崔振丰,温双兰,魏秋林.2型糖尿病辨治思路刍议[J].河北中医,2000,22(4):279
[6]刘喜明.中医药治疗2型糖尿病方法集粹[J].中医药学刊,2002,20(5):693-694
[7]徐丹慧.补肾阳法治疗糖尿病[J].河南中医,1998,18(5):314-315
[8]段尚勤.消渴之治勿忘调肝[J].光明中医,1996,11(6):5-6.
[9]程汉桥.肝气郁结与消渴病关系的理论研究[J].江苏中医,1997,18(9):49-50.
[10]邹如政.糖尿病从肝论治[J].中国医药学报,1998,13(1):17-23.
[11]郭俊杰.消渴从肝论治初探[J].中医研究,1997,10(3):12-13.
[12]赵泉霖,史秀珍.试论元气亏虚是消渴病发病的根本病机[J].山东中医药大学学报,2000,7(4):24
[13]王海云,徐建民.糖尿病气虚论[J].新疆中医药,2000,18(2):5-6
[14]詹锐文.第四届全国糖尿病(消渴病)学术研讨会论文集[M].284.
[15]康亚国.活血化淤法在糖尿病治疗中的应用探析[J].时珍国医国药,2006 17(6):1072-1074
[16]严晓华,梁彬强.糖尿病气阴两虚型证治探讨[J].山西中医,2007,23(1):78-80
[17]宋福印,孙灵娇,王迎新,等.消渴停胶囊治疗Ⅱ型糖尿病60例临床疗效观察[J].中国中医药科技,2001,8(1):44-45.
[18]刘志龙.消渴从阳虚论治临床体会[J].中国现代医药杂志,2007,2(9) 124-126
[19]曹忠贞.论消渴与痰[J].中医药研究,1997,13(2):8-9.
[20]程汗桥,马启明.糖尿病从痰湿论治的理论探讨[J].中国中医基础医学杂志,1999,5(4):49-50.
[21]彭万年.消渴病湿热证治探讨.新中医,1998,30(12):3.
[22]李赛美.糖尿病中医“湿热致消”研究近况.浙江中医杂志.2006,41(4):242-245.
[23]邱海江.消渴病的标本探析-火热为本[J].中医研究,2002,15(2):8-10
[24]仝小林.消渴六论[J].中医杂志,2001,42(4):253-253
[25]赵进喜.糖尿病内热伤阴耗气病机与清热类中成药[J].糖尿病新世界
[26]吴深涛.糖尿病中医病机新识[J].中国中医基础医学杂志,2005,11(11)808-810.
[27]仝小林.糖尿病中医新论.中华中医药杂志,2006,(6):349-352.
[28]吕仁和.糖尿病及其并发症中西医诊疗学[M].科学技术出版社.1991.97-98
[29]林兰.糖尿病的中西医结合论治[M].北京:北京科学技术出版社,1992.143-151.
[30]张延群,韩清,李瑛,等.2080例糖尿病患者证候与并发症相关性流行病学调查报告[J].上海中医药杂志,2000,22(1):15-16
[31]于青云,张德宪,杨浚宪,等.糖尿病证群调查及证型研究[J].山东中医药大学学报,2001,25(3):185-188
[32]张清梅,陈择奇,刘英哲,等.1490例2型糖尿病临床辨证分型调查分析[J].湖南中医学院学报,2004,24(5):33-35
[33]余学庆,李建生.2型糖尿病患者中医证候分布规律研究[J].上海中医药大学学报,2004,19(3):22-25
[34]刘喜明.试论消渴病临床面貌与概念的变化[J].世界中西医结合杂志 2007,2(4):187
[1]刘畅,于杰,梁惠芝等.老年及老年前期糖尿病辨证分型与胰岛素释放曲线关系的探讨[J].中西医结合杂志,1989,16(9):338-340.
[2]周国英,武雪萍,衡先培,等.Ⅱ型糖尿病中医辨证分型与胰岛素抵抗的关系[J].福建中医学院学报,2002,12(4):3-5.
[3]丁学屏.NIDDM中医辨证分型与胰高糖素、胰岛素敏感性的相关研究[J].曙光医刊,1998,14(1):3.
[4]王晖,马伟明.瘦素、胰岛素样生长因子-Ⅰ与阴虚热盛、气阴两虚型2型糖尿病关系的探讨[J]中国中医药科技,2006 13(4):211
[5]陆颢,丁学屏,蔡淦.84例NIDDM辨证分型与IR GLucagon的关系[J].辽宁中医志,1998,25(9):387-289.
[6]高玉芳,张玉璞.糖尿病中医辨证分型与客观指标相关性的探讨[J].安徽中医临床杂志,1998,10(4):206-207.
[7]李秋贵,贾太平,赵展荣,等.Ⅱ型糖尿病患者中医辨证分型与胰岛β细胞功能关系的研究[J].中医杂志,1998,39(7):428.
[8]宋家瑛.Ⅱ糖尿病患者血脂变化与中医辨证分型的关系[J].天津中医,2001,18(4):28.
[9]徐洁,宋宇.糖尿病患者脂质代谢紊乱与中医辨证分型的关系[J]湖北中医学院学报,2001,3(1):43.
[10]迟志超,李墨华,杨艳华,等.糖尿病的中医辨证与血液流变学关系观察60例[J].实用中西医结合杂志,1998,11(1):24.
[11]黄腾蛟,姚木铭,嵇美霞,等.糖尿病中医辨证分型与血、尿β微球蛋白相关性研究[J].福建中医药,2004,35(2):8-9.
[12]陈思兰,林兰,楚晓燕,等Ⅱ型糖尿病中医辨证分型与胰岛素抵抗的相关性分析[J].中国中医药信息杂志,2001,8(6):49.
[13]姜华.老年Ⅱ型糖尿病C肽水平与辨证分型的关系[J].中华实用中西医杂志,2004,17(11):1645-1646
[14]林寿宁,刘鹏,王彬,等.Ⅱ型糖尿病中医辨证分型与血清胃动素,胰高糖素、P物质关系的临床研究[J].中华实用中西医杂志,2002,2(15):1498-1499。
[15]蒋开平,简小云.Ⅱ型糖尿病患者中医辨证分型与空腹血胰高糖素含量的关系[J]辽宁中医杂志,1995,(01).
[16]祁建生,张恩平,李秀娟,等.Ⅱ型糖尿病不同中医证型红细胞Ins2PTRK活性变化机理探讨[J].浙江中西医结合杂志,2001,12(2):71-73.
[17]张崇祥,张庆云,苏天水,等.糖尿病辨证分型与激素关系的研究[J].中国中西医结合杂志,1998,8(12):714-716.
[18]袁效涵,张明利,韩伟峰.Ⅱ型糖尿病中医辨证分型与尿3种微量蛋白的关系[J].中国工医药科技,2000,7(5):318.
[19]徐洁.糖尿病中医辨证与血浆内皮素、心钠素及泌乳素的关系分析[J]中国中医药科技2001,8(3):153
[20]许军英,陈泽奇,胡瑛,等.糖尿病患者血清IL-6,IL-8和TN F-A变化与中医辨证分型关系的探讨[J].中国现代医学杂志,2003,13(11):66-67
[21]吴同玉,李植延,刘燕池.2型糖尿病(消渴病)微观辨证的临床研究[J]北京中医药大学学报(中医临床版),2003,10(3):1-4
[22]梁晓春,肖殿模,郭赛珊,等.糖尿病患者血浆TXB2、6-Keto-PGF1a水平、全血黏 度与血瘀证及微血管病的关系[J].中国中西医结合杂志1992,12(5):297-298.
[23]陈剑秋,施赛珠,石志芸.糖尿病血瘀证与血浆α—颗粒膜蛋白和内皮素关系的研究[J].中国中医基础医学杂志,1998,4(7)
[24]郭聂涛,祝向红,林棉,等.Ⅱ型糖尿病中医辨证分型与红细胞CD35粘附活性及数量表达的相关性[J].中国中医药信息杂志,2004,11(2):109-110.
[25]唐亚平,戴芳.Ⅱ型糖尿病中医辨证分型与血清骨钙素、甲状旁腺素水平的相关性研究[J].山西中医,2003,19(6):47-49.
[26]Steppan CM,Bailey ST.Bhats.et al The hormone resistin links obesity to diabetes[J]Nature,2001.409:307-312
[27]Vasselli JR.Behavioral and biological determinants of leptin resistance[J].Appetite,2001,37(2):115-117.
[28]Steppan CM,Bailey ST,Bhat S,et al.The hormone resistin links obesity to diabetes.Nature,2001,409:307-312.
[29]Satoh H,Nguyen MT,Miles PD,et al.Adenovirus-mediated chronic “hyperre-sistinemia” leads to in vivo insulin resistance in normal rats.J Clin Invest2004,114:224-231.
[30]章建梁,秦永文,郑兴,等.高血压病患者血清抵抗素浓度与游离脂肪酸水平的相关性研究[J].中国综合临床,2004,20(4):289-291.
[31]李慧,邹大进,张乐之,等.血清抵抗素水平与肥胖及2型糖尿病的关[J].中华糖尿病杂志,2004,12(3):199-201.
[32]Iqbal N,Seshadri P,Stern L,et al.Serum resistin is not associated with obesity or insulin resistance in humans.Eur Rev Med Pharmacol Sci,2005,9:161-165.
[33]Ruan H,Lodish HF.Insulin resistance in adipose tissue:direct and indirect effects of tumor necrosis factor-alpha[J].Cytokine Growth Factor Rev,2003,14:447-455.
[34]Rotter V,Nagaev I,Smith U.Interleukin-6 induces insulin resistance in3T3-L1 adipocytes and is,like IL-8 and TNF-alpha overexpressed inhuman fat cells from insulin-resistant subjects[J]J BiolChem,2003,278(46):45777-45784.
[35]王东,李敬林.肿瘤坏死因子与胰岛素抵抗的研究[J].中医药学刊.2003,21(4):560-562
[36]HofmannC,LorenzK,BraithwaiteSS,etal.Alteredgene expression for tumor necrosis factor-a and its receptors during drug and dietary modulation of insulin resistance.Endocrinology,1994,134:264
[37]Stefan N,Stumvoll M,Vozarova B et al.Plasma adiponectin and endogenous glucose production in humans[J].Diabetes Care,2003,26:3315-3319
[38]Yamauchi T,Kamon J,Waki H,et al.Globulal adiponectin protected ob/ob mice from diabetes and ApoE-deficient mice from atherosclerosis[J].J Biol Chem,2003,278:2461-2468.
[39]Lihn AS,Ostergard T,Nyholm B,et al.Adiponectin expression in adipose tissue is reduced in first-degree relatives of type 2diabetic patients.Am J Physiol EndocrinolMetab,2003,284:E443-E448.
[40]Lindsay RS,Funahashi T,Hanson RL,et al.Adiponectin and development of type 2diabetes in the Pima Indian population.Lancet,2002,360:57-58.
[41]Daimon M.Yaraaguchi H,Oizumi T,et al.Decreased serum levels of adiponectin are a risk factor for the progression to type 2 diabetes in the Japanese population:the Funagata study.Diabetes Care,2003,26:2015-2020.
[42]Yatagai T,Nagasaka S,Taniguchi A,et al.Hypoadiponectinemia is associated with visceral fat accumulation and insulin resistance in Japanese men with type 2 diabetes mellitus[J].Metabolism,2003,52(10):1274—1278.
[43]Philip KG,Gregorio D,Lu T,et al.Adiponectin expression from human adipose tissue:relation to obesity,insulin resistance and tumour necrosis-a expression.Diabetes,2003,52;1779-1785.
[44]Kamimura D,Ishihara K,Hirano T:IL-6 signal transduction and its physiological roles:the signal orchestration model.Rev Physiol Biochem Pharmacol.2003;149:1-38.
[45]Jones SA,Horiuchi S,Topley N,Yamamoto N,Fuller GM:The soluble interleukin 6 receptor:mechanisms of production and implications in disease.FASEB J.2001;15:43-58.
[46]Boulanger MJ,Chow DC,Brevnova EE,Garcia KC:Hexameric structure and assemblyofthe interleukin-6/IL-6alpha-receptor/gpl30complex.Science.2003;300:210-2104.
[47]Bruun JM,Verdich C,ToubroS et al.Association between measures of insulin sensitivity and circulating levels of interleukin-8interleukin-6 and tumor necrosis factor-alpha[J].Effect of weight loss in obesemen.Eur J Endocrinol,2003148:535-542.
[48]Rotter V,Nagaev I,Smith U.Interleukin-6 induces insulin resistance in3T3-Ll adipocytes and is,like IL-8 and TNF-alpha overexpressed inhuman fat cells from insulin2resistant subjects[J].J BiolChem,278(46):45777-45784.
[49]Senn JJ,Klover PJ,Nowak IA,et al Suppressor of cytokinesignaling23(SOCS),apotential mediator of interleukin262dependent insulin resistance inhepatocytes[J].J BiolChem,2003,278(16):13740-13746.
[50]Fasshauer M,Kralisch S,Kliver M,et al.Adiponectin gene expression and secretion is inhibited by interleukin-6 in 3T3-L1 adipocytes[J].Biochem Biophys Res Commun,2003,301(4):1045-1050.
[51]Haraldsen G,Kvale D,Lien $,et al.cytokine-regulated expression ofE-selectin,intercellular adhension molecule-1(ICAM-1),and vascular cell adhesion molecule-1(VCAM-1) in human intestinal mircrovascular endothelial cells[J].Immunol,1996,156:2558
[52]Shyu KG,Chang H,lin.CC,et al.Circulating intercellular adhesion molecule-1 and E-selectin in patients with acute with acute coronary syndrome.Chest,1996,109:1627-1630.
[53]Zheng F,Chevalier JA,Zhang LQ,et al.An Hphl polymorphism in the E-selectin gene is associated with premature coronary artery disease.Clin Genet,2001,59:58-64
[54]Ye SQ,Usher D,Virgil D,et al.A Pstl polymorphism detects the mutation of serine 128 to arginine in CD62E gene-a risk factor for coronary artery disease.J Biomed Sci,1999,6:18-21
[55]Limb GA,Hickman-Casey J,Hollif ield RD,et al.Vascular adhesio molecules in vitreous from eyes with proliferative diabetic retinopath[J].Invest Ophthalmol Vis Sci,1999,40(10):2453-2457.
[56]Matsumoto K,Sera Y,Ueki Y,et al.Comparison of serum concentrations of soluble adhesion molecules in diabetic microangiopathy an macroangiopathy[J].Diabet Med,2002,19(10):822-826.
[57]Matsumoto K,SeraY,UekiY,et a.1 Comparison of serum concentra-tions of soluble adhesion molecules in diabetic microangiopathy and macroangiopathy[J].DiabetMed,2002,19(10):822-826.
[58]MatsumotoK,Sera Y,NakamuraH.Serum concentrations of soluble adhesionmolecules are related to degree ofhyperglycemia and insulin resistance in patientswith type 2 diabetesmellitus[J].DiabetesRes Clin Pract,2002,55(2):131-138.
[59]Meigs JB,Hu FB,RifaiN,et a.l Biomarkers ofEndothelialDysfunc-tion and Risk of Type 2 DiabetesMellitus[J].JAMA,2004,291(16):1978-1986.
[60]Sokup A.Adhesion molecules in type 2 diabetes[J].Przegl Lek,2005,62(4):234-237.
[61]Horand B,Lowel H,Scheider A,et al.C-reactive protein as a predictor for incident diabetes mellitus among middle-aged men:results from the MONICA Augsberg cohort study,1984-1998.Arch Intern Med,2003,163(1):93-99.
[62]Wolford JK,Gruber JD,Ossowski VM,et al.A C-reactive protein promoter polymorphism is associated with type 2 diabetes mellitus in Pima Indians.MolGenet Metab,2003,78(2):136-144.
[63]VisserM,Bouter LM,McQuillan GM,et al.Elevated C-reactive protein levels in overweight and obeseadults.JAMA,1999,282(22):2131-2135.
[64]Diamantopoulos EJ,Andreadis EA,Tsourous GI,et al.Metabolic syndrome and prediabetes identify overlapping but not identical populations.Exp Clin Endocrinol Diabetes,2006,114(7):377-383.
[65]Rodilla E,Costa JA,Mares S,et al.Impact of metabolic syndrome on CRP levels.Rev Clin Esp,2006,206(8):363-368.
[66]Ridker PM,Buring JE,Cook NR,et al.C-reactiveprotein,the metabolic syndrome,and risk of incident cardiovascular events:an 8-year follow-up of 14,719 initiallyhealthy American women.Circulation.2003,07(3):391-397.
[67]Kieffer TJ,Habener JF.The glucagon-1ike peptides[J].Endocr Rev,1999,20(6):876-913.
[68]Deacon CF,Johnsen AH,Hoist JJ.Degradation of glucagon-1ike peptide-1 by human plasma in vitro yields an N-terminal-ly truncated peptide that is a major endogenous metabolite invivo[J].J Clin Endocrinol Metab,1995,80(3):952-957.
[69]Nakagawa A,Satake H,Nakabayashi H,et al.Receptorgene expression of glucagons-likepeptide-lbutnotglucose-dependentinsulinotropicpolypeptide in rat nodose ganglincells[J].Auton Neurosci,2004,110(1):36-43.
[70]ZerM,MadsbadS,Madsen JL,etal.Effect of 6-weekcourse of glucagons-1 ike peptide on glycaemic control,insu-lin sensitivity,and beta cell function in type 2 diabetes:aparallel group study[J].Lancet,2002,359(9309):824-830.
[71]Kieffer TJ,Habener JF.The glucagon-like peptides[J].Endocr Rev,1999,20(6):876-913.
[72]Stoffers DA,KiefferTJ,Hussain MA,et al.Insulinotropicglucagons-like peptide 1 agonists stimalte expression ofhomeodomain protein IDX-1 and increase islet size in mousepancreas[J].Diabetes,2000,49(5):741-748.
[73]Bulotta A,Hui H,Anastasi E,et al.Cultured pancreaticductal cells undergo cell cycle re-distribution and beta-cell-like differentiation in response to glucagons-like peptide-1[J].J Mol Endocrinol,2002,29(3):347-360.
[74]Wang X,Zhou J,Doyle ME,et al.Glucagon-like peptide-lcauses pancreatic duodenal homeobox-1 protein translocation from the cytoplasm to the nucleus of pancreatic beta-cells bya cyclic adenosine monophosphate/protein kinase A-dependent mechanism[J].Endocrinology,2001,142(5):1820-1827.
[75]Li L,El-Kholy W,Rhodes CJ,et al.Glucagon-like peptide-lprotects beta cells from cytokine-induced apoptosis and necro-sis:role of protein kinase B[J].Diabetologia,2005,48(7):1339-1349.
[1]陈黎亚,李志远,糖尿病与膳食因素及其它相关因素的研究[J],河南预防医学杂志,2004,15(30):140。
[2]Carlsson S,Midthjell K,Grill V.Smoking is associatedwith an increased risk of type 2 diabetes but a decreasedrisk of autoimmune diabetes in adults:an 11-year fol2low-up of incidence of diabetes in the Nord Trondela-gstudy.D iabetologia,2004,47(11):1953
[3]马林茂,富振英,王克安等.2型糖尿病危险因素的Logistic回归分析[J],中国糖尿病杂志,1999,7(5):26-27
[4]冯世纶等.经方传真.中国中医药出版社,1994:15
[5]清·徐灵胎.慎疾刍言.江苏科学技术出版社,1984:16
[6]邢锡波.伤寒论临床实验录.天津科技出版社,1984:10
[7]成友仁.伤寒论阐释.陕西科学技术出版社,1983:426
[8]国家计量总局.中国古代度量衡图集.文物出版社,1981
[1]国际生命科学学会中国办事处中国肥胖问题工作组.中国成人体质指数分类的推荐意见简介[J],中华预防医学杂志,2001,35(5):349-350.
[2]中国肥胖问题工作组数据汇总分析协作组.我国成人体重指数和腰围对相关疾病危险因素异常的预测价值:适宜体重指数和腰围切点的研究[J],中华流行病学杂志,2002,23(1):5-10.
[3]糖尿病中医防治指南 中国中医药出版社,2006
[4]项坤三 糖尿病临床面貌及概念的变化[J].中国糖尿病杂志,2003,11(1):2-3
[5]李光伟.纠正肥胖与胰岛素抵抗对2型糖尿病防治的重要性[J].中国糖尿病杂志,2003,11(2):77
[6]刘喜明.试论消渴病临床面貌与概念的变化[J].世界中西医结合杂志2007,2(4):187
[1]International Diabetes Federation:Diabetes and impaired glucose tolerance:prevalence and projections.In:Diabetes Atlas2nd edition[M]1WorldDiabetes Foundationl 2003.17
[2]唐晓君,卢仙娥.2型糖尿病的危险因素分析.中国公共卫生.2004,20(1):74-76
[3]王玉芳,孟凡杰.糖尿病人血液流变学改变及其与血糖水平的相关性分析 医学检验与临床 2007 18(4):31-33
[4]黎万凤 尿微量白蛋白检测在糖尿病患者中的诊断价值中国实用医药 2008 7(3):76
[5]Jianping Ye 代谢综合征研究新进展.中国糖尿病杂志.2009,17(2):81-84.
[6]kim JY,Van de.Obesity-associated improvements in metabolic profile through exnansion of adipose tissule J Clin Invest.2007.117:2621-2637
[7]李小英,温俊平,脂肪因子与中枢对话.中国糖尿病杂志.2008,16(7):441-443.
[8]RexfordS.Ahima,1YongQi.BrainAdipocytokineActionandMetabolicRegulationDIA BETES,2006,55:SUPPLEMENT,Supplerue,S145-154
[9]李久红.对瘦素的进一步认识.武警医学院学报.2008,17(1):75-78.
[10]李慧,邹大进,张乐之等.血清抵抗素水平与肥胖及2型糖尿病的关[J].中华糖尿病杂志,2004,12(3):199-201.
[11]HofmannC,LorenzK,BraithwaiteSS,etal.Alteredgene expression for tumor necrosis factor-a and its receptors during drug and dietary modulation of insulin resistance.Endocrinology,1994,134:264
[12]Daimon M.Yamaguchi H,Oizumi T,et al.Decreased serum levels of adiponectin are a risk factor for the progression to type 2 diabetes in the Japanese population:the Funagata study.Diabetes Care,2003,26:2015-2020.
[13]Sokup A.Adhesionmoleculesintype 2 diabetes[J].PrzeglLek200562(4):234-237.
[14]Zer M,Madsbad S,Madsen JL,etal.Effect of 6-weekcourse of glucagons-like peptide 1 on glycaemic control,insu-lin sensitivity,and beta cell function in type 2 diabetes:aparallel group study[J].Lancet,2002,359(9309):824-830.
[15]Steppan CM,Mitchell A.Resistin and obesity-associated insulin resistance.Trends Endocrinol Metab,2002,13:18-23
[16]Yang WS,Lee WJ,Funahashi T,et al.Plasma adiponect in levels in over weight and obese Asians.Obes Res,2002,10:1104-1110
[17]Bruun JM,Verdich C,Toubro S,et al.Association between measure of insulin sensivity and circulating levels of interleukin-8,interleukin-6 and tumor factor-alpha.Effect of weight loss in obese men.Eur J Endocrinol,2003,278:45777-45784
[18]杨玉莲,孙新宇.黄连温胆汤加味治疗肥胖型消渴30例[J].中医研究,2007,20(4):48.
[19]乔玉秋.论糖尿病与痰的关系[J].实用中医内科学杂志,1993,(2):44-45.
[20]张镜人.祖国医学对冠心病的辨证施治.资料 1997.
[21]屠浩明.高脂血症血脂水平与中医辨证分型的相关性研究[J].福建中医药,2003,34(6):3.
[22]郭蕾,王永炎,张志斌.关于证候概念的诠释[J].北京中医药大学学报,2003,26(2):5-8
[23]陈小野.证候实质研究中弱特异性的正面观[J].医学与哲学,1995,16(6):311-313
[24]江锋.中医证候本质研究的回顾与思考.中医药学刊[J].2005,23(1) 131-133
[2]页:14庞铁良.脾升理论在治疗2型糖尿病中的地位.四川中医.2006,24(4):62-63.
[3]页:14王东,李敬林从“脾主运化”论治消渴.中国中医基础医学杂志.2002,8(12):43-44.
[4]页:14张凌志.试论糖尿病脾虚湿滞证.北京中医药大学学报.2002,25(3):71.
[5]崔振丰,温双兰,魏秋林.2型糖尿病辨治思路刍议[J].河北中医,2000,22(4):279
[6]刘喜明.中医药治疗2型糖尿病方法集粹[J].中医药学刊,2002,20(5):693-694
[7]徐丹慧.补肾阳法治疗糖尿病[J].河南中医,1998,18(5):314-315
[8]段尚勤.消渴之治勿忘调肝[J].光明中医,1996,11(6):5-6.
[9]程汉桥.肝气郁结与消渴病关系的理论研究[J].江苏中医,1997,18(9):49-50.
[10]邹如政.糖尿病从肝论治[J].中国医药学报,1998,13(1):17-23.
[11]郭俊杰.消渴从肝论治初探[J].中医研究,1997,10(3):12-13.
[12]赵泉霖,史秀珍.试论元气亏虚是消渴病发病的根本病机[J].山东中医药大学学报,2000,7(4):24
[13]王海云,徐建民.糖尿病气虚论[J].新疆中医药,2000,18(2):5-6
[14]詹锐文.第四届全国糖尿病(消渴病)学术研讨会论文集[M].284.
[15]康亚国.活血化淤法在糖尿病治疗中的应用探析[J].时珍国医国药,2006 17(6):1072-1074
[16]严晓华,梁彬强.糖尿病气阴两虚型证治探讨[J].山西中医,2007,23(1):78-80
[17]宋福印,孙灵娇,王迎新,等.消渴停胶囊治疗Ⅱ型糖尿病60例临床疗效观察[J].中国中医药科技,2001,8(1):44-45.
[18]刘志龙.消渴从阳虚论治临床体会[J].中国现代医药杂志,2007,2(9) 124-126
[19]曹忠贞.论消渴与痰[J].中医药研究,1997,13(2):8-9.
[20]程汗桥,马启明.糖尿病从痰湿论治的理论探讨[J].中国中医基础医学杂志,1999,5(4):49-50.
[21]彭万年.消渴病湿热证治探讨.新中医,1998,30(12):3.
[22]李赛美.糖尿病中医“湿热致消”研究近况.浙江中医杂志.2006,41(4):242-245.
[23]邱海江.消渴病的标本探析-火热为本[J].中医研究,2002,15(2):8-10
[24]仝小林.消渴六论[J].中医杂志,2001,42(4):253-253
[25]赵进喜.糖尿病内热伤阴耗气病机与清热类中成药[J].糖尿病新世界
[26]吴深涛.糖尿病中医病机新识[J].中国中医基础医学杂志,2005,11(11)808-810.
[27]仝小林.糖尿病中医新论.中华中医药杂志,2006,(6):349-352.
[28]吕仁和.糖尿病及其并发症中西医诊疗学[M].科学技术出版社.1991.97-98
[29]林兰.糖尿病的中西医结合论治[M].北京:北京科学技术出版社,1992.143-151.
[30]张延群,韩清,李瑛,等.2080例糖尿病患者证候与并发症相关性流行病学调查报告[J].上海中医药杂志,2000,22(1):15-16
[31]于青云,张德宪,杨浚宪,等.糖尿病证群调查及证型研究[J].山东中医药大学学报,2001,25(3):185-188
[32]张清梅,陈择奇,刘英哲,等.1490例2型糖尿病临床辨证分型调查分析[J].湖南中医学院学报,2004,24(5):33-35
[33]余学庆,李建生.2型糖尿病患者中医证候分布规律研究[J].上海中医药大学学报,2004,19(3):22-25
[34]刘喜明.试论消渴病临床面貌与概念的变化[J].世界中西医结合杂志 2007,2(4):187
[1]刘畅,于杰,梁惠芝等.老年及老年前期糖尿病辨证分型与胰岛素释放曲线关系的探讨[J].中西医结合杂志,1989,16(9):338-340.
[2]周国英,武雪萍,衡先培,等.Ⅱ型糖尿病中医辨证分型与胰岛素抵抗的关系[J].福建中医学院学报,2002,12(4):3-5.
[3]丁学屏.NIDDM中医辨证分型与胰高糖素、胰岛素敏感性的相关研究[J].曙光医刊,1998,14(1):3.
[4]王晖,马伟明.瘦素、胰岛素样生长因子-Ⅰ与阴虚热盛、气阴两虚型2型糖尿病关系的探讨[J]中国中医药科技,2006 13(4):211
[5]陆颢,丁学屏,蔡淦.84例NIDDM辨证分型与IR GLucagon的关系[J].辽宁中医志,1998,25(9):387-289.
[6]高玉芳,张玉璞.糖尿病中医辨证分型与客观指标相关性的探讨[J].安徽中医临床杂志,1998,10(4):206-207.
[7]李秋贵,贾太平,赵展荣,等.Ⅱ型糖尿病患者中医辨证分型与胰岛β细胞功能关系的研究[J].中医杂志,1998,39(7):428.
[8]宋家瑛.Ⅱ糖尿病患者血脂变化与中医辨证分型的关系[J].天津中医,2001,18(4):28.
[9]徐洁,宋宇.糖尿病患者脂质代谢紊乱与中医辨证分型的关系[J]湖北中医学院学报,2001,3(1):43.
[10]迟志超,李墨华,杨艳华,等.糖尿病的中医辨证与血液流变学关系观察60例[J].实用中西医结合杂志,1998,11(1):24.
[11]黄腾蛟,姚木铭,嵇美霞,等.糖尿病中医辨证分型与血、尿β微球蛋白相关性研究[J].福建中医药,2004,35(2):8-9.
[12]陈思兰,林兰,楚晓燕,等Ⅱ型糖尿病中医辨证分型与胰岛素抵抗的相关性分析[J].中国中医药信息杂志,2001,8(6):49.
[13]姜华.老年Ⅱ型糖尿病C肽水平与辨证分型的关系[J].中华实用中西医杂志,2004,17(11):1645-1646
[14]林寿宁,刘鹏,王彬,等.Ⅱ型糖尿病中医辨证分型与血清胃动素,胰高糖素、P物质关系的临床研究[J].中华实用中西医杂志,2002,2(15):1498-1499。
[15]蒋开平,简小云.Ⅱ型糖尿病患者中医辨证分型与空腹血胰高糖素含量的关系[J]辽宁中医杂志,1995,(01).
[16]祁建生,张恩平,李秀娟,等.Ⅱ型糖尿病不同中医证型红细胞Ins2PTRK活性变化机理探讨[J].浙江中西医结合杂志,2001,12(2):71-73.
[17]张崇祥,张庆云,苏天水,等.糖尿病辨证分型与激素关系的研究[J].中国中西医结合杂志,1998,8(12):714-716.
[18]袁效涵,张明利,韩伟峰.Ⅱ型糖尿病中医辨证分型与尿3种微量蛋白的关系[J].中国工医药科技,2000,7(5):318.
[19]徐洁.糖尿病中医辨证与血浆内皮素、心钠素及泌乳素的关系分析[J]中国中医药科技2001,8(3):153
[20]许军英,陈泽奇,胡瑛,等.糖尿病患者血清IL-6,IL-8和TN F-A变化与中医辨证分型关系的探讨[J].中国现代医学杂志,2003,13(11):66-67
[21]吴同玉,李植延,刘燕池.2型糖尿病(消渴病)微观辨证的临床研究[J]北京中医药大学学报(中医临床版),2003,10(3):1-4
[22]梁晓春,肖殿模,郭赛珊,等.糖尿病患者血浆TXB2、6-Keto-PGF1a水平、全血黏 度与血瘀证及微血管病的关系[J].中国中西医结合杂志1992,12(5):297-298.
[23]陈剑秋,施赛珠,石志芸.糖尿病血瘀证与血浆α—颗粒膜蛋白和内皮素关系的研究[J].中国中医基础医学杂志,1998,4(7)
[24]郭聂涛,祝向红,林棉,等.Ⅱ型糖尿病中医辨证分型与红细胞CD35粘附活性及数量表达的相关性[J].中国中医药信息杂志,2004,11(2):109-110.
[25]唐亚平,戴芳.Ⅱ型糖尿病中医辨证分型与血清骨钙素、甲状旁腺素水平的相关性研究[J].山西中医,2003,19(6):47-49.
[26]Steppan CM,Bailey ST.Bhats.et al The hormone resistin links obesity to diabetes[J]Nature,2001.409:307-312
[27]Vasselli JR.Behavioral and biological determinants of leptin resistance[J].Appetite,2001,37(2):115-117.
[28]Steppan CM,Bailey ST,Bhat S,et al.The hormone resistin links obesity to diabetes.Nature,2001,409:307-312.
[29]Satoh H,Nguyen MT,Miles PD,et al.Adenovirus-mediated chronic “hyperre-sistinemia” leads to in vivo insulin resistance in normal rats.J Clin Invest2004,114:224-231.
[30]章建梁,秦永文,郑兴,等.高血压病患者血清抵抗素浓度与游离脂肪酸水平的相关性研究[J].中国综合临床,2004,20(4):289-291.
[31]李慧,邹大进,张乐之,等.血清抵抗素水平与肥胖及2型糖尿病的关[J].中华糖尿病杂志,2004,12(3):199-201.
[32]Iqbal N,Seshadri P,Stern L,et al.Serum resistin is not associated with obesity or insulin resistance in humans.Eur Rev Med Pharmacol Sci,2005,9:161-165.
[33]Ruan H,Lodish HF.Insulin resistance in adipose tissue:direct and indirect effects of tumor necrosis factor-alpha[J].Cytokine Growth Factor Rev,2003,14:447-455.
[34]Rotter V,Nagaev I,Smith U.Interleukin-6 induces insulin resistance in3T3-L1 adipocytes and is,like IL-8 and TNF-alpha overexpressed inhuman fat cells from insulin-resistant subjects[J]J BiolChem,2003,278(46):45777-45784.
[35]王东,李敬林.肿瘤坏死因子与胰岛素抵抗的研究[J].中医药学刊.2003,21(4):560-562
[36]HofmannC,LorenzK,BraithwaiteSS,etal.Alteredgene expression for tumor necrosis factor-a and its receptors during drug and dietary modulation of insulin resistance.Endocrinology,1994,134:264
[37]Stefan N,Stumvoll M,Vozarova B et al.Plasma adiponectin and endogenous glucose production in humans[J].Diabetes Care,2003,26:3315-3319
[38]Yamauchi T,Kamon J,Waki H,et al.Globulal adiponectin protected ob/ob mice from diabetes and ApoE-deficient mice from atherosclerosis[J].J Biol Chem,2003,278:2461-2468.
[39]Lihn AS,Ostergard T,Nyholm B,et al.Adiponectin expression in adipose tissue is reduced in first-degree relatives of type 2diabetic patients.Am J Physiol EndocrinolMetab,2003,284:E443-E448.
[40]Lindsay RS,Funahashi T,Hanson RL,et al.Adiponectin and development of type 2diabetes in the Pima Indian population.Lancet,2002,360:57-58.
[41]Daimon M.Yaraaguchi H,Oizumi T,et al.Decreased serum levels of adiponectin are a risk factor for the progression to type 2 diabetes in the Japanese population:the Funagata study.Diabetes Care,2003,26:2015-2020.
[42]Yatagai T,Nagasaka S,Taniguchi A,et al.Hypoadiponectinemia is associated with visceral fat accumulation and insulin resistance in Japanese men with type 2 diabetes mellitus[J].Metabolism,2003,52(10):1274—1278.
[43]Philip KG,Gregorio D,Lu T,et al.Adiponectin expression from human adipose tissue:relation to obesity,insulin resistance and tumour necrosis-a expression.Diabetes,2003,52;1779-1785.
[44]Kamimura D,Ishihara K,Hirano T:IL-6 signal transduction and its physiological roles:the signal orchestration model.Rev Physiol Biochem Pharmacol.2003;149:1-38.
[45]Jones SA,Horiuchi S,Topley N,Yamamoto N,Fuller GM:The soluble interleukin 6 receptor:mechanisms of production and implications in disease.FASEB J.2001;15:43-58.
[46]Boulanger MJ,Chow DC,Brevnova EE,Garcia KC:Hexameric structure and assemblyofthe interleukin-6/IL-6alpha-receptor/gpl30complex.Science.2003;300:210-2104.
[47]Bruun JM,Verdich C,ToubroS et al.Association between measures of insulin sensitivity and circulating levels of interleukin-8interleukin-6 and tumor necrosis factor-alpha[J].Effect of weight loss in obesemen.Eur J Endocrinol,2003148:535-542.
[48]Rotter V,Nagaev I,Smith U.Interleukin-6 induces insulin resistance in3T3-Ll adipocytes and is,like IL-8 and TNF-alpha overexpressed inhuman fat cells from insulin2resistant subjects[J].J BiolChem,278(46):45777-45784.
[49]Senn JJ,Klover PJ,Nowak IA,et al Suppressor of cytokinesignaling23(SOCS),apotential mediator of interleukin262dependent insulin resistance inhepatocytes[J].J BiolChem,2003,278(16):13740-13746.
[50]Fasshauer M,Kralisch S,Kliver M,et al.Adiponectin gene expression and secretion is inhibited by interleukin-6 in 3T3-L1 adipocytes[J].Biochem Biophys Res Commun,2003,301(4):1045-1050.
[51]Haraldsen G,Kvale D,Lien $,et al.cytokine-regulated expression ofE-selectin,intercellular adhension molecule-1(ICAM-1),and vascular cell adhesion molecule-1(VCAM-1) in human intestinal mircrovascular endothelial cells[J].Immunol,1996,156:2558
[52]Shyu KG,Chang H,lin.CC,et al.Circulating intercellular adhesion molecule-1 and E-selectin in patients with acute with acute coronary syndrome.Chest,1996,109:1627-1630.
[53]Zheng F,Chevalier JA,Zhang LQ,et al.An Hphl polymorphism in the E-selectin gene is associated with premature coronary artery disease.Clin Genet,2001,59:58-64
[54]Ye SQ,Usher D,Virgil D,et al.A Pstl polymorphism detects the mutation of serine 128 to arginine in CD62E gene-a risk factor for coronary artery disease.J Biomed Sci,1999,6:18-21
[55]Limb GA,Hickman-Casey J,Hollif ield RD,et al.Vascular adhesio molecules in vitreous from eyes with proliferative diabetic retinopath[J].Invest Ophthalmol Vis Sci,1999,40(10):2453-2457.
[56]Matsumoto K,Sera Y,Ueki Y,et al.Comparison of serum concentrations of soluble adhesion molecules in diabetic microangiopathy an macroangiopathy[J].Diabet Med,2002,19(10):822-826.
[57]Matsumoto K,SeraY,UekiY,et a.1 Comparison of serum concentra-tions of soluble adhesion molecules in diabetic microangiopathy and macroangiopathy[J].DiabetMed,2002,19(10):822-826.
[58]MatsumotoK,Sera Y,NakamuraH.Serum concentrations of soluble adhesionmolecules are related to degree ofhyperglycemia and insulin resistance in patientswith type 2 diabetesmellitus[J].DiabetesRes Clin Pract,2002,55(2):131-138.
[59]Meigs JB,Hu FB,RifaiN,et a.l Biomarkers ofEndothelialDysfunc-tion and Risk of Type 2 DiabetesMellitus[J].JAMA,2004,291(16):1978-1986.
[60]Sokup A.Adhesion molecules in type 2 diabetes[J].Przegl Lek,2005,62(4):234-237.
[61]Horand B,Lowel H,Scheider A,et al.C-reactive protein as a predictor for incident diabetes mellitus among middle-aged men:results from the MONICA Augsberg cohort study,1984-1998.Arch Intern Med,2003,163(1):93-99.
[62]Wolford JK,Gruber JD,Ossowski VM,et al.A C-reactive protein promoter polymorphism is associated with type 2 diabetes mellitus in Pima Indians.MolGenet Metab,2003,78(2):136-144.
[63]VisserM,Bouter LM,McQuillan GM,et al.Elevated C-reactive protein levels in overweight and obeseadults.JAMA,1999,282(22):2131-2135.
[64]Diamantopoulos EJ,Andreadis EA,Tsourous GI,et al.Metabolic syndrome and prediabetes identify overlapping but not identical populations.Exp Clin Endocrinol Diabetes,2006,114(7):377-383.
[65]Rodilla E,Costa JA,Mares S,et al.Impact of metabolic syndrome on CRP levels.Rev Clin Esp,2006,206(8):363-368.
[66]Ridker PM,Buring JE,Cook NR,et al.C-reactiveprotein,the metabolic syndrome,and risk of incident cardiovascular events:an 8-year follow-up of 14,719 initiallyhealthy American women.Circulation.2003,07(3):391-397.
[67]Kieffer TJ,Habener JF.The glucagon-1ike peptides[J].Endocr Rev,1999,20(6):876-913.
[68]Deacon CF,Johnsen AH,Hoist JJ.Degradation of glucagon-1ike peptide-1 by human plasma in vitro yields an N-terminal-ly truncated peptide that is a major endogenous metabolite invivo[J].J Clin Endocrinol Metab,1995,80(3):952-957.
[69]Nakagawa A,Satake H,Nakabayashi H,et al.Receptorgene expression of glucagons-likepeptide-lbutnotglucose-dependentinsulinotropicpolypeptide in rat nodose ganglincells[J].Auton Neurosci,2004,110(1):36-43.
[70]ZerM,MadsbadS,Madsen JL,etal.Effect of 6-weekcourse of glucagons-1 ike peptide on glycaemic control,insu-lin sensitivity,and beta cell function in type 2 diabetes:aparallel group study[J].Lancet,2002,359(9309):824-830.
[71]Kieffer TJ,Habener JF.The glucagon-like peptides[J].Endocr Rev,1999,20(6):876-913.
[72]Stoffers DA,KiefferTJ,Hussain MA,et al.Insulinotropicglucagons-like peptide 1 agonists stimalte expression ofhomeodomain protein IDX-1 and increase islet size in mousepancreas[J].Diabetes,2000,49(5):741-748.
[73]Bulotta A,Hui H,Anastasi E,et al.Cultured pancreaticductal cells undergo cell cycle re-distribution and beta-cell-like differentiation in response to glucagons-like peptide-1[J].J Mol Endocrinol,2002,29(3):347-360.
[74]Wang X,Zhou J,Doyle ME,et al.Glucagon-like peptide-lcauses pancreatic duodenal homeobox-1 protein translocation from the cytoplasm to the nucleus of pancreatic beta-cells bya cyclic adenosine monophosphate/protein kinase A-dependent mechanism[J].Endocrinology,2001,142(5):1820-1827.
[75]Li L,El-Kholy W,Rhodes CJ,et al.Glucagon-like peptide-lprotects beta cells from cytokine-induced apoptosis and necro-sis:role of protein kinase B[J].Diabetologia,2005,48(7):1339-1349.
[1]陈黎亚,李志远,糖尿病与膳食因素及其它相关因素的研究[J],河南预防医学杂志,2004,15(30):140。
[2]Carlsson S,Midthjell K,Grill V.Smoking is associatedwith an increased risk of type 2 diabetes but a decreasedrisk of autoimmune diabetes in adults:an 11-year fol2low-up of incidence of diabetes in the Nord Trondela-gstudy.D iabetologia,2004,47(11):1953
[3]马林茂,富振英,王克安等.2型糖尿病危险因素的Logistic回归分析[J],中国糖尿病杂志,1999,7(5):26-27
[4]冯世纶等.经方传真.中国中医药出版社,1994:15
[5]清·徐灵胎.慎疾刍言.江苏科学技术出版社,1984:16
[6]邢锡波.伤寒论临床实验录.天津科技出版社,1984:10
[7]成友仁.伤寒论阐释.陕西科学技术出版社,1983:426
[8]国家计量总局.中国古代度量衡图集.文物出版社,1981
[1]国际生命科学学会中国办事处中国肥胖问题工作组.中国成人体质指数分类的推荐意见简介[J],中华预防医学杂志,2001,35(5):349-350.
[2]中国肥胖问题工作组数据汇总分析协作组.我国成人体重指数和腰围对相关疾病危险因素异常的预测价值:适宜体重指数和腰围切点的研究[J],中华流行病学杂志,2002,23(1):5-10.
[3]糖尿病中医防治指南 中国中医药出版社,2006
[4]项坤三 糖尿病临床面貌及概念的变化[J].中国糖尿病杂志,2003,11(1):2-3
[5]李光伟.纠正肥胖与胰岛素抵抗对2型糖尿病防治的重要性[J].中国糖尿病杂志,2003,11(2):77
[6]刘喜明.试论消渴病临床面貌与概念的变化[J].世界中西医结合杂志2007,2(4):187
[1]International Diabetes Federation:Diabetes and impaired glucose tolerance:prevalence and projections.In:Diabetes Atlas2nd edition[M]1WorldDiabetes Foundationl 2003.17
[2]唐晓君,卢仙娥.2型糖尿病的危险因素分析.中国公共卫生.2004,20(1):74-76
[3]王玉芳,孟凡杰.糖尿病人血液流变学改变及其与血糖水平的相关性分析 医学检验与临床 2007 18(4):31-33
[4]黎万凤 尿微量白蛋白检测在糖尿病患者中的诊断价值中国实用医药 2008 7(3):76
[5]Jianping Ye 代谢综合征研究新进展.中国糖尿病杂志.2009,17(2):81-84.
[6]kim JY,Van de.Obesity-associated improvements in metabolic profile through exnansion of adipose tissule J Clin Invest.2007.117:2621-2637
[7]李小英,温俊平,脂肪因子与中枢对话.中国糖尿病杂志.2008,16(7):441-443.
[8]RexfordS.Ahima,1YongQi.BrainAdipocytokineActionandMetabolicRegulationDIA BETES,2006,55:SUPPLEMENT,Supplerue,S145-154
[9]李久红.对瘦素的进一步认识.武警医学院学报.2008,17(1):75-78.
[10]李慧,邹大进,张乐之等.血清抵抗素水平与肥胖及2型糖尿病的关[J].中华糖尿病杂志,2004,12(3):199-201.
[11]HofmannC,LorenzK,BraithwaiteSS,etal.Alteredgene expression for tumor necrosis factor-a and its receptors during drug and dietary modulation of insulin resistance.Endocrinology,1994,134:264
[12]Daimon M.Yamaguchi H,Oizumi T,et al.Decreased serum levels of adiponectin are a risk factor for the progression to type 2 diabetes in the Japanese population:the Funagata study.Diabetes Care,2003,26:2015-2020.
[13]Sokup A.Adhesionmoleculesintype 2 diabetes[J].PrzeglLek200562(4):234-237.
[14]Zer M,Madsbad S,Madsen JL,etal.Effect of 6-weekcourse of glucagons-like peptide 1 on glycaemic control,insu-lin sensitivity,and beta cell function in type 2 diabetes:aparallel group study[J].Lancet,2002,359(9309):824-830.
[15]Steppan CM,Mitchell A.Resistin and obesity-associated insulin resistance.Trends Endocrinol Metab,2002,13:18-23
[16]Yang WS,Lee WJ,Funahashi T,et al.Plasma adiponect in levels in over weight and obese Asians.Obes Res,2002,10:1104-1110
[17]Bruun JM,Verdich C,Toubro S,et al.Association between measure of insulin sensivity and circulating levels of interleukin-8,interleukin-6 and tumor factor-alpha.Effect of weight loss in obese men.Eur J Endocrinol,2003,278:45777-45784
[18]杨玉莲,孙新宇.黄连温胆汤加味治疗肥胖型消渴30例[J].中医研究,2007,20(4):48.
[19]乔玉秋.论糖尿病与痰的关系[J].实用中医内科学杂志,1993,(2):44-45.
[20]张镜人.祖国医学对冠心病的辨证施治.资料 1997.
[21]屠浩明.高脂血症血脂水平与中医辨证分型的相关性研究[J].福建中医药,2003,34(6):3.
[22]郭蕾,王永炎,张志斌.关于证候概念的诠释[J].北京中医药大学学报,2003,26(2):5-8
[23]陈小野.证候实质研究中弱特异性的正面观[J].医学与哲学,1995,16(6):311-313
[24]江锋.中医证候本质研究的回顾与思考.中医药学刊[J].2005,23(1) 131-133