单纯性肥胖人群2型糖尿病发病相关危险因素分析
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摘要
目的:了解单纯性肥胖人群发生2型糖尿病的流行病学情况,探讨该人群发生2型糖尿病的相关危险因素,进而对其2型糖尿病的预测和预防提供依据。
研究对象及方法:
1研究对象:石家庄市区的单纯性肥胖人群(从本院体检中心健康查体人群中筛选,据2002年亚太地区的肥胖标准,体重指数(BMI)≥25kg/m~2,经临床和实验室检查除外高血压、冠心病、血脂异常、糖尿病或糖耐量异常及其他疾病,女性排除绝经者。年龄在35-55岁)共583例,其中男性316例,女性267例。
2研究方法:2000年采集入组人群信息:记录基本信息(包括性别、年龄、日常生活习惯、糖尿病家族史等),测定心率(heart rate, HR)、血压、身高、体重、腰围、臀围、血脂(包括总胆固醇(TC)、甘油三脂(TG)、低密度脂蛋白胆固醇(LDL-c)、高密度脂蛋白胆固醇(HDL-c))、空腹血糖及胰岛素浓度、血管内皮依赖性舒张功能(endothelium dependent dilatation,EDD)。计算体重指数(body mass index, BMI)、腰臀比(waist hip ratio, WHR)、胰岛素抵抗指数(homeostasis model assessment of insulin resistance index, HOMA-IR)。2007年对入组人群进行随访,回顾其历年体检报告及病历医疗本。详细了解随访对象7年间个人疾病史(尤其是否有2型糖尿病、高血压、冠心病、脂代谢异常等病史),按照相同方法再次测定上述指标,并行口服葡萄糖耐量试验,测定2小时血糖。按随访终点是否发生2型糖尿病将随访人群分为糖尿病组和非糖尿病组。
3统计分析:计量资料以X|-±S表示,各组数据均经正态性检验,非正态分布者经对数转换成正态分布资料后进行统计分析。使用统计软件spss15.0对所得数据进行处理。两组间计量资料的比较采用t检验,计数资料比较采用卡方检验;各研究因素与2型糖尿病的相关性采用双变量相关分析、Logistic回归分析进行研究,以P<0.05为差异具有统计学意义。
结果:
1初访时纳入583例,共随访到524例,随访率为89.88%。其中糖尿病组96例,非糖尿病组428例。两组间基线资料比较:糖尿病组收缩压(systolic blood pressure,SBP)、舒张压(diastolic blood pressure,DBP)、BMI、WHR、TC、LDL-c、HOMA-IR,以及男性、2型糖尿病家族史、吸烟、饮酒史所占百分比均高于非糖尿病组;EDD、HDL-c低于非糖尿病组;年龄、HR、TG在两组间无显著性差异。
2入组前后BMI分别为28.51±1.86、28.63±2.20,二者无统计学差异。统计2型糖尿病7年累积发病率为18.3%。
3各研究因素分别与2型糖尿病发病情况进行双变量相关分析显示:性别、年龄、SBP、BMI、WHR、TC、LDL-c、HDL-c、HOMA-IR、EDD、2型糖尿病家族史、吸烟、饮酒与糖尿病发病均有相关性;HR、DBP、TG与糖尿病的相关分析无统计学意义。
4对所有可能危险因素进行Logistic回归分析,结果显示:HOMA-IR(OR=2.067)、WHR(OR=1.889)、EDD (OR=1.856)、BMI(OR=1.847)、2型糖尿病家族史(OR=1.842)、男性(OR=1.759)、年龄(OR=1.451)、吸烟史(OR=1.375)、HDL-c(OR=0.645)均与2型糖尿病的发病有相关性,而SBP、TC、LDL-c、饮酒习惯未能纳入回归模型。
5统计高血压、冠心病、脂代谢异常的累积发病率为17.4%、13.5%、22.5%。糖尿病组与非糖尿病组比较,前者(26.0%、20.8%、33.3%)均明显高于后者(15.7%、11.9%、20.1%),有统计学差异,显示在单纯性肥胖人群2型糖尿病的发病与高血压、冠心病、脂代谢异常有相关性,上述慢性疾病间存在明显的聚集性。
结论:
1肥胖人群2型糖尿病的发病率较体重正常人群明显增高,肥胖人群的健康状况令人担忧,值得引起广大医务工作者及肥胖者本人注意。
2在单纯性肥胖人群发生2型糖尿病的过程中存在多重危险因素,对具有该特征的人群实行一级预防,通过行为干预、药物干预消除部分危险因素,可能达到降低2型糖尿病发病率的目的。
3 2型糖尿病与高血压、冠心病、脂代谢异常的发病有聚集性,对已经出现并发症的肥胖患者,采取积极干预措施,防止或延缓其它并发症的发生、发展是很有必要的。
Objective: To find out the prevalence of type 2 diabetes mellitus (T2DM) in the obesity and investigate the risk factors of T2DM, in order to provide evidence for the prevention and forecast of T2DM.
Subjects and Methods:
1 Subjects: The simple obesity of Shijiazhuang (selected from the medical examination center of our hospital, body mass index (BMI)≥25kg/m~2, age:35-55, without hypertension, coronary artery disease, dyslipidemia, diabetes or impaired gluc- ose tolerance and other diseases. Menopause female were also excluded.) The total subjects were 583, including 316 male and 267 female.
2 Methods: In 2000, their basic information was collected, including sex, age, daily habits and family history of T2DM.The data was measured, including heart rate (HR), blood pressure (BP), height, weight, waist circumference, hip circumference, total cholesterol(TC), triglyceride(TG), low-density lipoprotein cholesterol (LDL-c), high-density lipoprotein cholesterol (HDL-c), fasting blood glucose and insulin, and endothelium dependent dilatation (EDD). Moreover, body mass index (BMI), waist hip ratio (WHR) and homeostasis model assessment of insulin resistance index (HOMA-IR) were calculated. In 2007 the health status of subjects was followed-up. With the same method, the above mentioned measurements and 2 hour blood glucose after glucose loading were measured. According to occurrence of T2DM or not, the subjects were divided into diabetic group and non-diabetic group.
3 Statistical analysis: The measurement data was presented with mean±standard deviation. The normality test of every group was took firstly. Abnormal data was analyzed after log- transformed. All data was analyzed by statistical software SPSS15.0 version. It applied independent-samples t-test to compare the measurement data, and chi-square test to compare the numeration data between diabetic group and non-diabetic group. Using Bivariate correlation and Logistic Regression the risk factors of T2DM were investigated. A value of P<0.05 was considered to be statistically significant.
Results:
1 524 of 583 subjects were followed up, and the percentage was 89.88%. There were 96 subjects in diabetic group, and 428 subjects in non-diabetic group. Compared with non-diabetic group, the systolic blood pressure(SBP), diastolic blood pressure (DBP), BMI, WHR, TC, LDL-c, HOMA-IR and the percentage of male, family history of T2DM, smoking and drinking all were higher in diabetic group. And EDD, HDL-c were lower in diabetic group. There was no significant difference in age, HR and TG between the two groups.
2 The BMI before and after follow-up were 28.51±1.86 and 28.63±2.20, and there was no significant difference. Seven-year cumulative incidence of T2DM is 18.3%.
3 Bivariate correlation between T2DM and all analytic factors showed that, sex, age, SBP, BMI, WHR, TC, LDL-c, HDL-c, HOMA-IR, EDD, family history of T2DM, smoking and drinking were correlated with T2DM, and HR, DBP, TG were not correlated.
4 Logistic Regression about risk factors of T2DM showed that,HOMA-IR(OR=2.067),WHR(OR=1.889),EDD(OR=1.856),BMI (OR=1.847), family history of T2DM(OR=1.842), male (OR=1.759), age (OR=1.451), smoking (OR=1.375) and HDL-c (OR=0.645) were influential factors. SBP, TC, LDL-c and drin- king could not enter the regression model.
5 The cumulative incidence of hypertension, coronary artery disease and dyslipidemia were 17.4%, 13.5%and 22.5%. All were higher in diabetic group (26.0%、20.8%、33.3%) than non-diabetic group(15.7%、11.9%、20.1%)(p<0.05).It showed the cooccurence of T2DM, the high blood, coronary artery disease and dyslipidemia in the obesity.
Conclusion:
1 The prevalence of T2DM in the obesity is higher than the normal. Their healthy is worrisome. It should catch the attention of medical worker and the obesity.
2 There are some influential factors in the occurrence of T2DM. If first-level prevention was enforced, and some risk fa- ctors were eliminated in the high-risk group, the morbidity of T2DM would decrease.
3 T2DM, hypertension, coronary artery disease and dyslipi- demia often concur in the obesity simultaneously. Therefore, it is important to take active intervention method to prevent or delay the complications of the obesity.
研究对象及方法:
1研究对象:石家庄市区的单纯性肥胖人群(从本院体检中心健康查体人群中筛选,据2002年亚太地区的肥胖标准,体重指数(BMI)≥25kg/m~2,经临床和实验室检查除外高血压、冠心病、血脂异常、糖尿病或糖耐量异常及其他疾病,女性排除绝经者。年龄在35-55岁)共583例,其中男性316例,女性267例。
2研究方法:2000年采集入组人群信息:记录基本信息(包括性别、年龄、日常生活习惯、糖尿病家族史等),测定心率(heart rate, HR)、血压、身高、体重、腰围、臀围、血脂(包括总胆固醇(TC)、甘油三脂(TG)、低密度脂蛋白胆固醇(LDL-c)、高密度脂蛋白胆固醇(HDL-c))、空腹血糖及胰岛素浓度、血管内皮依赖性舒张功能(endothelium dependent dilatation,EDD)。计算体重指数(body mass index, BMI)、腰臀比(waist hip ratio, WHR)、胰岛素抵抗指数(homeostasis model assessment of insulin resistance index, HOMA-IR)。2007年对入组人群进行随访,回顾其历年体检报告及病历医疗本。详细了解随访对象7年间个人疾病史(尤其是否有2型糖尿病、高血压、冠心病、脂代谢异常等病史),按照相同方法再次测定上述指标,并行口服葡萄糖耐量试验,测定2小时血糖。按随访终点是否发生2型糖尿病将随访人群分为糖尿病组和非糖尿病组。
3统计分析:计量资料以X|-±S表示,各组数据均经正态性检验,非正态分布者经对数转换成正态分布资料后进行统计分析。使用统计软件spss15.0对所得数据进行处理。两组间计量资料的比较采用t检验,计数资料比较采用卡方检验;各研究因素与2型糖尿病的相关性采用双变量相关分析、Logistic回归分析进行研究,以P<0.05为差异具有统计学意义。
结果:
1初访时纳入583例,共随访到524例,随访率为89.88%。其中糖尿病组96例,非糖尿病组428例。两组间基线资料比较:糖尿病组收缩压(systolic blood pressure,SBP)、舒张压(diastolic blood pressure,DBP)、BMI、WHR、TC、LDL-c、HOMA-IR,以及男性、2型糖尿病家族史、吸烟、饮酒史所占百分比均高于非糖尿病组;EDD、HDL-c低于非糖尿病组;年龄、HR、TG在两组间无显著性差异。
2入组前后BMI分别为28.51±1.86、28.63±2.20,二者无统计学差异。统计2型糖尿病7年累积发病率为18.3%。
3各研究因素分别与2型糖尿病发病情况进行双变量相关分析显示:性别、年龄、SBP、BMI、WHR、TC、LDL-c、HDL-c、HOMA-IR、EDD、2型糖尿病家族史、吸烟、饮酒与糖尿病发病均有相关性;HR、DBP、TG与糖尿病的相关分析无统计学意义。
4对所有可能危险因素进行Logistic回归分析,结果显示:HOMA-IR(OR=2.067)、WHR(OR=1.889)、EDD (OR=1.856)、BMI(OR=1.847)、2型糖尿病家族史(OR=1.842)、男性(OR=1.759)、年龄(OR=1.451)、吸烟史(OR=1.375)、HDL-c(OR=0.645)均与2型糖尿病的发病有相关性,而SBP、TC、LDL-c、饮酒习惯未能纳入回归模型。
5统计高血压、冠心病、脂代谢异常的累积发病率为17.4%、13.5%、22.5%。糖尿病组与非糖尿病组比较,前者(26.0%、20.8%、33.3%)均明显高于后者(15.7%、11.9%、20.1%),有统计学差异,显示在单纯性肥胖人群2型糖尿病的发病与高血压、冠心病、脂代谢异常有相关性,上述慢性疾病间存在明显的聚集性。
结论:
1肥胖人群2型糖尿病的发病率较体重正常人群明显增高,肥胖人群的健康状况令人担忧,值得引起广大医务工作者及肥胖者本人注意。
2在单纯性肥胖人群发生2型糖尿病的过程中存在多重危险因素,对具有该特征的人群实行一级预防,通过行为干预、药物干预消除部分危险因素,可能达到降低2型糖尿病发病率的目的。
3 2型糖尿病与高血压、冠心病、脂代谢异常的发病有聚集性,对已经出现并发症的肥胖患者,采取积极干预措施,防止或延缓其它并发症的发生、发展是很有必要的。
Objective: To find out the prevalence of type 2 diabetes mellitus (T2DM) in the obesity and investigate the risk factors of T2DM, in order to provide evidence for the prevention and forecast of T2DM.
Subjects and Methods:
1 Subjects: The simple obesity of Shijiazhuang (selected from the medical examination center of our hospital, body mass index (BMI)≥25kg/m~2, age:35-55, without hypertension, coronary artery disease, dyslipidemia, diabetes or impaired gluc- ose tolerance and other diseases. Menopause female were also excluded.) The total subjects were 583, including 316 male and 267 female.
2 Methods: In 2000, their basic information was collected, including sex, age, daily habits and family history of T2DM.The data was measured, including heart rate (HR), blood pressure (BP), height, weight, waist circumference, hip circumference, total cholesterol(TC), triglyceride(TG), low-density lipoprotein cholesterol (LDL-c), high-density lipoprotein cholesterol (HDL-c), fasting blood glucose and insulin, and endothelium dependent dilatation (EDD). Moreover, body mass index (BMI), waist hip ratio (WHR) and homeostasis model assessment of insulin resistance index (HOMA-IR) were calculated. In 2007 the health status of subjects was followed-up. With the same method, the above mentioned measurements and 2 hour blood glucose after glucose loading were measured. According to occurrence of T2DM or not, the subjects were divided into diabetic group and non-diabetic group.
3 Statistical analysis: The measurement data was presented with mean±standard deviation. The normality test of every group was took firstly. Abnormal data was analyzed after log- transformed. All data was analyzed by statistical software SPSS15.0 version. It applied independent-samples t-test to compare the measurement data, and chi-square test to compare the numeration data between diabetic group and non-diabetic group. Using Bivariate correlation and Logistic Regression the risk factors of T2DM were investigated. A value of P<0.05 was considered to be statistically significant.
Results:
1 524 of 583 subjects were followed up, and the percentage was 89.88%. There were 96 subjects in diabetic group, and 428 subjects in non-diabetic group. Compared with non-diabetic group, the systolic blood pressure(SBP), diastolic blood pressure (DBP), BMI, WHR, TC, LDL-c, HOMA-IR and the percentage of male, family history of T2DM, smoking and drinking all were higher in diabetic group. And EDD, HDL-c were lower in diabetic group. There was no significant difference in age, HR and TG between the two groups.
2 The BMI before and after follow-up were 28.51±1.86 and 28.63±2.20, and there was no significant difference. Seven-year cumulative incidence of T2DM is 18.3%.
3 Bivariate correlation between T2DM and all analytic factors showed that, sex, age, SBP, BMI, WHR, TC, LDL-c, HDL-c, HOMA-IR, EDD, family history of T2DM, smoking and drinking were correlated with T2DM, and HR, DBP, TG were not correlated.
4 Logistic Regression about risk factors of T2DM showed that,HOMA-IR(OR=2.067),WHR(OR=1.889),EDD(OR=1.856),BMI (OR=1.847), family history of T2DM(OR=1.842), male (OR=1.759), age (OR=1.451), smoking (OR=1.375) and HDL-c (OR=0.645) were influential factors. SBP, TC, LDL-c and drin- king could not enter the regression model.
5 The cumulative incidence of hypertension, coronary artery disease and dyslipidemia were 17.4%, 13.5%and 22.5%. All were higher in diabetic group (26.0%、20.8%、33.3%) than non-diabetic group(15.7%、11.9%、20.1%)(p<0.05).It showed the cooccurence of T2DM, the high blood, coronary artery disease and dyslipidemia in the obesity.
Conclusion:
1 The prevalence of T2DM in the obesity is higher than the normal. Their healthy is worrisome. It should catch the attention of medical worker and the obesity.
2 There are some influential factors in the occurrence of T2DM. If first-level prevention was enforced, and some risk fa- ctors were eliminated in the high-risk group, the morbidity of T2DM would decrease.
3 T2DM, hypertension, coronary artery disease and dyslipi- demia often concur in the obesity simultaneously. Therefore, it is important to take active intervention method to prevent or delay the complications of the obesity.
引文
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27 Ivandic A,Prpic-Krizeval I, Bozic D, et al. Insulin resistance and androgens in healthy women with different body fat distributions. Wien Klin Wochenschr,2002,114:321~326
28 Holst D, Grimaldi PA. New factors in the regulation of adipose differentiation and metabolism. Curr-opin-Lipidol 2002,13(2):241-245
29 Rattarasarn C, Leelawattana R, Soonthornpun S, et al. Gender differences of regional abdominal fat distribution and their relationships with insulin sensitivity in healthy and glucose intolerant Thais. J Clin Endocrinol Metab,2004, 89:6266~6270
30 卓连坤,闫道春,陈秀美,等.中老年男性胰岛素抵抗和相关激素水平变化规律及临床意义的研究. 标记免疫分析与临床 2005,12(1):17~21
31 Muzumdar R, Max, Atzmon G, et al. Decrease in glucose- stimulated insulin secretion with aging is independent of insulin action. Dabetes,2004,53(2):441~446
32 李江源,李小鹰. 年龄依赖性胰岛素抵抗与睾酮水平的相关性. 中华老年医学杂志,2007,26(2):104~106
33 Oh JY, Barret-connor E, wedick NM, et al. Endogenous sex hormones and development of type 2 diabetes in older men and women: the Rancho Bernardo study. Diabetes care, 2002,25:55~60
34 王继旺,张素华,汪志红,等. 吸烟与胰岛素抵抗关系的实验研究. 中国糖尿病杂志,2007,15(1),52~55
35 Eliasson B, Attvall S, Taskinen MR, et al. The insulin resistance syndrome in smokers is related to smoking habits. Arterioscler Thromb,1994,14:1946~1950
36 Targher G, Alberiche M, Zenere B, et al. Cigarette smokingand insulin resistance in patients with noninsulin-dependent diabetes mellitus. J Clin Endocrinol Metab, 1997,82: 3619~ 3624
37 American Diabetes Association. Smoking and diabetes. Dia- betes Care,2000,23:93~94
38 黎健. 血脂异常导致血管内皮细胞的氧化损伤. Chin J Arterioscler 2007,15:524
39 Nofer JR,van der Giet M, Tolle M, et al. HDL induces NO- dependent Vasorelaxation via the Lysophospholipid receptor S1P3. Clin Invest, 2004,113: 569~581
40 Rubins H, Robins SJ, Collins D, et al. For the Veterans Affa- irs High-Density Lipoprotein Chlesterol Intervention Trial Study Group. N Engl J Med,1999,341:96~97
41 邹大进,吴鸿. 腹型肥胖致胰岛素抵抗的机制及治疗展望. 中国糖尿病杂志,2006,1(4):309~312
42 Sharma AM, Chetty VT. Obesity, hypertension and insulin resistance. Acta Diabetologica,2005,42(suppl1):3~8
43 陶军,靳亚非,王礼春,等. 年龄对血管弹性和内皮细胞功能的影响. 中华心血管病杂志,2003,31(4):250~253
44 蒲素,余叶蓉,喻红玲,等. 雌激素对肥胖女性内皮依赖性血管舒张功能的保护作用. 中国糖尿病杂志,2006,14(5): 363~365
45 张伟. 高血压与血管内皮功能.中国误诊学杂志 2005, 5 (16):3024~3026
46 Vita JA,Keaney JF. Endothelial function:a barometer for cardiovascular risk. Circulation,2002,106:639~641
1 赵文华,翟屹,胡建平,等. 中国超重和肥胖造成相关慢性疾病的经济负担研究. 中国流行病学杂志,2006,27(7):555~ 559
2 武阳丰,马冠生,胡永华,等. 中国居民的超重和肥胖流行现状. 中华预防医学杂志,2005,39(5):316~320
3 马冠生,李艳平,武阳丰,等. 1992 至 2002 年间中国居民超重率 和 肥 胖 率 的 变 化 . 中 华 预 防 医 学 杂 志 ,2005,39(5): 311~315
4 栗华,张敬一,张中朝,等. 河北省成年居民超重肥胖流行特征及相关因素的调查分析. 实用预防学,2007,14(2): 283~286
5 裴海成. 实用肥胖病治疗学(人民军医出版社,2006 版):3~5.
6 张爱萍,叶山东. 游离脂肪酸在 2 型糖尿病发病中作用的研究进展. 国外医学老年医学分册,2005,26(2):76~80
7 陈伟,向红丁. 游离脂肪酸在胰岛素抵抗和 2 型糖尿病发生中的作用. 中国临床营养杂志,2003,11(3):223~226
8 Griu V, Qvigstad E. Fatty acids and insulin secretion. Br J Nutr,2000,83 (suppl):79~84
9 Chu C A,Sherck S M,Igawa K,et al. Effects of free fatty acids on hepatic glycogenolysis and gluconeogenesis in conscious dogs. Am J physiol Endocrinol Metab,2002,282(2):402~411.
10 Fujiwara K, Maekawa F, Yada T. Oleic acid interacts with GPk40 to induce ca2+ signaling in rat islet ?-cell: Mediation by PLC and L-type ca2+ channel and link to insulin release. Am J Physiol Endocrinol metal,2005,289(4):670~677
11 Boden G, Shulman GL. Free fatty acids in obesity and type2 diabetes: Defining their role in the development of insulin resistance and beta-cell dysfunction. Eur J Clin Invest, 2002, 32(3):14~23
12 柳红芳,陆菊明,潘长玉,等. 游离脂肪酸与胰岛素抵抗. 中华老年多器官疾病杂志,2003,2(3):236~240
13 Krysiak R,Okopien B. Adipose tissue: a new endocrine organ. Przegl-Lek,2005,62(9):919~923
14 赵乃倩,余叶蓉. 脂联素对血管内皮细胞的保护作用及其作用机制. 中国综合临床,2007,23(1)91~93
15 Yamauchi T,Kamon J,Waki H,et al. The fat-derived hormone adiponectin reverses insulin resistance associated with both lipoatrophy and obesity. Nat Med,2001,7:941~946
16 魏涛,陈艳萍,段文若,等. 脂联素、瘦素、胰岛素的调节与女性单纯性肥胖. 放射免疫学杂志,2004,17(4): 258~261
17 Sandoval DE, Davis SN. Leptin: metabolic control and regula- tion. Diabetes Complications,2003,17(2):108~113
18 Denomary, Naour N, Aubourg A, et al. Insulin and leptin induce Glut-4 plasma membrane translocation and glucose up take in a human meuronal cell line by a PI3-kinase dependent. Endocrinology, 2006,147(5):2550~2556
19 郑宪玲. 抵抗素与胰岛素抵抗及 2 型糖尿病. 医学综述, 2007,13(3):221~222
20 Skilton MR, Nakhla S, Sieveking DP, et al. Pathophysiological levels of the obesity related peptides resistin and ghrelin increase adhesion molecule expression on human vascular endothelial cells. Clini-Exp-Phar-Physiol,2005,32(10): 839~ 844
21 Trayhurn P. Adipose tissue in obesity-an inflammatory tissue. Endocrinology,2005,146(3):1003~1005
22 Mishima Y, Kuyama A, Tada A, et al. Relationship betweenserum tumor necrosis factor-alpha and insulin resistance in obese men with type2 diabetes mellitus. Diabetes-Res-Clin- Pract,2001,52(2):119~123
23 李若男,林哲章. 肿瘤坏死因子-α 与 2 型糖尿病及其大血管并发症的关系. 中国现代医药杂志,2007,9(1): 49~51
24 邹大进,吴鸿. 腹型肥胖致胰岛素抵抗的机制及治疗展望. 中国糖尿病杂志, 2006,14(4):309~312
25 Gacka M,Adamiec R. Mutations of peroxisome proliferator activated receptor gamma: clinical implications Postepy- Hig -Med-Dosw. 2004,58: 483~489
26 胡晓抒,郭志容,武鸣,等. 体重指数、腰围与代谢性健康风险的关系. 中华流行病学杂志,2005,26(12):967~970
27 邵新宇,贾伟平,陆俊茜,等. 正常糖调节人群中腹内脂肪积聚与糖脂代谢的早期变化. Shanghai Med ,2004,(12),27:906 ~908.
28 Hayashi T, Boyko EJ,Leonetti DL, et al. Visceral adiposity and the risk of impaired glucose tolerance: aprospective study among Japanese Americans. Diabetes Care, 2003, 26: 650~ 655
29 WP Jia, JX Lu, KS Xiang, et al. Prediction of abdominal visceral obesity from body mass index, waist circumference and waist-hip ratio in Chinese adults: receiver operating characteristic curves analysis. Biomedical and environmental sciences,2003,16:206~211
30 Dietz WH. Health consequences of obesity in youth: childhood predictors of adult disease. Pediatrics, 1998,101:518~525
31 杜东梅,张景玲,杨艳芬,等. 2 型糖尿病患者正常糖耐量一级亲属炎症因子与胰岛素抵抗的相关性.中国糖尿病杂2007,15(4):213~214
32 李妍妍. 老年糖尿病高危人群胰岛素抵抗、B 细胞功能评估及高胰岛素血症流行现状. 军医进修学院硕士学位论文.
33 Jequier E. Pathways to obesity. Int J Obes Relat Metab Disord. 2002,26:12
34 Muzumdar R, Max, Atzmon G, et al. Decrease in glucose stim- ulated insulin secretion with aging is independent of insulin action. Dabetes,2004,53(2):441~446
35 李江源,李小鹰. 年龄依赖性胰岛素抵抗与睾酮水平的相关性. 中华老年医学杂志,2007,26(2):104~106
36 Oh JY, Barret-connor E, wedick NM, et al. Endogenous sex hormones and development of type 2 diabetes in older men and women: the Rancho Bernardo study. Diabetes care, 2002, 25: 55~60
37 付正菊,袁鹰,阎胜利,等. 绝经后肥胖女性胰岛素抵抗与IGFBP-1 及 SHBG 的相关性研究. 山东医药,2005,45(1): 45 ~46
38 McTernan PG, Anwar A, Eggo MC, et al. Gender differences in the regulation of P450 aromatase expression and activity in human adipose tissue. Int-J-Obes-Relat-Metab Disord, 2000, 24(7):875~881
39 蒲素,余叶蓉,喻红玲,等. 雌激素对肥胖女性内皮依赖性血管舒张功能的保护作用. 中国糖尿病杂,2006,14(5): 363~365
40 王继旺,张素华,任伟,等.吸烟与代谢综合征的相关性调查与分析.重庆医学,2004,23:382~384
41 Kong C, Nimmo L, Elatrozy T, et al. Smoking is associated with increased hepatic lipase activity,insulin resistance, dyslip- idemia and early atherosclerosis in type 2diabetes. Atherocler- osis,2001,156:373~378
42 王继旺,张素华,汪志红,等. 吸烟与胰岛素抵抗关系的实验研究. 中国糖尿病杂志,2007,15(1):52~55
43 Eliasson B, Attlval S, Taskien MR, et al. The insulin resistance syndrome in smoker is related to smoking habits. Arterioscer Thromb,1994,14:1946~1950
44 Targher G, Alberiche M, Zenere MB, et al. Cigarette smoking and insulin resistance inpatients with noninsulin-dependent diabetes mellitus. J Clin Endocrinol Metab,1997, 82:3619~ 3624
45 杨俊坤.嗜酒与糖尿病相关性.医学综述,2006,(16): 993~994
2 赵文华,翟屹,胡建平,等. 中国超重和肥胖造成相关慢性疾病的经济负担研究. 中国流行病,2006,27(7):555~559
3 朱旅云. 超重和肥胖对血管内皮功能的影响. 中华心血管病杂志,2001,29(12)750~752
4 裴海成,邱明才,贾伟平,等. 肥胖病的定义. 实用肥胖病治疗学:2~5
5 The expert committee on the diagnosis and classification of diabetes mellitus: report of the export committee on the diagnosis and classification of diabetes mellitus. Diabetes Care, 1997, 20:1183~1197
6 中国高血压联盟.中国高血压防治指南(1999). 诊断学(陈文彬主编,2002 年版):143~144
7 第一届全国内科学术会议心血管病专业组. 关于冠状动脉粥样硬化性心脏病的临床诊断标准问题. 心血管病的现代观点(林容著,2005 年版):707~712
8 中国成人血脂异常防治指南制定联合委员会. 中国成人血脂异常防治指南. 中华心血管病,2007,35(5):390~409
9 孙纪新,朱俊卿,张建新,等. 河北省成年居民糖尿病患病及防治状况调查. 中国公共卫生,2006,22(7):801~803
10 毛斌,史玲,李晨曦,等. 肥胖与 2 型糖尿病. 实用全科医学,2006,4(1):91~92
11 Boden G, Shulman GL. Free fatty acids in obesity and type2 diabetes: Defining their role in the development of insulin resistance and beta-cell dysfunction. Eur J Clin Invest, 2002,32(3):14~23
12 Krysiak R, Okopien B. Adipose tissue: a new endocrine organ. Przegl-Lek,2005,62(9):919~923
13 Goodpaster B, Kelley D. Significance of high adipose tissue compartmentalization in insulin resistance. Diabetes, 1998, 47:1220~1223
14 Hayashi T, Boyko EJ, Leonetti DL, et al. Visceral Adiposity and the Risk of Impaired Glucose Tolerance. Diabetes care, 2003,26(3):649~652
15 李秀钧. 代谢综合征(人民卫生出版社,第二版):48~55
16 张家庆. 新的 HOMA-IR,从空腹血糖、空腹胰岛素测胰岛素抵抗. 中华糖尿病杂志,2005,13(4):245~246
17 谢爱霞,吴胜利,李农,等. 肥胖与糖尿病、高血压病的相关性探讨. 中国糖尿病杂志,2007,15(9): 556~557
18 裴新军. 脂肪细胞因子与胰岛素抵抗关系的研究进展. 医学综述,2007,13(16):1201~1203
19 郭文彬,刘宗明,朱梅,等. 肥胖对血管内皮依赖性舒张功能的影响. 医学影像学杂,2004,14(8):651~653
20 葛倩. 肥胖与内皮细胞损伤的关系和相关机制研究进展. 国外医学内分泌学分册,2005,25(4):254~256
21 朱旅云. 肥胖者内皮功能障碍与胰岛素抵抗关系的研究. 解放军医学杂志.2006,31(1):72~73
22 Kim JA, Montagnani M. Reciprocal relationships between insulin resistance and endothelial dysfunction: molecular and pathophysiological mechanisms. Circulation, 2006,113 (15):1888~1904
23 娄金荣. 胰岛素抵抗与内皮功能障碍. 心血管病进展, 2005,26:117~119
24 Bloomgarden zt. Genes and the cell biology of insulin secretion and insulin resistance. Diabetes care,2000, 23(2): 248~252
25 余劲明,黄莹,颜晓东,等. 2 型糖尿病家系正常血糖一级亲属腰围与胰岛功能的关系. 广西医学,2007,29(1):27~29
26 杜东梅,张景玲,杨艳芬,等. 2 型糖尿病患者正常糖耐量一级亲属炎症因子与胰岛素抵抗的相关性. 中国糖尿病杂志,2007,15(4):213~214
27 Ivandic A,Prpic-Krizeval I, Bozic D, et al. Insulin resistance and androgens in healthy women with different body fat distributions. Wien Klin Wochenschr,2002,114:321~326
28 Holst D, Grimaldi PA. New factors in the regulation of adipose differentiation and metabolism. Curr-opin-Lipidol 2002,13(2):241-245
29 Rattarasarn C, Leelawattana R, Soonthornpun S, et al. Gender differences of regional abdominal fat distribution and their relationships with insulin sensitivity in healthy and glucose intolerant Thais. J Clin Endocrinol Metab,2004, 89:6266~6270
30 卓连坤,闫道春,陈秀美,等.中老年男性胰岛素抵抗和相关激素水平变化规律及临床意义的研究. 标记免疫分析与临床 2005,12(1):17~21
31 Muzumdar R, Max, Atzmon G, et al. Decrease in glucose- stimulated insulin secretion with aging is independent of insulin action. Dabetes,2004,53(2):441~446
32 李江源,李小鹰. 年龄依赖性胰岛素抵抗与睾酮水平的相关性. 中华老年医学杂志,2007,26(2):104~106
33 Oh JY, Barret-connor E, wedick NM, et al. Endogenous sex hormones and development of type 2 diabetes in older men and women: the Rancho Bernardo study. Diabetes care, 2002,25:55~60
34 王继旺,张素华,汪志红,等. 吸烟与胰岛素抵抗关系的实验研究. 中国糖尿病杂志,2007,15(1),52~55
35 Eliasson B, Attvall S, Taskinen MR, et al. The insulin resistance syndrome in smokers is related to smoking habits. Arterioscler Thromb,1994,14:1946~1950
36 Targher G, Alberiche M, Zenere B, et al. Cigarette smokingand insulin resistance in patients with noninsulin-dependent diabetes mellitus. J Clin Endocrinol Metab, 1997,82: 3619~ 3624
37 American Diabetes Association. Smoking and diabetes. Dia- betes Care,2000,23:93~94
38 黎健. 血脂异常导致血管内皮细胞的氧化损伤. Chin J Arterioscler 2007,15:524
39 Nofer JR,van der Giet M, Tolle M, et al. HDL induces NO- dependent Vasorelaxation via the Lysophospholipid receptor S1P3. Clin Invest, 2004,113: 569~581
40 Rubins H, Robins SJ, Collins D, et al. For the Veterans Affa- irs High-Density Lipoprotein Chlesterol Intervention Trial Study Group. N Engl J Med,1999,341:96~97
41 邹大进,吴鸿. 腹型肥胖致胰岛素抵抗的机制及治疗展望. 中国糖尿病杂志,2006,1(4):309~312
42 Sharma AM, Chetty VT. Obesity, hypertension and insulin resistance. Acta Diabetologica,2005,42(suppl1):3~8
43 陶军,靳亚非,王礼春,等. 年龄对血管弹性和内皮细胞功能的影响. 中华心血管病杂志,2003,31(4):250~253
44 蒲素,余叶蓉,喻红玲,等. 雌激素对肥胖女性内皮依赖性血管舒张功能的保护作用. 中国糖尿病杂志,2006,14(5): 363~365
45 张伟. 高血压与血管内皮功能.中国误诊学杂志 2005, 5 (16):3024~3026
46 Vita JA,Keaney JF. Endothelial function:a barometer for cardiovascular risk. Circulation,2002,106:639~641
1 赵文华,翟屹,胡建平,等. 中国超重和肥胖造成相关慢性疾病的经济负担研究. 中国流行病学杂志,2006,27(7):555~ 559
2 武阳丰,马冠生,胡永华,等. 中国居民的超重和肥胖流行现状. 中华预防医学杂志,2005,39(5):316~320
3 马冠生,李艳平,武阳丰,等. 1992 至 2002 年间中国居民超重率 和 肥 胖 率 的 变 化 . 中 华 预 防 医 学 杂 志 ,2005,39(5): 311~315
4 栗华,张敬一,张中朝,等. 河北省成年居民超重肥胖流行特征及相关因素的调查分析. 实用预防学,2007,14(2): 283~286
5 裴海成. 实用肥胖病治疗学(人民军医出版社,2006 版):3~5.
6 张爱萍,叶山东. 游离脂肪酸在 2 型糖尿病发病中作用的研究进展. 国外医学老年医学分册,2005,26(2):76~80
7 陈伟,向红丁. 游离脂肪酸在胰岛素抵抗和 2 型糖尿病发生中的作用. 中国临床营养杂志,2003,11(3):223~226
8 Griu V, Qvigstad E. Fatty acids and insulin secretion. Br J Nutr,2000,83 (suppl):79~84
9 Chu C A,Sherck S M,Igawa K,et al. Effects of free fatty acids on hepatic glycogenolysis and gluconeogenesis in conscious dogs. Am J physiol Endocrinol Metab,2002,282(2):402~411.
10 Fujiwara K, Maekawa F, Yada T. Oleic acid interacts with GPk40 to induce ca2+ signaling in rat islet ?-cell: Mediation by PLC and L-type ca2+ channel and link to insulin release. Am J Physiol Endocrinol metal,2005,289(4):670~677
11 Boden G, Shulman GL. Free fatty acids in obesity and type2 diabetes: Defining their role in the development of insulin resistance and beta-cell dysfunction. Eur J Clin Invest, 2002, 32(3):14~23
12 柳红芳,陆菊明,潘长玉,等. 游离脂肪酸与胰岛素抵抗. 中华老年多器官疾病杂志,2003,2(3):236~240
13 Krysiak R,Okopien B. Adipose tissue: a new endocrine organ. Przegl-Lek,2005,62(9):919~923
14 赵乃倩,余叶蓉. 脂联素对血管内皮细胞的保护作用及其作用机制. 中国综合临床,2007,23(1)91~93
15 Yamauchi T,Kamon J,Waki H,et al. The fat-derived hormone adiponectin reverses insulin resistance associated with both lipoatrophy and obesity. Nat Med,2001,7:941~946
16 魏涛,陈艳萍,段文若,等. 脂联素、瘦素、胰岛素的调节与女性单纯性肥胖. 放射免疫学杂志,2004,17(4): 258~261
17 Sandoval DE, Davis SN. Leptin: metabolic control and regula- tion. Diabetes Complications,2003,17(2):108~113
18 Denomary, Naour N, Aubourg A, et al. Insulin and leptin induce Glut-4 plasma membrane translocation and glucose up take in a human meuronal cell line by a PI3-kinase dependent. Endocrinology, 2006,147(5):2550~2556
19 郑宪玲. 抵抗素与胰岛素抵抗及 2 型糖尿病. 医学综述, 2007,13(3):221~222
20 Skilton MR, Nakhla S, Sieveking DP, et al. Pathophysiological levels of the obesity related peptides resistin and ghrelin increase adhesion molecule expression on human vascular endothelial cells. Clini-Exp-Phar-Physiol,2005,32(10): 839~ 844
21 Trayhurn P. Adipose tissue in obesity-an inflammatory tissue. Endocrinology,2005,146(3):1003~1005
22 Mishima Y, Kuyama A, Tada A, et al. Relationship betweenserum tumor necrosis factor-alpha and insulin resistance in obese men with type2 diabetes mellitus. Diabetes-Res-Clin- Pract,2001,52(2):119~123
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