2型糖尿病患者腹部脂肪分布特征及其与C反应蛋白的关系
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摘要
目的:通过测量2型糖尿病内脏型肥胖患者、非内脏型肥胖患者以及非肥胖型患者腹部内脏、皮下脂肪面积及C反应蛋白水平,探讨2型糖尿病患者腹部脂肪分布特征及其与C反应蛋白之间的关系。
方法:按照1999年世界卫生组织(WHO)制定的糖尿病诊断标准,选取我院2型糖尿病病人36例,根据腰围(男性≥85cm,女性≥90cm,将病人分为腹型肥胖组26例和非肥胖10例(C)组,再根据CT测量值将腹型肥胖糖尿病病人分为内脏肥胖14例(A)组(内脏脂肪面积≥100cm2)和非内脏肥胖12例(B)组。健康对照(NC)组15例。受试者均测量身高、腰围、体重、臀围,检测空腹血糖(FPG)、血脂(TC、TG、LDL-C及HDL-C)、载脂蛋白(A、B)、血压、空腹胰岛素(FINS)及C反应蛋白(CRP)水平。根据CT扫描,测量腹部皮下脂肪面积(SA)、腹部内脏脂肪面积(VA)。计算体重指数(BMI)、腰臀比(WHR)、胰岛素抵抗指数(HOMA-IR)、内脏/皮下面积比值(VA/SA)。比较四组间空腹血糖、血脂、血压、空腹胰岛素、胰岛素抵抗指数、体重指数、腰臀比、C反应蛋白、皮下脂肪面积、内脏脂肪面积、内脏/皮下面积比值;观察C反应蛋白与腹部脂肪面积分布的相关性。采用SPSS12.0软件进行统计学处理。组间比较采用方差分析或秩检验,采用Pearson和Spearman进行相关分析。
结果: 1、C反应蛋白水平在A组和B组均值分别为5.03±1.06mg/L和4.73±1. 12mg/L,C组为4.68±1.13 mg/L,NC组均值为3.85±1.45 mg/L。A组C反应蛋白水平高于NC组,差异有统计学意义(P<0.01);B组和C组C反应蛋白水平高于NC组,差异有统计学意义(P<0.05); A组C反应蛋白水平高于B组和C组,差异有统计学意义(P<0.05);B组CRP水平高于C组,差异无统计学意义(P>0.05)。NC组、C组、B组至A组,C反应蛋白水平依次升高。
2、A组内脏脂肪面积(VA)和皮下脂肪面积(SA)分别为129.06±38.55cm2和137.13±35.15cm2;B组内脏脂肪面积和皮下脂肪面积分别为90.52±40.26cm2和123.42±37.14cm2;C组内脏脂肪面积和皮下脂肪面积分别为87.57±38.14cm2和112.36±40.73cm2;NC组内脏脂肪面积和皮下脂肪面积分别为79.23±35.13cm2和110.26±40.73cm2。内脏脂肪面积:A组和B组高于NC组,差异有统计学意义(P<0.01); C组高于NC组,差异有统计学意义(P<0.05); B组高于C组,差异有统计学意义(P<0.05); A组高于B组和C组,差异无统计学意义(P>0.05);皮下脂肪面积:A组和B组高于NC组,差异有统计学意义(P<0.05); B组高于C组,差异有统计学意义(P<0.05); A组高于B组和C组,差异有统计学意义(P<0.05);内脏/皮下脂肪面积比值:A组高于C组和NC组,差异有统计学意义(P<0.01); B组高于C组和NC组,差异有统计学意义(P<0.05); A组高于B组,差异有统计学意义(P<0.05).
4、研究结果表明:C反应蛋白与内脏脂肪面积、皮下脂肪面积、内脏面积/皮下面积比、腰围、胰岛素抵抗指数、血糖、体重指数、低密度脂蛋白、腰臀比呈正相关,在控制血糖和胰岛素抵抗指数后,C反应蛋白与内脏脂肪、内脏脂肪/皮下脂肪比、腰围呈正相关(相关系数分别为γ=0.446 p<0.01,γ=0.341 p<0.05,γ=0.374 p<0.05)。
结论: 2型糖尿病患者存在C反应蛋白水平升高,提示2型糖尿病患者体内存在一定的炎症反应;合并内脏型肥胖的患者这种异常更加明显,提示C反应蛋白水平的升高和内脏脂肪的增多密切相关。减少内脏脂肪的增加是减少2型糖尿病患者体内炎症重要措施。
Objective: By measuring visceral fat area (VA), subcutaneous fat area (SA) and C-reactive protein levels in the normal(NC group), type 2 diabetes patients without obesity(C group) ,type 2 diabetes patients with non-visceral obesity(B group) and type 2 diabetes patients with visceral obesity(A group) to explore relationship between C-reactive protein and abdominal fat distribution in type 2 diabetic patients.
Methods: In accordance with the 1999 World Health Organization (WHO) diagnostic criteria for diabetes to develop, select 36 patients with type 2diabetes for this study our hospital. According to waist circumference (man≥85cm, females≥90cm,to navel horizontal), they were divided into two groups: type 2daibetes patients with or without obesity. According to area of visceral fat, type 2 diabetes patients with obesity were divided into two group: type 2daibetes patients with or without visceral obesity. Take 15 people as normal controls. The subjects were measured height, waist circumference, weight, hip circumference, fasting blood glucose testing(FPG), lipid(TC, TG, LDL-C, HDL-C), Apo lipoprotein(A, B), blood pressure, fasting insulin(FINS) and C-reactive protein levels, subcutaneous fat area and visceral fat area. All of body mass index (BMI), waist-hip ratio(WHR), insulin resistance index(HOMS-IR), and visceral/subcutaneous area ratio(VA/SA) were calculated. Comparison among the three groups of fasting blood glucose, blood lipids, blood pressure, fasting insulin, insulin resistance index, waist-hip ratio, C-reactive protein, subcutaneous fat area, visceral fat area, visceral/subcutaneous area ratio; observation of C-reactive protein and abdominal fat the relevance of the distribution area. All data were expressed as mean±SD, or median. Statistical comparisons were done by Pearson and Spearman analysis.
Result: 1. C-reactive protein in A group were significantly higher than the normal control (P<0.01); C-reactive protein levels of B group and C group higher than the normal control (P<0.05). C-reactive protein in A group were significantly higher than B group and C group (P<0.05); C-reactive protein in B group were significantly higher than C group(P>0.05); From the normal control, C group, B group to A group, C-reactive protein levels increased in turn.
2. Visceral fat area in A group, B group and C group was significantly higher than that of normal control (P<0.01); Visceral fat area in A group was significantly higher than that in B group and C group (P<0.05); visceral fat area in B group higher in C group (P>0.05); subcutaneous fat area of A group, B group, C group was higher than that of normal control (P<0.05); subcutaneous fat area in B group was higher than that in C group (P<0.05); subcutaneous fat area of A group and was higher than that in B group and C group(P<0.05); VA/SA ratio of A group, B group and C group was significantly higher than that of normal control (P<0.01); VA/SA ratio of A group and B group was significantly higher than that of C group (P<0.05); VA/SA ratio of A group was significantly higher than that of B group (P<0.05).
3. C-reactive protein levels were positively correlated with waist circumference, visceral fat area, subcutaneous fat area, waist hip ratio, insulin resistance index, low density protein, body mass index, fasting glucose testing. C-reactive protein levels were positively correlated with waist circumference, visceral fat area, subcutaneous fat area, VA/SA after adjusting HOMA-IR, FPG.
Conclusion: Compared with normal control group, C-reactive protein levels with type 2 diabetes patients significantly increased, suggesting that there is a certain degree of chronic inflammation process in type 2 diabetes patients. C-reactive protein levels activity increased with visceral fat. Visceral fat reduction is very important solution for type 2 diabetes patients to reduce inflammation in vivo.
方法:按照1999年世界卫生组织(WHO)制定的糖尿病诊断标准,选取我院2型糖尿病病人36例,根据腰围(男性≥85cm,女性≥90cm,将病人分为腹型肥胖组26例和非肥胖10例(C)组,再根据CT测量值将腹型肥胖糖尿病病人分为内脏肥胖14例(A)组(内脏脂肪面积≥100cm2)和非内脏肥胖12例(B)组。健康对照(NC)组15例。受试者均测量身高、腰围、体重、臀围,检测空腹血糖(FPG)、血脂(TC、TG、LDL-C及HDL-C)、载脂蛋白(A、B)、血压、空腹胰岛素(FINS)及C反应蛋白(CRP)水平。根据CT扫描,测量腹部皮下脂肪面积(SA)、腹部内脏脂肪面积(VA)。计算体重指数(BMI)、腰臀比(WHR)、胰岛素抵抗指数(HOMA-IR)、内脏/皮下面积比值(VA/SA)。比较四组间空腹血糖、血脂、血压、空腹胰岛素、胰岛素抵抗指数、体重指数、腰臀比、C反应蛋白、皮下脂肪面积、内脏脂肪面积、内脏/皮下面积比值;观察C反应蛋白与腹部脂肪面积分布的相关性。采用SPSS12.0软件进行统计学处理。组间比较采用方差分析或秩检验,采用Pearson和Spearman进行相关分析。
结果: 1、C反应蛋白水平在A组和B组均值分别为5.03±1.06mg/L和4.73±1. 12mg/L,C组为4.68±1.13 mg/L,NC组均值为3.85±1.45 mg/L。A组C反应蛋白水平高于NC组,差异有统计学意义(P<0.01);B组和C组C反应蛋白水平高于NC组,差异有统计学意义(P<0.05); A组C反应蛋白水平高于B组和C组,差异有统计学意义(P<0.05);B组CRP水平高于C组,差异无统计学意义(P>0.05)。NC组、C组、B组至A组,C反应蛋白水平依次升高。
2、A组内脏脂肪面积(VA)和皮下脂肪面积(SA)分别为129.06±38.55cm2和137.13±35.15cm2;B组内脏脂肪面积和皮下脂肪面积分别为90.52±40.26cm2和123.42±37.14cm2;C组内脏脂肪面积和皮下脂肪面积分别为87.57±38.14cm2和112.36±40.73cm2;NC组内脏脂肪面积和皮下脂肪面积分别为79.23±35.13cm2和110.26±40.73cm2。内脏脂肪面积:A组和B组高于NC组,差异有统计学意义(P<0.01); C组高于NC组,差异有统计学意义(P<0.05); B组高于C组,差异有统计学意义(P<0.05); A组高于B组和C组,差异无统计学意义(P>0.05);皮下脂肪面积:A组和B组高于NC组,差异有统计学意义(P<0.05); B组高于C组,差异有统计学意义(P<0.05); A组高于B组和C组,差异有统计学意义(P<0.05);内脏/皮下脂肪面积比值:A组高于C组和NC组,差异有统计学意义(P<0.01); B组高于C组和NC组,差异有统计学意义(P<0.05); A组高于B组,差异有统计学意义(P<0.05).
4、研究结果表明:C反应蛋白与内脏脂肪面积、皮下脂肪面积、内脏面积/皮下面积比、腰围、胰岛素抵抗指数、血糖、体重指数、低密度脂蛋白、腰臀比呈正相关,在控制血糖和胰岛素抵抗指数后,C反应蛋白与内脏脂肪、内脏脂肪/皮下脂肪比、腰围呈正相关(相关系数分别为γ=0.446 p<0.01,γ=0.341 p<0.05,γ=0.374 p<0.05)。
结论: 2型糖尿病患者存在C反应蛋白水平升高,提示2型糖尿病患者体内存在一定的炎症反应;合并内脏型肥胖的患者这种异常更加明显,提示C反应蛋白水平的升高和内脏脂肪的增多密切相关。减少内脏脂肪的增加是减少2型糖尿病患者体内炎症重要措施。
Objective: By measuring visceral fat area (VA), subcutaneous fat area (SA) and C-reactive protein levels in the normal(NC group), type 2 diabetes patients without obesity(C group) ,type 2 diabetes patients with non-visceral obesity(B group) and type 2 diabetes patients with visceral obesity(A group) to explore relationship between C-reactive protein and abdominal fat distribution in type 2 diabetic patients.
Methods: In accordance with the 1999 World Health Organization (WHO) diagnostic criteria for diabetes to develop, select 36 patients with type 2diabetes for this study our hospital. According to waist circumference (man≥85cm, females≥90cm,to navel horizontal), they were divided into two groups: type 2daibetes patients with or without obesity. According to area of visceral fat, type 2 diabetes patients with obesity were divided into two group: type 2daibetes patients with or without visceral obesity. Take 15 people as normal controls. The subjects were measured height, waist circumference, weight, hip circumference, fasting blood glucose testing(FPG), lipid(TC, TG, LDL-C, HDL-C), Apo lipoprotein(A, B), blood pressure, fasting insulin(FINS) and C-reactive protein levels, subcutaneous fat area and visceral fat area. All of body mass index (BMI), waist-hip ratio(WHR), insulin resistance index(HOMS-IR), and visceral/subcutaneous area ratio(VA/SA) were calculated. Comparison among the three groups of fasting blood glucose, blood lipids, blood pressure, fasting insulin, insulin resistance index, waist-hip ratio, C-reactive protein, subcutaneous fat area, visceral fat area, visceral/subcutaneous area ratio; observation of C-reactive protein and abdominal fat the relevance of the distribution area. All data were expressed as mean±SD, or median. Statistical comparisons were done by Pearson and Spearman analysis.
Result: 1. C-reactive protein in A group were significantly higher than the normal control (P<0.01); C-reactive protein levels of B group and C group higher than the normal control (P<0.05). C-reactive protein in A group were significantly higher than B group and C group (P<0.05); C-reactive protein in B group were significantly higher than C group(P>0.05); From the normal control, C group, B group to A group, C-reactive protein levels increased in turn.
2. Visceral fat area in A group, B group and C group was significantly higher than that of normal control (P<0.01); Visceral fat area in A group was significantly higher than that in B group and C group (P<0.05); visceral fat area in B group higher in C group (P>0.05); subcutaneous fat area of A group, B group, C group was higher than that of normal control (P<0.05); subcutaneous fat area in B group was higher than that in C group (P<0.05); subcutaneous fat area of A group and was higher than that in B group and C group(P<0.05); VA/SA ratio of A group, B group and C group was significantly higher than that of normal control (P<0.01); VA/SA ratio of A group and B group was significantly higher than that of C group (P<0.05); VA/SA ratio of A group was significantly higher than that of B group (P<0.05).
3. C-reactive protein levels were positively correlated with waist circumference, visceral fat area, subcutaneous fat area, waist hip ratio, insulin resistance index, low density protein, body mass index, fasting glucose testing. C-reactive protein levels were positively correlated with waist circumference, visceral fat area, subcutaneous fat area, VA/SA after adjusting HOMA-IR, FPG.
Conclusion: Compared with normal control group, C-reactive protein levels with type 2 diabetes patients significantly increased, suggesting that there is a certain degree of chronic inflammation process in type 2 diabetes patients. C-reactive protein levels activity increased with visceral fat. Visceral fat reduction is very important solution for type 2 diabetes patients to reduce inflammation in vivo.
引文
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13 Grievink L,Alberty JF,Oniel J,et al.Waist circunference as a measurement of obesity in the Netherlands Antilles; associations with hypertension and diabetes mellitus. Eur J Clin Nutr,2004,58:1159-1165.
14 Wang Z,Hoy WE. Body size measurements as predictors of type 2 diabetes in Aboriginal people. Int J Obe Relat Metab Disord,2004,28:1580-1584.
15 Lopatynski J, Mardarowicz G,Szczesniak G, A comparative evaluation of waist circumference, waist-to-hip ratio, waist-to-height ratio and body mass index as indicators of impaired glucose tolerance and as risk factors for type-2 diabetes mellitus,Ann Univ Mariae Curie Sklodowaka,2003,58:413-419.
16 Sethi JK et al. Trends Mol Med, 2005,11(8):344-347.
17 Visser M, Bouter LM, Mc Quillan GM, et al. Elevated C-reactive protein level in overweight and obese adults. JAMA,1999,282(22):2131-2135.
18谷春华,杨立波等.代谢综合征临床研究进展[J].中国中医药信息杂志,2004,11(6):548-560.
19王树海,王文健.胰岛素抵抗的发病机制及中西医结合防治策略[J].中西医结合学报,2004,2(1):14-16.
20崔丽娟,都健.脂联素与炎症及胰岛素抵抗关系的研究进展[J].国际内分泌代谢杂志,2006,26(增刊):44-46.
21余劲明.胰岛素抵抗遗传学研究进展[J].中国医学文摘内科学,2006,27(1):11-13 .
22李秀钧.肥胖与胰岛素抵抗[J].中国糖尿病杂志,2005,13(6):401-402.
23黎明,吴从愿,詹志伟,等.瘦素与代谢综合征级成成分的聚集特性分析[J].中华预防医学杂志,2004,38(4):226-229.
24 Kiffer TJ,Heller RS,Leech CA,et al. Leptin suppression of insulin secretion by the activation of ATP-sensitive K channels in pancreatic ?-cells[J].Diabetes,1997,6(6):1087-1093.
25 Emilsson V,Liu YL,Cawthorne MA,et al. Expression of the functional leptin receptor mRNA in pancreatic islets and direct inhibitory action of leptin on insulin secretion[J].Diabetes,1997,46(2):313 -316.
26 Steppan CM,Bailey ST,Bhat S, et al. The hormone resistance links obesity to diabetes[J].Nature,2001,50(9):2094-2099.
27徐伟斌,俞璐,罗敏.抵抗素的研究进展[J].国际内分泌代谢杂志,2006,26(1):23-25.
28陆静尔.过氧化物酶体增殖体激活受体与胰岛素抵抗的研究进展[J].国外医学老年医学分册,2006,27(5):222-224.
29 Wolf AM,Wolf D,Rnmpiod H et al. The kinase inhibitor imatinib maculate inhibits TNF-alpha production in vitro and prevents TNF- dependent acute hepatic inflammation. Proc Natl Acad Sci USA, 2005,102(38):13622-13627.
30 Sheng WH Ching BL , Chang SC , et al. Clinical manifestations and inflammatory cytokine responses in patients with severe acute respiratory syndrome [J]. Formos Med Assoc,2005,104(10):715-723.
31 Path G,Bomstein SR,Gumiak M,at al. Human breast adipocytes express interleukin-6(IL-6)and its receptor system:increased IL-6 production by beta–adrenergic activation and effects of IL-6 on adipocyte function[J].Clin Endocrinol Me tab,2001,86(6):2281-2288.
32 Fukuhara A,Matsuda M,Nishizawa M,et al. Visfatin:a protein secreted by visceral fat that mimics the effects of insulin [J].Science,2005,307(5708):426-430.
33 Chen MP,Chung FM Chang DM,et al. Elevated Plasma Level of Visfatin/Pre-B Cell Colony-Enhancing Factor inPatients with Type 2 Diabetes Mellitus[J].Clin Endocrinol Me tab,2006,91(1):295-299.
34 Qin Yang, Timothy E. Graham1,Nimesh Moldy, et al. Serum retinol binding protein 4 contributes to insulin resistance in obesity and type 2 diabetes [J]. Nature, 2005, 436 (7049):356-362.
35 Rattarasarn C,Leelawattana R,Soomthornpun S,et al. Regional abdominal fat distribution in lean and obese Thai type 2 diabetes mellitus women; relationships with insulin sensitivity and cardiovascular risk factors. Metabolism,2003,52:1444-1447.
36 Ross R,Aru J,et al. Abdominal adiposity and insulin resistance in obese men. Am J Physiologic Endocrinal Me tab,2002,282:E657-E663.
37任颖,刘伟,陆广华,2型糖尿病病人的内脏脂肪性肥胖和胰岛素抵抗,中国糖尿病杂志,2003,11(2):84-87.
38苏丽,王中心.血脂异常2型糖尿病与代谢综合征。医学综述,2005,11(12):1102-1104.
39杉杉。联合减肥对2型糖尿病患者有益.中华医学信息导报,2005,20(15):11.
40顾全霞,杨东辉,佟爱华,等.运动疗法对肥胖的糖耐量低减患者胰岛素抵抗的影响.中华物理医学与康复杂志,2006,28(4):279-280.
41赵向东,史雪茄.减肥对肥胖型2型糖尿病的影响.徐州医学报,2002,22(2):160-1621.
42史楠,马晓伟.血糖控制对糖尿病并发症的影响.中华糖尿病杂志,2006,14(1):77.
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5 Tulloch-Reid MK,Williams DE,Looker HC,et al. Do measures of body fat distribution provide information on the risk of type 2 diabetes in addition to measures of general obesity? Comparison of anthropometric predictors of type 2 diabetes in Indians. Diabetes Care, 2003,26, 2556-25 61.
6 Derma,D’Addato S,Cicero A,et al. Relative role of BMI and reduced glucose tolerance as risk factors for diabetes development in the Brisighella Heart Study. The 18th International Diabetes Federatio–n Congress,Paris,France,2003.Diabetes Me tab,2003,29:24-28.
7陈仆,肥胖、糖尿病和代谢综合征越来越流行(上).世界核心医学期刊文摘心脏病学分册,2005,6:12-15.
8 Jia WP,Xiang KS,Chen L,et al. Epidemiological study on obesity and its comorbidities in urban Chinese older than 20 years of age in Shanghai, China. Obesity Rev,2002,3:157-165.
9 Lara Esqueda A ,Aguilar-Salinas CA,Velazquez-MonroyO,et al. The body mass index is a less is a less-sensitive tool for detecting cases with obesity-associated co-morbidities in short stature subjects,Int J Obe Relat Metab Disord,2004,28:1443-1450.
10 Ogawa K,Ueda K,Sasaki H ,et al. History of obesity as a risk factors for both carotid atherosclerosis and microangiopathy. Diabetes Res Clin Pract,2004,66:S165-S168.
11 Stokic EJ,Tomic DD,Ivkovic-Lazar TA,et al. Total and intra abdominal fat mass in NIDDM patients with normal BMI. The 18th International Diabetes Federation Congress, Paris ,France, 2003. Diabetes Me tab,2003,29:4S148.
12董砚虎,孙黎明,李利.肥胖的新定义及亚太地区肥胖诊断的重新评估与探讨.辽宁实用糖尿病杂志,2001,9:3-6.
13 Grievink L,Alberty JF,Oniel J,et al.Waist circunference as a measurement of obesity in the Netherlands Antilles; associations with hypertension and diabetes mellitus. Eur J Clin Nutr,2004,58:1159-1165.
14 Wang Z,Hoy WE. Body size measurements as predictors of type 2 diabetes in Aboriginal people. Int J Obe Relat Metab Disord,2004,28:1580-1584.
15 Lopatynski J, Mardarowicz G,Szczesniak G, A comparative evaluation of waist circumference, waist-to-hip ratio, waist-to-height ratio and body mass index as indicators of impaired glucose tolerance and as risk factors for type-2 diabetes mellitus,Ann Univ Mariae Curie Sklodowaka,2003,58:413-419.
16 Sethi JK et al. Trends Mol Med, 2005,11(8):344-347.
17 Visser M, Bouter LM, Mc Quillan GM, et al. Elevated C-reactive protein level in overweight and obese adults. JAMA,1999,282(22):2131-2135.
18谷春华,杨立波等.代谢综合征临床研究进展[J].中国中医药信息杂志,2004,11(6):548-560.
19王树海,王文健.胰岛素抵抗的发病机制及中西医结合防治策略[J].中西医结合学报,2004,2(1):14-16.
20崔丽娟,都健.脂联素与炎症及胰岛素抵抗关系的研究进展[J].国际内分泌代谢杂志,2006,26(增刊):44-46.
21余劲明.胰岛素抵抗遗传学研究进展[J].中国医学文摘内科学,2006,27(1):11-13 .
22李秀钧.肥胖与胰岛素抵抗[J].中国糖尿病杂志,2005,13(6):401-402.
23黎明,吴从愿,詹志伟,等.瘦素与代谢综合征级成成分的聚集特性分析[J].中华预防医学杂志,2004,38(4):226-229.
24 Kiffer TJ,Heller RS,Leech CA,et al. Leptin suppression of insulin secretion by the activation of ATP-sensitive K channels in pancreatic ?-cells[J].Diabetes,1997,6(6):1087-1093.
25 Emilsson V,Liu YL,Cawthorne MA,et al. Expression of the functional leptin receptor mRNA in pancreatic islets and direct inhibitory action of leptin on insulin secretion[J].Diabetes,1997,46(2):313 -316.
26 Steppan CM,Bailey ST,Bhat S, et al. The hormone resistance links obesity to diabetes[J].Nature,2001,50(9):2094-2099.
27徐伟斌,俞璐,罗敏.抵抗素的研究进展[J].国际内分泌代谢杂志,2006,26(1):23-25.
28陆静尔.过氧化物酶体增殖体激活受体与胰岛素抵抗的研究进展[J].国外医学老年医学分册,2006,27(5):222-224.
29 Wolf AM,Wolf D,Rnmpiod H et al. The kinase inhibitor imatinib maculate inhibits TNF-alpha production in vitro and prevents TNF- dependent acute hepatic inflammation. Proc Natl Acad Sci USA, 2005,102(38):13622-13627.
30 Sheng WH Ching BL , Chang SC , et al. Clinical manifestations and inflammatory cytokine responses in patients with severe acute respiratory syndrome [J]. Formos Med Assoc,2005,104(10):715-723.
31 Path G,Bomstein SR,Gumiak M,at al. Human breast adipocytes express interleukin-6(IL-6)and its receptor system:increased IL-6 production by beta–adrenergic activation and effects of IL-6 on adipocyte function[J].Clin Endocrinol Me tab,2001,86(6):2281-2288.
32 Fukuhara A,Matsuda M,Nishizawa M,et al. Visfatin:a protein secreted by visceral fat that mimics the effects of insulin [J].Science,2005,307(5708):426-430.
33 Chen MP,Chung FM Chang DM,et al. Elevated Plasma Level of Visfatin/Pre-B Cell Colony-Enhancing Factor inPatients with Type 2 Diabetes Mellitus[J].Clin Endocrinol Me tab,2006,91(1):295-299.
34 Qin Yang, Timothy E. Graham1,Nimesh Moldy, et al. Serum retinol binding protein 4 contributes to insulin resistance in obesity and type 2 diabetes [J]. Nature, 2005, 436 (7049):356-362.
35 Rattarasarn C,Leelawattana R,Soomthornpun S,et al. Regional abdominal fat distribution in lean and obese Thai type 2 diabetes mellitus women; relationships with insulin sensitivity and cardiovascular risk factors. Metabolism,2003,52:1444-1447.
36 Ross R,Aru J,et al. Abdominal adiposity and insulin resistance in obese men. Am J Physiologic Endocrinal Me tab,2002,282:E657-E663.
37任颖,刘伟,陆广华,2型糖尿病病人的内脏脂肪性肥胖和胰岛素抵抗,中国糖尿病杂志,2003,11(2):84-87.
38苏丽,王中心.血脂异常2型糖尿病与代谢综合征。医学综述,2005,11(12):1102-1104.
39杉杉。联合减肥对2型糖尿病患者有益.中华医学信息导报,2005,20(15):11.
40顾全霞,杨东辉,佟爱华,等.运动疗法对肥胖的糖耐量低减患者胰岛素抵抗的影响.中华物理医学与康复杂志,2006,28(4):279-280.
41赵向东,史雪茄.减肥对肥胖型2型糖尿病的影响.徐州医学报,2002,22(2):160-1621.
42史楠,马晓伟.血糖控制对糖尿病并发症的影响.中华糖尿病杂志,2006,14(1):77.