2型糖尿病患者血清3-硝基酪氨酸水平及其与膳食的关系研究
|
摘要
目的:以2型糖尿病患者和非糖尿病患者为研究对象,观察两组人群血清3-硝基酪氨酸(3-NT)水平的差异;探讨糖尿病患者血糖控制与体内蛋白质硝基化的关系;探讨糖尿病患者心血管疾病的危险因素与血清3-NT水平之间的关系;分析糖尿病患者不同类别的食物选择和消费数量与血清3-NT水平的关系,通过回归分析找出与3-NT关系最为密切的食物类别和营养素摄入量,为探讨糖尿病抗硝基化损伤进而防治其并发症提供基础研究依据。
方法:
分组和观察指标:单盲随机病例对照研究。筛选2型糖尿病患者109例,与其匹配的非糖尿病对照人群57例,对入选的糖尿病患者和对照人群进行膳食调查、人体测量、血生化检测和血清3-NT水平的测定。膳食调查采用“食物频率询问法(FFQ)”,回顾年限为1年。人体测量指标包括身高、体重、BMI等;血生化指标包括空腹血糖、GSP、HbA1c、血浆胰岛素、TC、TG和载脂蛋白。
人体测量采用TZ-1型身高体重秤和中体同方体育科技有限公司生产的BCA-2A人体成份分析仪测定;空腹血生化指标采用日立7600全自动生化分析仪。
3-NT检测:血清3-NT检测采用ELISA试剂盒(Hycult biotechnology bv,Lot#:5822k19),按试剂盒操作说明进行。血样均为新鲜血清,稀释25倍。每个样品均设平行样,Unico UV-2000紫外分光光度计测量450nm吸收光值。
质量控制:膳食调查时,提供食物模型,作为膳食调查的参考。对于主食米、面、蛋类、奶类、水果、食用油及酒和茶的量化估计,提供量具,并有实物参考。所有调查员均经统一培训,由专人进行计算机录入。
统计方法:数据统计采用SPSS13.0进行。两组之间比较采用t检验,单因素多水平资料采用方差分析,相关分析采用多元线性逐步回归方法。
结果
T2DM患者血清3-NT水平显著高于非糖尿病对照人群,且3-NT在男性糖尿病组高于男性对照组,在女性T2DM组高于女性对照组(p<0.05);随着BMI的增加,T2DM患者的血清3-NT水平有逐渐增高的趋势;男性T2DM患者中,BMI≥24kg/m2者其3-NT值显著高于BMI正常的T2DM患者(p<0.05);空腹血糖>6.1mmol/LT2DM患者,其血清3-NT水平显著高于血糖≤6.1mmol/LT2DM患者(p<0.05);HDL-c高于1.6mmol/L的所有T2DM患者及男性T2DM患者,其血清3-NT值均显著低于正常HDL-c的相应对照组(p<0.05);TC高于5.7mmol/L的T2DM患者,其血清3-NT水平显著低于正常TC的T2DM患者(p<0.05)。
两组人群的脂肪产能比均高于推荐产能比,T2DM患者的日均脂肪摄入量明显高于非糖尿病对照组,碳水化合物产能比较推荐产能比低;T2DM组患者的日均主食量显著低于对照组,奶类和豆类以及食盐的日均摄入量显著高于对照组(p<0.05);T2DM组患者日均VitB1、VitB2摄入量明显低于对照组,钠盐的摄入量高于对照组;全部受试者平均每日VitC摄入量、钠、铁、锰、铜、磷摄入量均高于RNI,非糖尿病组的VitA、VitB1、钙摄入量显著低于RNI;T2DM患者中HDL-c<1.6mmol/L组的3-NT、胡萝卜素、VitC、叶酸均高于HDL-c≥1.6mmol/L组(p<0.05);在T2DM患者中,血清3-NT水平与LDL-c、GSP、HbAlc有线性回归关系;男性T2DM患者中,与血清3-NT水平相关性最大的是ApoA II和ApoC3;女性T2DM患者中,与血清3-NT水平相关性最大的是GSP和HbAlc;在血糖高于6.1mmol/L的T2DM患者中,与血清3-NT水平相关性最大的是TG和ApoC3;在HDL-c低于1.6mmol/L的T2DM患者中,与血清3-NT水平相关性最大的是HbAlc、GSP和LDL-c;3-NT与营养素摄入量的线性关系中,T2DM患者血清3-NT水平与每日钠、钾、铁的摄入量有线性回归关系。
结论
T2DM患者血清3-NT水平显著高于正常人。此结果再次证明了T2DM患者体内硝基化损伤的存在,为抗硝基化预防和治疗T2DM及并发症奠定了理论基础;血糖控制不好的T2DM患者其血清3-NT水平较高,为T2DM患者控制血糖提供了新的理论依据;超重和肥胖的T2DM患者其血清3-NT水平较高,为饮食干预控制体重以防治T2DM心血管并发症奠定了理论基础;3-NT与糖尿病心血管并发症危险因素的关系如下:血清LDL-c、TC与3-NT呈显著负相关,ApoC3在血糖控制不好的T2DM患者中,与3-NT呈负相关。可能的机制是血清3-NT高的T2DM患者体内过氧化损伤也大量存在,导致了TC和载脂蛋白的过氧化损伤。所以控制体内的过氧化损伤、减少3-NT的生成对糖尿病患者并发心血管并发症有显著意义;T2DM患者血清3-NT与膳食摄入VitB1、VitB2呈负相关,与膳食摄入钠、钾、铁呈线性相关。建议T2DM患者在目前的膳食摄入基础上增加B族维生素和钾的摄入量,减少钠盐和铁的摄入,进而减少3-NT的生成,减少糖尿病及其并发症发生的可能性。
Objective
In order to provide a clinical evidence of avoiding or attenuating diabetic complications by a novel way of anti-nitrition of proteins in type 2 diabetic patients, the present study was done to try to find out a possible correlation between diabetic blood glucose control and protein nitrition, a relationship between 3-NT levels and risk factors of cardiovascular disease in diabetic patients, a relationship between 3-NT levels and different food categories and their intakes of diabetic patients by detecting serum 3-nitrotyrosine levels of type 2 diabetic patients and their matched control subjects patients.
Methods
Subjects and measurements:A randomized case-control trial was carried out, in which 109 type 2 diabetic patients (diabetic case group) and 57 non-diabetic patients (control group) were enrolled. Dietary survey, anthropometric measurements, blood biochemical markers and serum 3-NT levels were done in all subjects. Food Frequency Questionnaire (FFQ) was used for the dietary survey, and duration of the diet retrospect was one year. Anthropometric measurements included body height, body weight, body mass index (BMI). Blood biochemicals were fasting blood glucose, glucosylated serum protein (GSP), HbAlc, insulin, total cholesterol (TC), triglyceride (TG) and apolipoproteins.
Apparatus: Body weight were carried on a TZ-1 weighing scale and anthropometric measurements were meadsured on a BCA-2 body analyzer manufactured by Zhongti Tongfang Sports Tech, Ltd. Blood biochemicals were measured by Hitachi 7600 automatic biochemical analyzer.
3-NT detection: 3-NT in blood was determined by ELISA kit (Hycult biotechnology bv, Lot#:5822k19). Blood samples were freshly-collected serum, diluted by 25 times. Each sample was set by a parallel reference. 450nm absorption spectrum was measured by Unico UV-2000 Spectrophotometer.
Quality control: Specific food models were adopted for the subjects as references of dietary survey to estimate daily intakes of foods such as rice, flour, eggs, milk, fruits, oil, alcohol, tea and so on. All researchers were trained uniformly and data was collected by particular persons.
Statistical analysis: Data are expressed as means±s.d. SPSS 13.0 Version for Windows was used for statistical analysis. The level of significant difference was set at P<0.05. Different groups were compared by repeated-measures analysis of variance. When significant differences occurred, related means were then compared by Student’s t-test between the two groups, and between the initial and final means in the same group.
Results
Levels of 3-NT in diabetic case group were much higher than those in their matched control group, while 3-NT levels were higher in both male and female diabetic patients than those in non-diabetic male and female patients, respectively(p<0.05). In diabetic case group, 3-NT levels increased with elevation of Body Mass Index (BMI). Male patients with BMI>24kg/m2 had much higher 3-NT levels than those with normal BMI(18.5-23.9) (p<0.05). Diabetic patients with blood glucose >6.1mmol/L had much higher 3-NT levels than those with glucose≤6.1mmol/L (p<0.05). Diabetic patients with HDL-c >1.6mmol/L had lower 3-NT levels than those with normal HDL-c concentration(p<0.05). In diabetic case group, patients with TC more than 5.7mmol/L had lower 3-NT level than those with TC less than 5.7mmol/L (p<0.05). The percentage of energy from dietary fat was significantly higher than RNI in both groups, and the dietary patterns were significantly unreasonable. Daily fat intake in diabetic group was much higher than in control group (p<0.05), while the percentage of energy from carbohydrate was lower than RNI;Daily intake of vitamin B1 and B2 were much lower in diabetic group than in control group (p<0.05), however, daily intake of sodium showed the opposite trend. Daily intake of vitamin C, sodium, iron, manganese, copper, phosphorus were higher than RNIs in both groups, as well as daily intake of vitamin A, vitamin B1, calcium in control group were lower than RNIs (p<0.05). Daily intake of staple food were much lower in diabetic group than in control group (p<0.05). However, daily intake of milk, beans and salt were on the contrary (p<0.05). Daily intakes of carotene, ascorbic acid, folic acid were higher in the HDL-c<1.6 mmol/L group than the HDL-c>1.6 mmol/L group. Serum 3-NT levels had a linear regressive relationship to LDL-c, GSP, and HbAlc in diabetic group. ApoA II and ApoC3 had the most relevant to serum 3-NT levels in male diabetic patients. GSP and HbAlc had the the most relevant to serum 3-NT levels in female diabetic patients. Triglyceride and ApoC3 were the most related with serum 3-NT levels in patients with blood glucose higher than 6.1mmol/L.HbAlc, GSP and ApoC3 were the most highly relevant to serum 3-NT levels in diabetic subjects with HDL-c concentration lower than 1.6mmol/L. Daily intakes of Na, K, Fe had accordingly linear regressive relationships to serum 3-NT levels among 3-NT levels and nutrient intakes.
Conclusions
3-NT levels in type 2 diabetics patients were much higher than those in their non-diabetic control subjects, which demonstrated that nitrosative injury indeed existed in diabetes. This provides the theoretical basis of anti-nitrition for type 2 diabetics and their cardiovascular complications.3-NT levels in type 2 diabetic patients with poorly controlled blood glucose were much higher than those in the corresponding control group. This conclusion further expands the importance of blood glucose control in diabetes. 3-NT levels in overweight and obese diabetic patients were much higher than those in the corresponding control group. This has laid a theoretical basis for dietary intervention for body weight control to reduce complications of diabetes.The relationships of 3-NT levels to risk factors of diabetic cardiovascular complications are as follows: The serum 3-NT levels and LDL-c, TC showed significant negative correlation. In diabetic patients with poor control of blood, the serum 3-NT levels and Apo C3 showed negative correlation. The possible mechanism is that excessive oxidative damages exist in diabetic patients, whose serum 3-NT levels are high, resulting in the peroxidation of lipids. Therefore, reducing oxidation and production of 3-NT might be a great significance to controlling diabetes and their cardiovascular complications.Daily intakes of Na, K, Fe had respective linear regressive relationships to serum 3-NT levels in diabetic patients, while VitB1 and VitB2 had negative relationship to 3-NT. Therefore, increasing dietary intakes of vitamin B and potassium and reducing dietary intakes of sodium and iron may be beneficial to reducing generation of 3-NT and its related diabetic complications.
方法:
分组和观察指标:单盲随机病例对照研究。筛选2型糖尿病患者109例,与其匹配的非糖尿病对照人群57例,对入选的糖尿病患者和对照人群进行膳食调查、人体测量、血生化检测和血清3-NT水平的测定。膳食调查采用“食物频率询问法(FFQ)”,回顾年限为1年。人体测量指标包括身高、体重、BMI等;血生化指标包括空腹血糖、GSP、HbA1c、血浆胰岛素、TC、TG和载脂蛋白。
人体测量采用TZ-1型身高体重秤和中体同方体育科技有限公司生产的BCA-2A人体成份分析仪测定;空腹血生化指标采用日立7600全自动生化分析仪。
3-NT检测:血清3-NT检测采用ELISA试剂盒(Hycult biotechnology bv,Lot#:5822k19),按试剂盒操作说明进行。血样均为新鲜血清,稀释25倍。每个样品均设平行样,Unico UV-2000紫外分光光度计测量450nm吸收光值。
质量控制:膳食调查时,提供食物模型,作为膳食调查的参考。对于主食米、面、蛋类、奶类、水果、食用油及酒和茶的量化估计,提供量具,并有实物参考。所有调查员均经统一培训,由专人进行计算机录入。
统计方法:数据统计采用SPSS13.0进行。两组之间比较采用t检验,单因素多水平资料采用方差分析,相关分析采用多元线性逐步回归方法。
结果
T2DM患者血清3-NT水平显著高于非糖尿病对照人群,且3-NT在男性糖尿病组高于男性对照组,在女性T2DM组高于女性对照组(p<0.05);随着BMI的增加,T2DM患者的血清3-NT水平有逐渐增高的趋势;男性T2DM患者中,BMI≥24kg/m2者其3-NT值显著高于BMI正常的T2DM患者(p<0.05);空腹血糖>6.1mmol/LT2DM患者,其血清3-NT水平显著高于血糖≤6.1mmol/LT2DM患者(p<0.05);HDL-c高于1.6mmol/L的所有T2DM患者及男性T2DM患者,其血清3-NT值均显著低于正常HDL-c的相应对照组(p<0.05);TC高于5.7mmol/L的T2DM患者,其血清3-NT水平显著低于正常TC的T2DM患者(p<0.05)。
两组人群的脂肪产能比均高于推荐产能比,T2DM患者的日均脂肪摄入量明显高于非糖尿病对照组,碳水化合物产能比较推荐产能比低;T2DM组患者的日均主食量显著低于对照组,奶类和豆类以及食盐的日均摄入量显著高于对照组(p<0.05);T2DM组患者日均VitB1、VitB2摄入量明显低于对照组,钠盐的摄入量高于对照组;全部受试者平均每日VitC摄入量、钠、铁、锰、铜、磷摄入量均高于RNI,非糖尿病组的VitA、VitB1、钙摄入量显著低于RNI;T2DM患者中HDL-c<1.6mmol/L组的3-NT、胡萝卜素、VitC、叶酸均高于HDL-c≥1.6mmol/L组(p<0.05);在T2DM患者中,血清3-NT水平与LDL-c、GSP、HbAlc有线性回归关系;男性T2DM患者中,与血清3-NT水平相关性最大的是ApoA II和ApoC3;女性T2DM患者中,与血清3-NT水平相关性最大的是GSP和HbAlc;在血糖高于6.1mmol/L的T2DM患者中,与血清3-NT水平相关性最大的是TG和ApoC3;在HDL-c低于1.6mmol/L的T2DM患者中,与血清3-NT水平相关性最大的是HbAlc、GSP和LDL-c;3-NT与营养素摄入量的线性关系中,T2DM患者血清3-NT水平与每日钠、钾、铁的摄入量有线性回归关系。
结论
T2DM患者血清3-NT水平显著高于正常人。此结果再次证明了T2DM患者体内硝基化损伤的存在,为抗硝基化预防和治疗T2DM及并发症奠定了理论基础;血糖控制不好的T2DM患者其血清3-NT水平较高,为T2DM患者控制血糖提供了新的理论依据;超重和肥胖的T2DM患者其血清3-NT水平较高,为饮食干预控制体重以防治T2DM心血管并发症奠定了理论基础;3-NT与糖尿病心血管并发症危险因素的关系如下:血清LDL-c、TC与3-NT呈显著负相关,ApoC3在血糖控制不好的T2DM患者中,与3-NT呈负相关。可能的机制是血清3-NT高的T2DM患者体内过氧化损伤也大量存在,导致了TC和载脂蛋白的过氧化损伤。所以控制体内的过氧化损伤、减少3-NT的生成对糖尿病患者并发心血管并发症有显著意义;T2DM患者血清3-NT与膳食摄入VitB1、VitB2呈负相关,与膳食摄入钠、钾、铁呈线性相关。建议T2DM患者在目前的膳食摄入基础上增加B族维生素和钾的摄入量,减少钠盐和铁的摄入,进而减少3-NT的生成,减少糖尿病及其并发症发生的可能性。
Objective
In order to provide a clinical evidence of avoiding or attenuating diabetic complications by a novel way of anti-nitrition of proteins in type 2 diabetic patients, the present study was done to try to find out a possible correlation between diabetic blood glucose control and protein nitrition, a relationship between 3-NT levels and risk factors of cardiovascular disease in diabetic patients, a relationship between 3-NT levels and different food categories and their intakes of diabetic patients by detecting serum 3-nitrotyrosine levels of type 2 diabetic patients and their matched control subjects patients.
Methods
Subjects and measurements:A randomized case-control trial was carried out, in which 109 type 2 diabetic patients (diabetic case group) and 57 non-diabetic patients (control group) were enrolled. Dietary survey, anthropometric measurements, blood biochemical markers and serum 3-NT levels were done in all subjects. Food Frequency Questionnaire (FFQ) was used for the dietary survey, and duration of the diet retrospect was one year. Anthropometric measurements included body height, body weight, body mass index (BMI). Blood biochemicals were fasting blood glucose, glucosylated serum protein (GSP), HbAlc, insulin, total cholesterol (TC), triglyceride (TG) and apolipoproteins.
Apparatus: Body weight were carried on a TZ-1 weighing scale and anthropometric measurements were meadsured on a BCA-2 body analyzer manufactured by Zhongti Tongfang Sports Tech, Ltd. Blood biochemicals were measured by Hitachi 7600 automatic biochemical analyzer.
3-NT detection: 3-NT in blood was determined by ELISA kit (Hycult biotechnology bv, Lot#:5822k19). Blood samples were freshly-collected serum, diluted by 25 times. Each sample was set by a parallel reference. 450nm absorption spectrum was measured by Unico UV-2000 Spectrophotometer.
Quality control: Specific food models were adopted for the subjects as references of dietary survey to estimate daily intakes of foods such as rice, flour, eggs, milk, fruits, oil, alcohol, tea and so on. All researchers were trained uniformly and data was collected by particular persons.
Statistical analysis: Data are expressed as means±s.d. SPSS 13.0 Version for Windows was used for statistical analysis. The level of significant difference was set at P<0.05. Different groups were compared by repeated-measures analysis of variance. When significant differences occurred, related means were then compared by Student’s t-test between the two groups, and between the initial and final means in the same group.
Results
Levels of 3-NT in diabetic case group were much higher than those in their matched control group, while 3-NT levels were higher in both male and female diabetic patients than those in non-diabetic male and female patients, respectively(p<0.05). In diabetic case group, 3-NT levels increased with elevation of Body Mass Index (BMI). Male patients with BMI>24kg/m2 had much higher 3-NT levels than those with normal BMI(18.5-23.9) (p<0.05). Diabetic patients with blood glucose >6.1mmol/L had much higher 3-NT levels than those with glucose≤6.1mmol/L (p<0.05). Diabetic patients with HDL-c >1.6mmol/L had lower 3-NT levels than those with normal HDL-c concentration(p<0.05). In diabetic case group, patients with TC more than 5.7mmol/L had lower 3-NT level than those with TC less than 5.7mmol/L (p<0.05). The percentage of energy from dietary fat was significantly higher than RNI in both groups, and the dietary patterns were significantly unreasonable. Daily fat intake in diabetic group was much higher than in control group (p<0.05), while the percentage of energy from carbohydrate was lower than RNI;Daily intake of vitamin B1 and B2 were much lower in diabetic group than in control group (p<0.05), however, daily intake of sodium showed the opposite trend. Daily intake of vitamin C, sodium, iron, manganese, copper, phosphorus were higher than RNIs in both groups, as well as daily intake of vitamin A, vitamin B1, calcium in control group were lower than RNIs (p<0.05). Daily intake of staple food were much lower in diabetic group than in control group (p<0.05). However, daily intake of milk, beans and salt were on the contrary (p<0.05). Daily intakes of carotene, ascorbic acid, folic acid were higher in the HDL-c<1.6 mmol/L group than the HDL-c>1.6 mmol/L group. Serum 3-NT levels had a linear regressive relationship to LDL-c, GSP, and HbAlc in diabetic group. ApoA II and ApoC3 had the most relevant to serum 3-NT levels in male diabetic patients. GSP and HbAlc had the the most relevant to serum 3-NT levels in female diabetic patients. Triglyceride and ApoC3 were the most related with serum 3-NT levels in patients with blood glucose higher than 6.1mmol/L.HbAlc, GSP and ApoC3 were the most highly relevant to serum 3-NT levels in diabetic subjects with HDL-c concentration lower than 1.6mmol/L. Daily intakes of Na, K, Fe had accordingly linear regressive relationships to serum 3-NT levels among 3-NT levels and nutrient intakes.
Conclusions
3-NT levels in type 2 diabetics patients were much higher than those in their non-diabetic control subjects, which demonstrated that nitrosative injury indeed existed in diabetes. This provides the theoretical basis of anti-nitrition for type 2 diabetics and their cardiovascular complications.3-NT levels in type 2 diabetic patients with poorly controlled blood glucose were much higher than those in the corresponding control group. This conclusion further expands the importance of blood glucose control in diabetes. 3-NT levels in overweight and obese diabetic patients were much higher than those in the corresponding control group. This has laid a theoretical basis for dietary intervention for body weight control to reduce complications of diabetes.The relationships of 3-NT levels to risk factors of diabetic cardiovascular complications are as follows: The serum 3-NT levels and LDL-c, TC showed significant negative correlation. In diabetic patients with poor control of blood, the serum 3-NT levels and Apo C3 showed negative correlation. The possible mechanism is that excessive oxidative damages exist in diabetic patients, whose serum 3-NT levels are high, resulting in the peroxidation of lipids. Therefore, reducing oxidation and production of 3-NT might be a great significance to controlling diabetes and their cardiovascular complications.Daily intakes of Na, K, Fe had respective linear regressive relationships to serum 3-NT levels in diabetic patients, while VitB1 and VitB2 had negative relationship to 3-NT. Therefore, increasing dietary intakes of vitamin B and potassium and reducing dietary intakes of sodium and iron may be beneficial to reducing generation of 3-NT and its related diabetic complications.
引文
[1]池泉.蛋白质酪氨酸硝化的研究[J].化学进展, 2006,18.
[2]赵玉玲.蛋白质硝基化反应的途径[J].生命的化学, 2003,25.
[3]孙士铸.过氧化物酶催化的硝化反应研究进展[J]. Science Technology and Engineering, 2007,7:1671-1819.
[4] Koo JR, Vaziri ND. Effects of diabetes, insulin and antioxidants on NO synthase abundance and NO interaction with reactive oxygen species[J]. Kidney Int, 2003,63:195-201.
[5] Piconi I, Ceriello A. Oxidative stress in diabetes[J]. Clin Chem Lab Med, 2003,41:1144-1149.
[6]高平章,卢乃浩,高中洪.蛋白质酪氨酸硝化检测方法[J].化学进展, 2007,19.
[7] Delatour T GPA, Stadler R H. 3-Nitrotyrosine butyl ester: a novel derivative to assess tyrosine nitration in rat plasma by liquid chromatography-tandem mass spectrometry detection[J]. Analytical Biochemistry 2002,302:10-18.
[8] Hermo R. Circulating levels of nitrated apolipoprotein A-I are increased in type 2 diabetic patients[J]. clin chem lab med, 2005,43:601-606.
[9] Ceriello A. New findings as a marker of postprandial oxidative stress[J]. Int J Clin Pract Suppl, 2002:51-58.
[10] Turko IV, Marcondes S, Murad F. Diabetes-associated nitration of tyrosine and inactivation of succinyl-CoA:3-oxoacid CoA-transferase [J]. Am J Physiol Heart Circ Physiol, 2001,281:2289-2294.
[11] Ishii N. Nitricoxide synthesis and oxidative stress in the renal cortex of rats with diabetes mellitus[J]. J Am Soc Nephrol, 2001,12:1630-1639.
[12] Ahmed N, Babaei-Jadidi R, Howell S.K, et al. Degradation products of proteins damaged by glycation, oxidation and nitration in clinical type 1 diabetes[J]. Diabetologia, 2005,48:1590-1603.
[13] Ceriello A, Mercuri F, Quagliaro L, et al. Detection of nitrotyrosine in the diabetic plasma: evidence of oxidative stress[J]. Diabetologia, 2001,44:834-838.
[14] Ceriello A. Acute hyperglycemia induces nitrotyrosine formation and apoptosis in perfused heart from rat[J]. Diabetes 2002,51:1076-1082.
[15] Ceriello A. Pramlintide reduced markers of oxidative stress in the postprandialperiod in patients with type 2 diabetes[J]. Diabetes/metabolism research and reviews, 2008,24:103-108.
[16] Tseng KH. Standards of medical care in diabetes--2006: response to the American Diabetes Association[J]. Diabetes Care, 2006,29:2563-2564; author reply 2564-2565.
[17]刘新民,潘长玉,张达青,等.实用内分泌学.北京:人民军医出版社, 2004.
[18]葛可佑.中国营养科学全书.北京:人民卫生出版社, 2004.
[19]刘人伟.现代实验诊断学检验与临床.化学工业出版社, 2002.
[20] Bo S, Gambino R, Guidi S, et al. Plasma nitrotyrosine levels, antioxidant vitamins and hyperglycaemia[J]. Diabet Med, 2005,22:1185-1189.
[21] M.Cowell R, W.Russell J. Nitrosative injury and antioxidant therapy in the management of diabetic neuropathy[J]. Journal of Investigative, 2004,52.
[22] Franceschina mercuri, quagliaro L, ceriello A. Oxidative stress evaluation in diabetes[J]. Diabetes technology & therapeutics, 2000,2:589-601.
[23] Turko IV, Murad F. Protein nitration in cardiovascular diseases[J]. Pharmacol Rev, 2002,54:619-639.
[24] Wang XL, Rainwater DL, Leone A, et al. Effects of diabetes on plasma nitrotyrosine levels[J]. Diabet Med, 2004,21:577-580.
[25] Sun YC, Chang PY, Tsao KC, et al. Establishment of a sandwich ELISA using commercial antibody for plasma or serum 3-nitrotyrosine (3NT). Elevation in inflammatory diseases and complementary between 3NT and myeloperoxidase[J]. Clin Chim Acta, 2007,378:175-180.
[26] Safinowski M, Wilhelm B, Reimer T, et al. Determination of nitrotyrosine concentrations in plasma samples of diabetes mellitus patients by four different immunoassays leads to contradictive results and disqualifies the majority of the tests[J]. clin chem lab med, 2009,47:483-488.
[27] Zou MH, Shi C, Cohen RA. High glucose via peroxynitrite causes tyrosine nitration and inactivation of prostacyclin synthase that is associated with thromboxane/prostaglandin H(2) receptor-mediated apoptosis and adhesion molecule expression in cultured human aortic endothelial cells[J]. Diabetes, 2002,51:198-203.
[28] Ceriello A, Quagliaro L, Catone B, et al. Role of hyperglycemia in nitrotyrosine postprandial generation[J]. Diabetes Care, 2002,25:1439-1443.
[29] Cosentino F, Hishikawa K, S.Katusic Z. High glucose increases nitric oxidesynthase expression and superoxide anion generation in human aortic endothelial cells[J]. Circulation, 1997,96:25-28.
[30] Haun DR, Pitanga FJ, Lessa I. Waist-height ratio compared to other indicators of obesity as predictosr of high coronary risk.[J]. Rev Assoc Med Bras, 2009,55:705-711.
[31] Friedl CK. Waist circumference threshold values for type 2 diabetes risk[J]. J Diabetes Sci Technol, 2009,3:761-769.
[32]张荣欣,薛长勇,郑子新,等.成人BMI与体脂含量和脂肪分别得关系[J].营养学报, 2002,24:5.
[33]巫向前.临床检验结果的评价.人民卫生出版社, 2000,第一版.
[34]王俊玲,赵文华.用简化的食物频率询问法进行膳食评价[J].中国慢性病预防与控制, 2000,8.
[35] Ceriello A, Bortolotti N, Motz E, et al. Meal-generated oxidative stress in type 2 diabetic patients.[J]. Diabetes Care 1998,21:1529-1533.
[36] Rossi MC, Nicolucci A, Di Bartolo P, et al. Diabetes interactive diary: a new telemedicine system enabling flexible diet and insulin therapy while improving quality of life: an open-label, international, multicenter, randomized study[J]. Diabetes Care, 2010,33:109-115.
[37] Agte VV, Tarwadi KV. Combination of diabetes and cataract worsens the oxidative stress and micronutrient status in Indians[J]. Nutrition, 2008,24:617-624.
[38] Bonnefont-Rousselot D. The role of antioxidant micronutrients in the prevention of diabetic complications[J]. Treat Endocrinol, 2004,3:41-52.
[39] Guerrero-Romero F, Rodriguez-Moran M. Complementary therapies for diabetes: the case for chromium, magnesium, and antioxidants[J]. Arch Med Res, 2005,36:250-257.
[40] Faure P. Protective effects of antioxidant micronutrients (vitamin E, zinc and selenium) in type 2 diabetes mellitus[J]. Clin Chem Lab Med, 2003,41:995-998.
[41] Armstrong AM, Chestnutt JE, Gormley MJ, et al. The effect of dietary treatment on lipid peroxidation and antioxidant status in newly diagnosed noninsulin dependent diabetes[J]. Free Radic Biol Med, 1996,21:719-726.
[42] Ceriello A, Esposito K, Piconi L, et al. Glucose "peak" and glucose "spike": Impact on endothelial function and oxidative stress[J]. Diabetes Res Clin Pract,2008,82:262-267.
[43]王乐三. SPSS在医学科研中的应用.北京-化学工业出版社, 2007:143-151.
[44] Turko IV, Li L, Aulak KS. Protein tyrosine nitration in the mitochondria from diabetic mouse heart[J]. J.Biol.Chem, 2003,278:33972-33977.
[45] Cromheeke KM, Kockx MM, Meyer GR, et al. Inducible nitric oxide synthase colocalizes with signs of lipid oxidation/peroxidation in human atherosclerotic plaques[J]. Cardiovasc Res, 1999,43:744-754.
[46] Shin T, Tanuma N, Kim S, et al. An inhibitor of inducible nitric oxide synthase ameliorates experimental autoimmune myocarditis in Lewis rats[J]. J Neuroimmunol, 1998,92:133-138.
[47] Da Ros R, Quagliaro L, Gasparini D, et al. Nitrotyrosine in peripheral vascular disease[J]. J Thromb Haemost, 2003,1:382-383.
[48] Ferderbar S, Pereira EC, Apolinario E, et al. Cholesterol oxides as biomarkers of oxidative stress in type 1 and type 2 diabetes mellitus[J]. Diabetes Metab Res Rev, 2007,23:35-42.
[49] Zheng L, Nukuna B, Brennan ML, et al. Apolipoprotein A-I is a selective target for myeloperoxidase-catalyzed oxidation and functional impairment in subjects with cardiovascular disease[J]. J Clin Invest, 2004,114:529-541.
[1] Davies K J. Oxidative stress: the paradox of acrobic life [J]. Biochem Soc Symp, 1995, 61:1-31.
[2] Chan J C, Cheung J C, Laue M, et al. The metabolic syndrome in Hong Kong Chinese, The interrelationships among its components analyzed by structural equation modeling [J]. Dia J, 1996, 19(9): 953-959.
[3] Mercuri F, Quagliaro L. Oxidative stress evaluation in diabetes [J]. Dia Tech Ther, 2000:2(4) :589-600.
[4] Turko I V, Murad F. Protein nitration in cardiovascular diseases [J]. Pharmacol Rev, 2002, 54(4):619-639.
[5]池泉.蛋白质酪氨酸硝化的研究[J].化学进展, 2006, 18(7/8): 1019-1025.
[6] Antonio C. Role of hyperglycemia in nitrotyrosine postprandial generation [J].Diabetes Care, 2002, 25(8):1439-1443.
[7] Antonio C. New findings as a marker of postprandial oxidative stress [J]. Int J Clin Pract Suppl, 2002, (129): 51-58.
[8] Turko I V, Marcondes S. Diabetes-associated nitration of tyrosine and inactivation of succinyl-CoA-transferase [J]. Am J Physiol Heart Circ Physiol, 2001, 281:H2289- H2294.
[9] Antonio C. Reactive oxygen species mediate a cellular memory of high glucose stress signaling [J]. Diabetologia, 2007, 50(7):1523-1531.
[10] Ishii N. Nitric oxide synthesis and oxidative stress in the renal cortex of rats with diabetes mellitus [J]. J Am Soc Nephrol, 2001, 12 (8):1630-1639.
[11] Ahmed N, Babaei-Jadidi R. Degradation products of proteins damaged by glycation, oxidation and nitration in clinical type 1 diabetes [J]. Diabetologia, 2005, 48(8):1590-1603.
[12] Wang X L. Effects of diabetes on plasma nitrotyrosine levels.[J] Diabetes med, 2004, 21(6):577-580.
[13] Antonio C. Detection of nitrotyrosine in the diabetic plasma: evidence of oxidative stress [J]. Diabetologia, 2001, 44(7):834-838.
[14] Antonio C. Acute hyperglycemia induces nitrotyrosine formation and apoptosis in perfused heart from rat [J]. Diabetes, 2002, 51(4):1076-1082.
[15] Ccsentino F, Hishikawa K, S.Katusic Z. High glucose increases nitric oxide synthase expression and superoxide anion generation in human aortic endothelial cells [J] Circulation, 1997, 96(1):25-28.
[16] Antonio C. Pramlintide reduced markers of oxidative stress in the postprandial period in patients with type 2 diabetes [J]. Dia/Met Re And Rev, 2008, 24(2):103-108.
[17] Gambino R, Guidi S, Silli B, et al. Plasma nitrotyrosine levels, antioxidant vitamins and hyperglycaemia [J]. Dia Med, 2005, 22(9):1185-1189.
[18] Turko I V, Li L, Aulak K S. Protein tyrosine nitration in the mitochondria from diabetic mouse heart [J]. J Biol Chem, 2003, 278(36):33972-33977.
[19] Cromheeke K M, Kockx M M, De Meyer G R et al. Inducible nitric oxide synthase colocalizes with signs of lipid oxidation/peroxidation in human atherosclerotic plaques [J]. Cardiovasc Res, 1999, 43(3):744-754.
[20] Shin T, Tanuma N. An inhibitor of inducible nitric oxide synthase ameliorates exp-erimental autoimmune myocarditis in Lewis rats [J]. J Neuroimmunol, 1998, 92:133-138.
[21] Zhan X, Du Y. Targets of tyrosine nitration in diabetic rat retina [J]. Mol Cel Pro, 2008 ,7(5):864-874.
[22] Renu A.K CHAN P. Oxidative stress and diabetic retinopathy [J]. Experimental Diabetes Research,2007, 2007:1155-1167.
[23] Cowell R, Russell J. Nitrosative injury and antioxidant therapy in the management of diabetic neuropathy [J]. J of Investigative, 2004, 52 (1):33-44.
[24] Cameron N E, Eaton S E. Vascular factors and metabolic interactions in the pathogenesis of diabetic neuropathy [J]. Diabetologia, 2001, 44(11):1973-1988.
[25] Bauersachs J. Improvement of left ventricular remodeling and function by hydrox-ymethylglutaryl coenzyme A reductase inhibition with cerivastatin in rats with heart failure after myocardial infarction [J]. Circulation, 2001,104:982-985.
[26] Szabo C. Pathogenetic role of peroxynitrite in the development of diabetes and diabetic vascular complications: studies with FP15, a novel potent peroxynitrite decomposition catalyst [J]. Mol Med, 2002, 8(10):571-580.
[27] Antonio C. Effect of irbesartan on nitrotyrosine generation in non-hypertensive diabetic patients [J]. Diabetologia, 2004, 47(9):1535-1540.
[28] Antonio C, Piconi L, Esposito K. Telmisartan shows an equivalent effect of vitamin C in further improving endothelial dysfunction after glycemia normalization in type 1 diabetes [J]. Diabetes Care, 2007, 30(7):1694-1698.
[29] Droge W. Free radicals in the physiological control of cell function [J]. Physiol Rev, 2002, 82(7):47-95.
[30] Piconi I, Antonio C. Oxidative stress in diabetes [J]. Clin Chem Lab Med, 2003, 41(9):1144-1149.
[2]赵玉玲.蛋白质硝基化反应的途径[J].生命的化学, 2003,25.
[3]孙士铸.过氧化物酶催化的硝化反应研究进展[J]. Science Technology and Engineering, 2007,7:1671-1819.
[4] Koo JR, Vaziri ND. Effects of diabetes, insulin and antioxidants on NO synthase abundance and NO interaction with reactive oxygen species[J]. Kidney Int, 2003,63:195-201.
[5] Piconi I, Ceriello A. Oxidative stress in diabetes[J]. Clin Chem Lab Med, 2003,41:1144-1149.
[6]高平章,卢乃浩,高中洪.蛋白质酪氨酸硝化检测方法[J].化学进展, 2007,19.
[7] Delatour T GPA, Stadler R H. 3-Nitrotyrosine butyl ester: a novel derivative to assess tyrosine nitration in rat plasma by liquid chromatography-tandem mass spectrometry detection[J]. Analytical Biochemistry 2002,302:10-18.
[8] Hermo R. Circulating levels of nitrated apolipoprotein A-I are increased in type 2 diabetic patients[J]. clin chem lab med, 2005,43:601-606.
[9] Ceriello A. New findings as a marker of postprandial oxidative stress[J]. Int J Clin Pract Suppl, 2002:51-58.
[10] Turko IV, Marcondes S, Murad F. Diabetes-associated nitration of tyrosine and inactivation of succinyl-CoA:3-oxoacid CoA-transferase [J]. Am J Physiol Heart Circ Physiol, 2001,281:2289-2294.
[11] Ishii N. Nitricoxide synthesis and oxidative stress in the renal cortex of rats with diabetes mellitus[J]. J Am Soc Nephrol, 2001,12:1630-1639.
[12] Ahmed N, Babaei-Jadidi R, Howell S.K, et al. Degradation products of proteins damaged by glycation, oxidation and nitration in clinical type 1 diabetes[J]. Diabetologia, 2005,48:1590-1603.
[13] Ceriello A, Mercuri F, Quagliaro L, et al. Detection of nitrotyrosine in the diabetic plasma: evidence of oxidative stress[J]. Diabetologia, 2001,44:834-838.
[14] Ceriello A. Acute hyperglycemia induces nitrotyrosine formation and apoptosis in perfused heart from rat[J]. Diabetes 2002,51:1076-1082.
[15] Ceriello A. Pramlintide reduced markers of oxidative stress in the postprandialperiod in patients with type 2 diabetes[J]. Diabetes/metabolism research and reviews, 2008,24:103-108.
[16] Tseng KH. Standards of medical care in diabetes--2006: response to the American Diabetes Association[J]. Diabetes Care, 2006,29:2563-2564; author reply 2564-2565.
[17]刘新民,潘长玉,张达青,等.实用内分泌学.北京:人民军医出版社, 2004.
[18]葛可佑.中国营养科学全书.北京:人民卫生出版社, 2004.
[19]刘人伟.现代实验诊断学检验与临床.化学工业出版社, 2002.
[20] Bo S, Gambino R, Guidi S, et al. Plasma nitrotyrosine levels, antioxidant vitamins and hyperglycaemia[J]. Diabet Med, 2005,22:1185-1189.
[21] M.Cowell R, W.Russell J. Nitrosative injury and antioxidant therapy in the management of diabetic neuropathy[J]. Journal of Investigative, 2004,52.
[22] Franceschina mercuri, quagliaro L, ceriello A. Oxidative stress evaluation in diabetes[J]. Diabetes technology & therapeutics, 2000,2:589-601.
[23] Turko IV, Murad F. Protein nitration in cardiovascular diseases[J]. Pharmacol Rev, 2002,54:619-639.
[24] Wang XL, Rainwater DL, Leone A, et al. Effects of diabetes on plasma nitrotyrosine levels[J]. Diabet Med, 2004,21:577-580.
[25] Sun YC, Chang PY, Tsao KC, et al. Establishment of a sandwich ELISA using commercial antibody for plasma or serum 3-nitrotyrosine (3NT). Elevation in inflammatory diseases and complementary between 3NT and myeloperoxidase[J]. Clin Chim Acta, 2007,378:175-180.
[26] Safinowski M, Wilhelm B, Reimer T, et al. Determination of nitrotyrosine concentrations in plasma samples of diabetes mellitus patients by four different immunoassays leads to contradictive results and disqualifies the majority of the tests[J]. clin chem lab med, 2009,47:483-488.
[27] Zou MH, Shi C, Cohen RA. High glucose via peroxynitrite causes tyrosine nitration and inactivation of prostacyclin synthase that is associated with thromboxane/prostaglandin H(2) receptor-mediated apoptosis and adhesion molecule expression in cultured human aortic endothelial cells[J]. Diabetes, 2002,51:198-203.
[28] Ceriello A, Quagliaro L, Catone B, et al. Role of hyperglycemia in nitrotyrosine postprandial generation[J]. Diabetes Care, 2002,25:1439-1443.
[29] Cosentino F, Hishikawa K, S.Katusic Z. High glucose increases nitric oxidesynthase expression and superoxide anion generation in human aortic endothelial cells[J]. Circulation, 1997,96:25-28.
[30] Haun DR, Pitanga FJ, Lessa I. Waist-height ratio compared to other indicators of obesity as predictosr of high coronary risk.[J]. Rev Assoc Med Bras, 2009,55:705-711.
[31] Friedl CK. Waist circumference threshold values for type 2 diabetes risk[J]. J Diabetes Sci Technol, 2009,3:761-769.
[32]张荣欣,薛长勇,郑子新,等.成人BMI与体脂含量和脂肪分别得关系[J].营养学报, 2002,24:5.
[33]巫向前.临床检验结果的评价.人民卫生出版社, 2000,第一版.
[34]王俊玲,赵文华.用简化的食物频率询问法进行膳食评价[J].中国慢性病预防与控制, 2000,8.
[35] Ceriello A, Bortolotti N, Motz E, et al. Meal-generated oxidative stress in type 2 diabetic patients.[J]. Diabetes Care 1998,21:1529-1533.
[36] Rossi MC, Nicolucci A, Di Bartolo P, et al. Diabetes interactive diary: a new telemedicine system enabling flexible diet and insulin therapy while improving quality of life: an open-label, international, multicenter, randomized study[J]. Diabetes Care, 2010,33:109-115.
[37] Agte VV, Tarwadi KV. Combination of diabetes and cataract worsens the oxidative stress and micronutrient status in Indians[J]. Nutrition, 2008,24:617-624.
[38] Bonnefont-Rousselot D. The role of antioxidant micronutrients in the prevention of diabetic complications[J]. Treat Endocrinol, 2004,3:41-52.
[39] Guerrero-Romero F, Rodriguez-Moran M. Complementary therapies for diabetes: the case for chromium, magnesium, and antioxidants[J]. Arch Med Res, 2005,36:250-257.
[40] Faure P. Protective effects of antioxidant micronutrients (vitamin E, zinc and selenium) in type 2 diabetes mellitus[J]. Clin Chem Lab Med, 2003,41:995-998.
[41] Armstrong AM, Chestnutt JE, Gormley MJ, et al. The effect of dietary treatment on lipid peroxidation and antioxidant status in newly diagnosed noninsulin dependent diabetes[J]. Free Radic Biol Med, 1996,21:719-726.
[42] Ceriello A, Esposito K, Piconi L, et al. Glucose "peak" and glucose "spike": Impact on endothelial function and oxidative stress[J]. Diabetes Res Clin Pract,2008,82:262-267.
[43]王乐三. SPSS在医学科研中的应用.北京-化学工业出版社, 2007:143-151.
[44] Turko IV, Li L, Aulak KS. Protein tyrosine nitration in the mitochondria from diabetic mouse heart[J]. J.Biol.Chem, 2003,278:33972-33977.
[45] Cromheeke KM, Kockx MM, Meyer GR, et al. Inducible nitric oxide synthase colocalizes with signs of lipid oxidation/peroxidation in human atherosclerotic plaques[J]. Cardiovasc Res, 1999,43:744-754.
[46] Shin T, Tanuma N, Kim S, et al. An inhibitor of inducible nitric oxide synthase ameliorates experimental autoimmune myocarditis in Lewis rats[J]. J Neuroimmunol, 1998,92:133-138.
[47] Da Ros R, Quagliaro L, Gasparini D, et al. Nitrotyrosine in peripheral vascular disease[J]. J Thromb Haemost, 2003,1:382-383.
[48] Ferderbar S, Pereira EC, Apolinario E, et al. Cholesterol oxides as biomarkers of oxidative stress in type 1 and type 2 diabetes mellitus[J]. Diabetes Metab Res Rev, 2007,23:35-42.
[49] Zheng L, Nukuna B, Brennan ML, et al. Apolipoprotein A-I is a selective target for myeloperoxidase-catalyzed oxidation and functional impairment in subjects with cardiovascular disease[J]. J Clin Invest, 2004,114:529-541.
[1] Davies K J. Oxidative stress: the paradox of acrobic life [J]. Biochem Soc Symp, 1995, 61:1-31.
[2] Chan J C, Cheung J C, Laue M, et al. The metabolic syndrome in Hong Kong Chinese, The interrelationships among its components analyzed by structural equation modeling [J]. Dia J, 1996, 19(9): 953-959.
[3] Mercuri F, Quagliaro L. Oxidative stress evaluation in diabetes [J]. Dia Tech Ther, 2000:2(4) :589-600.
[4] Turko I V, Murad F. Protein nitration in cardiovascular diseases [J]. Pharmacol Rev, 2002, 54(4):619-639.
[5]池泉.蛋白质酪氨酸硝化的研究[J].化学进展, 2006, 18(7/8): 1019-1025.
[6] Antonio C. Role of hyperglycemia in nitrotyrosine postprandial generation [J].Diabetes Care, 2002, 25(8):1439-1443.
[7] Antonio C. New findings as a marker of postprandial oxidative stress [J]. Int J Clin Pract Suppl, 2002, (129): 51-58.
[8] Turko I V, Marcondes S. Diabetes-associated nitration of tyrosine and inactivation of succinyl-CoA-transferase [J]. Am J Physiol Heart Circ Physiol, 2001, 281:H2289- H2294.
[9] Antonio C. Reactive oxygen species mediate a cellular memory of high glucose stress signaling [J]. Diabetologia, 2007, 50(7):1523-1531.
[10] Ishii N. Nitric oxide synthesis and oxidative stress in the renal cortex of rats with diabetes mellitus [J]. J Am Soc Nephrol, 2001, 12 (8):1630-1639.
[11] Ahmed N, Babaei-Jadidi R. Degradation products of proteins damaged by glycation, oxidation and nitration in clinical type 1 diabetes [J]. Diabetologia, 2005, 48(8):1590-1603.
[12] Wang X L. Effects of diabetes on plasma nitrotyrosine levels.[J] Diabetes med, 2004, 21(6):577-580.
[13] Antonio C. Detection of nitrotyrosine in the diabetic plasma: evidence of oxidative stress [J]. Diabetologia, 2001, 44(7):834-838.
[14] Antonio C. Acute hyperglycemia induces nitrotyrosine formation and apoptosis in perfused heart from rat [J]. Diabetes, 2002, 51(4):1076-1082.
[15] Ccsentino F, Hishikawa K, S.Katusic Z. High glucose increases nitric oxide synthase expression and superoxide anion generation in human aortic endothelial cells [J] Circulation, 1997, 96(1):25-28.
[16] Antonio C. Pramlintide reduced markers of oxidative stress in the postprandial period in patients with type 2 diabetes [J]. Dia/Met Re And Rev, 2008, 24(2):103-108.
[17] Gambino R, Guidi S, Silli B, et al. Plasma nitrotyrosine levels, antioxidant vitamins and hyperglycaemia [J]. Dia Med, 2005, 22(9):1185-1189.
[18] Turko I V, Li L, Aulak K S. Protein tyrosine nitration in the mitochondria from diabetic mouse heart [J]. J Biol Chem, 2003, 278(36):33972-33977.
[19] Cromheeke K M, Kockx M M, De Meyer G R et al. Inducible nitric oxide synthase colocalizes with signs of lipid oxidation/peroxidation in human atherosclerotic plaques [J]. Cardiovasc Res, 1999, 43(3):744-754.
[20] Shin T, Tanuma N. An inhibitor of inducible nitric oxide synthase ameliorates exp-erimental autoimmune myocarditis in Lewis rats [J]. J Neuroimmunol, 1998, 92:133-138.
[21] Zhan X, Du Y. Targets of tyrosine nitration in diabetic rat retina [J]. Mol Cel Pro, 2008 ,7(5):864-874.
[22] Renu A.K CHAN P. Oxidative stress and diabetic retinopathy [J]. Experimental Diabetes Research,2007, 2007:1155-1167.
[23] Cowell R, Russell J. Nitrosative injury and antioxidant therapy in the management of diabetic neuropathy [J]. J of Investigative, 2004, 52 (1):33-44.
[24] Cameron N E, Eaton S E. Vascular factors and metabolic interactions in the pathogenesis of diabetic neuropathy [J]. Diabetologia, 2001, 44(11):1973-1988.
[25] Bauersachs J. Improvement of left ventricular remodeling and function by hydrox-ymethylglutaryl coenzyme A reductase inhibition with cerivastatin in rats with heart failure after myocardial infarction [J]. Circulation, 2001,104:982-985.
[26] Szabo C. Pathogenetic role of peroxynitrite in the development of diabetes and diabetic vascular complications: studies with FP15, a novel potent peroxynitrite decomposition catalyst [J]. Mol Med, 2002, 8(10):571-580.
[27] Antonio C. Effect of irbesartan on nitrotyrosine generation in non-hypertensive diabetic patients [J]. Diabetologia, 2004, 47(9):1535-1540.
[28] Antonio C, Piconi L, Esposito K. Telmisartan shows an equivalent effect of vitamin C in further improving endothelial dysfunction after glycemia normalization in type 1 diabetes [J]. Diabetes Care, 2007, 30(7):1694-1698.
[29] Droge W. Free radicals in the physiological control of cell function [J]. Physiol Rev, 2002, 82(7):47-95.
[30] Piconi I, Antonio C. Oxidative stress in diabetes [J]. Clin Chem Lab Med, 2003, 41(9):1144-1149.