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1.
目的 观察肥胖患者血清游离胰岛素样生长因子Ⅰ(IGF-Ⅰ)、胰岛素样生长因子结合蛋白1(IGFBP-1)及IGFBP-3水平,分析其与年龄、性别、体重指数(BMI)、糖代谢、脂代谢等指标的关系。方法应用ELSA法测定97例肥胖患者和84例正常人血清游离IGF-Ⅰ、IGFBP-3、IGFBP-1、真胰岛素和血脂水平。结果 肥胖组与对照组比较,IGFBP-3明显增高(P<0.01),IGFBP-1下降(P<0.05),而游离的IGF-Ⅰ水平差异无显著性。游离IGF-Ⅰ水平与年龄呈显著负相关(正常组r=-0.26,P<0.05;肥胖组r=-0.42,P<0.01)。在肥胖组,游离IGF-Ⅰ水平与空腹血糖(r=-0.31,P<0.01)、低密度脂蛋白(r=-0.23,P<0.05)及IGFBP-1(r=-0.24,P<0.05)呈负相关,IGFBP-1与BMI(r=-0.41,P<0.01)、空腹胰岛素(FINS)(r=-0.35,P<0.01)和Homa-IR指数呈负相关(r=-0.31,P<0.01),IGFBP-3与FINS呈正相关(r=0.26,P<0.05)。结论 游离IGF-Ⅰ水平随年龄的增长有下降的趋势,并可能参与糖代谢及脂代谢的调节。IGFBP-1浓度可能反映胰岛素抵抗状态。  相似文献   

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目的探讨胰岛素样生长因子(IGF)及其结合蛋白(IGFBP)在2型糖尿病肾脏病变中的变化及其相关关系。方法2000-02~2003-05对广东省人民医院的130例(男52例、女78例),年龄在37~75岁2型糖尿病患者,观察了IGFs、IGFBPs、血脂、空腹和餐后2hC肽(CP0、CP120)等与血、尿α1和β2-微球蛋白(MG)的相关性,比较不同肾脏病变组间的IGFs和IGFBPs改变。结果多元逐步回归分析,血α1-MG主要相关预测因子为IGF-2、TC、年龄(r=0.492,P=0.0001);尿α1-MG为IGF-2、年龄(r=0.307,P=0.007);血β2-MG为IGFBP-1、HDL、年龄(r=0.528,P=0.0001);尿β2-MG为IGFBP-1、CP120、年龄(r=0.407,P=0.0001);血肌酐(Cr)为IGFBP-1、CP0、年龄(r=0.499,P=0.0001)。IGF-2和IGFBP-1在糖尿病肾病组显著升高[IGF-2:(889.48±65.94)μg/L对(711.57±28.73)μg/L,P=0.03;IGFBP-1:(94.91±17.48)μg/L对(54.81±5.04)μg/L,P=0.009]。结论2型糖尿病患者血清IGFBP-1、IGF-2水平与血、尿微球蛋白水平有密切的相关性,糖尿病肾病的IGFBP-1和IGF-2明显升高。糖尿病的胰岛功能改变、IGF与IGFBP系统以及脂代谢异常,与糖尿病肾病的发生、发展有关。  相似文献   

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目的探讨糖、脂代谢不同人群的血清胰岛素样生长因子结合蛋白1(IGFBP-1)水平与胰岛素抵抗(IR)的关系。方法选取正常人(NC)、高TG血症患者、2型糖尿病(T2DM)患者及T2DM+高TG患者共66例,测定血清IGFBP-1、胰岛素、血糖和血脂水平。结果(1)血清IGFBP-1水平,高TG血症组较NC组、T2DM+高TG组较T2DM组均明显下降(P〈0.05)。(2)多元逐步回归分析显示血清IGFBP-1水平与TG、HOMA-IR负相关(P〈0.05),与HDL-C正相关(P〈0.05)。结论高TG血症人群血清IGFBP-1明显下降,提示存在明显肝脏IR。  相似文献   

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目的 探讨胰岛素样生长因子(IGF)-1及胰岛素样生长因子结合蛋白(IGFBP)-3在过敏性紫癜(HSP)中的作用.方法 采用放射免疫法方法测定45例HSP患儿不同时期的血清IGF-1及IGFBP-3、C反应蛋白(CRP)水平.采用t检验和直线相关关系.结果 HSP急性发作组血清IGF-1[(452±183)μg/L]、IGFBP-3[(13 897±3124)μg/L]及CRP[(20±8)mg/L]水平升高,与健康对照组和缓解组比较,差异均有统计学意义(t值分别为3.42、4.10、11.17、11.63、8.59、9.86.P均<0.01);HSP缓解组血清IGF-1、IGFBP-3及CRP与健康对照组比较,差异无统计学意义(t=0.3,4、0.34、0.52,P均>0.05).HSP急性期并发肾损害组血清IGF-1[(621±253)μg/L]、IGFBP-3[(18 763±3173)μg/L]水平升高,与无肾损害组比较,差异有统计学意义(t值分别为4.21、7.26,P均<0.01),有胃肠道症组血清IGF-1[(479±192)μg/L]、IGFBP-3[(13 986±3162)μg/L]水平与无胃肠道症状组比较,差异无统计学意义(t值分别为0.83、0.16,P均>0.05);血清CRP水平在肾损害组与非肾损害组及胃肠道症组与无胃肠道症状组问差异均无统计学意义(t值分别为0.56、0.32.P均>0.05).HSP急性期患儿血IGF-1、IGFBP-3与CRP浓度之间呈直线正相关(r值分别为0.624,0.672,JP均<0.01).结论 IGF-1、IGFBP-3参与了HSP疾病的病理生理过程,血清IGF-1、IGFBP-3测定对紫癜性肾损害的诊断、病情监测及预后判断有一定帮助.
Abstract:
Objecfive To investigate the role of serum Insulin-like growth factor(IGF)-1,insulinlike growth factor-binding potein(IGFBP)-3 in children with Henoch-Schonlein purpura(HSP).Methods The serum concentration of IGF-1,1GFBP-3 was measured by enzyme-linked immunosorbent assay(ELISA)method in 45 acute SHP patients,40 recoverv patients and 30 healthy controls.Results The serum levels of IGF-1 [(452±183)μg/L],IGFBP-3 [(13 897±3124)μg/L] and C-reactive protein(CRP)[(20±8)mg/L]in acute phase were significantly higher than those in healthy controls(P<0.0 1)and higher than those during recovery period.The serum level of IGF-1,IGFBP-3 for the HSP patients dropped back slowly and their levels during recovery period were the same as those in healthy controls(P>0.05).The serum levels of IGF-1[(621±253)μg/L] and IGFBP-3[(18 763±3173)μg/L] were higher in the renal damage group than in the non-renal damage group(P<0.01).and the same in patients with gastrointestinal symptoms group as in patients without gastrointestinal symptoms group(P>0.05).whereas the serum level of CRP was not significantly different(P>0.05).The serum levels of IGF-1,IGFBP-3 showed positive correlation with the level of CRP(r=0.624,0.672,P<0.01).Conclusion The IGF-1 and IGFBP-3 may play an important role in the pathological mechanism of HSP.The level of IGF-1 may be used as an indicator for HSP disease activity and progression.IGF-1 mav have a close relation with the damage"of renaJ system in HSP.  相似文献   

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目的观察新诊断的老年2型糖尿病患者胰岛素治疗前后血清胰岛素样生长因子Ⅰ(IGF-Ⅰ)的变化.方法选取用口服葡萄糖耐量试验新确诊的2型老年糖尿病患者60例,测定体重指数、血压、24小时尿微量白蛋白(24hUAlb)、空腹及餐后2h的血糖(FBG,P2hBG)、胰岛素(Ins)和C肽值、HbA1c、IGF-Ⅰ,予常规胰岛素(RI)8U、6U、6U,三餐前皮下注射,2天后,重复上述检查,计算胰岛素抵抗指数(IR);以40例健康老年人为正常对照.结果对照组、RI治疗前组和治疗后组IGF-Ⅰ的值分别为(349.0±49.5)μg/L、(231.8±64.4)μg/L和(294.2±46.2)μg/L.IGF-Ⅰ治疗前显著低于对照组(P<0.01),治疗后IGF-Ⅰ升高但仍低于对照组(P<0.05);和对照组相比,FBG、P2hBG、HbA1c、餐后2hIns和C肽及IR较高(P<0.01),RI治疗后2天,血糖下降但未达到正常,IR、空腹Ins及餐后2hIns和C肽仍显著升高(P<0.01).结论老年2型糖尿病患者血清IGF-Ⅰ的水平降低可能与胰岛素抵抗导致的高胰岛素血症及高血糖有关,RI治疗可恢复IGF-Ⅰ的水平,但同时可导致高胰岛素血症.  相似文献   

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目的 研究T2DM患者血清胰岛素样生长因子结合蛋白7(IGFBP7)与坂的相关性。方法选取新诊断T2DM患者(T2DM组)137例和健康体检者(NC组)96名,测定两组FPG、FInS、血脂、C-RP、肿瘤坏死因子a(TNF-a)和IGFBP7。结果T2DM组除TC和LDL-C外,其余指标与NC组比较差异有统计学意义(P〈0.05)。按T2DM组IGFBP7四分位数将其分成4组(Q1~4),各组间年龄、BMI、C-RP、TNF-a、Fins、HOMA-IR和HOMA-IS差异有统计学意义(P<0.05);新诊断T2DM患者IpFBP7与年龄、BMI、C-RP、TNF-a、Fins和HOMA-IR呈正相关(r=0.264、0.173、0.255、0.227、0.192、0.325,P〈0.05),与HOMA-IS呈负相关(r=-0.324,P〈0.01)。年龄、C-RP、TNF-n和HOMA-IR是影响新诊断T2DM患者IGFBP7水平的独立因素(β’=0.318、0.186、0.239、0.255,P〈0.05)。结论新诊断T2DM患者IGFBP7与年龄、C-RP、TNF-a和HOMA-IR密切相关。  相似文献   

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在新发病的1型糖尿病患儿和正常对照儿童测定血GH,胰岛素样生长因子(IGF),IGF结合蛋白(IGFBP)3的水平。结果显示新发病的1型糖尿病患儿可乐定刺激的生长激素分泌,血IGF,IGFBP-3水平低于正常对照儿童。  相似文献   

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目的 探讨胰岛素样生长因子 Ⅰ (IGF Ⅰ )与老年男性 2型糖尿病患者骨密度变化的关系。方法 选择 60岁以上男性 2型糖尿病患者 3 2例 ,用双能X线骨密度仪测量其骨密度(BMD) ,并测定血IGF Ⅰ及参与骨代谢有关的激素和生化指标 ,并与正常老年男性对照。结果 糖尿病组与对照组比较 ,BMD、IGF Ⅰ、血睾酮 (T)显著降低 ;生长激素 (GH )升高。IGF Ⅰ、T水平与BMD有显著相关性 (P <0 .0 5 )。糖尿病患者糖化血红蛋白 (HbA1c)、T与血清IGF Ⅰ显著相关(P <0 .0 5 ) ;IGF Ⅰ (P <0 .0 1)、空腹C肽 (FCP) (P <0 .0 1)、T(P <0 .0 5 )与糖尿病组BMD均显著相关。结论 IGF Ⅰ的减少可能是 2型老年男性糖尿病患者合并骨质疏松的原因之一。  相似文献   

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目的探讨格列吡嗪治疗对2型糖尿病病人血清胰岛素样生长因子(IGF)及其结合蛋白(IGFBP)的影响。方法采用病例对照及治疗前后自身对照研究,了解糖尿病病人空腹血清IGF-1、IGF-2和IGFBP-1、IGFBP-3水平及格列吡嗪治疗2周后的改变情况。其中糖尿病组40例,正常对照组90例,两组年龄无显著性差异,P>0.05。结果与正常对照组比,糖尿病组治疗前IGF-1水平降低(234.41±141.78vs181.76±104.48ng/mlP<0.05),IGFBP-1水平升高(47.65±31.78vs68.82±43.18ng/ml,P<0.01),IGF-2和IGFBP-3改变不明显。格列吡嗪治疗后IGF-I升高(181.8±104.5vs209.0±88.2ng/ml,P<0.05);IGFBP-1则明显下降(68.82±43.18vs43.72±34.35ng/ml,p=0.001);IGF-II,IGFBP-3无明显变化。结论格列吡嗪治疗可改善2型糖尿病所导致的血清IGF-I和IGFBP-1水平改变。  相似文献   

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Circulating levels of the low molecular weight insulin-like growth factor binding protein-1 (IGFBP-1) are insulin dependent and vary markedly throughout the day. IGFBP-1 levels are abnormally high in diabetes but the relationship between this and the metabolic status of the patient has not been defined. We have therefore measured fasting IGFBP-1 levels at 0800 h in 32 diabetic adolescents. IGFBP-1 was measured in 19 of these patients after a normal night and in 27 after a night of euglycaemia, maintained with a glucose clamp. In 13 patients both studies were performed and could be compared. Puberty-matched control data were obtained from 69 normal children. In normal prepubertal children IGFBP-1 levels were high; lower levels were found with advancing pubertal development. This fall in IGFBP-1 correlated with pubertal stage (r= 0.68, p less than 0.001) and with fasting insulin levels (r = 0.60, p less than 0.001) which rose with pubertal advancement. In the diabetic children IGFBP-1 levels also correlated inversely with the 0800 h free insulin level but there was no clear relationship with pubertal development. However, when measured after overnight euglycaemia IGFBP-1 levels correlated inversely with pubertal development (r = 0.67, p less than 0.001) as in the normal children. In the patients studied on two comparable occasions the IGFBP-1 level measured after a normal night relative to that measured under standardized euglycaemic conditions was found to correlate closely with the glycosylated haemoglobin level (r = 0.71, p less than 0.005).  相似文献   

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探讨胰岛素治疗对2型糖尿病患者血清中胰岛素样生长因子I(IGF-I)水平的影响以及两者之间的关系.结果 发现2型糖尿病患者外源性胰岛素治疗可增加血清中的IGF-I水平[(126.70±51.91对90.04±43.68)μg/L,P<0.01],并且IGF-I水平与胰岛素水平呈正相关(r=0.298,P<0.05).
Abstract:
To explore the effect of insulin therapy on serum level of insulin-like growth factor-I(IGF-I)in patients with type 2 diabetes mellitus.The results showed that serum IGF-I level increased[(126.70±51.91 vs 90.04±43.68)μg/L,P<0.01]and was positively correlated with insulin level in patients with type 2 diabetes mellitus after exogenous insulin therapy(r=0.298,P<0.05).  相似文献   

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Summary Previous studies have suggested that nerve regeneration may be defective in patients with diabetic polyneuropathy. Since insulin-like growth factor I (IGF-I) has been shown to stimulate nerve regeneration, and IGF binding protein-1 is acutely regulated by plasma insulin we have investigated the relationships between plasma IGF-I, IGFBP-1, glucose and insulin in Type 1 (insulin-dependent) diabetic patients with peripheral polyneuropathy. Plasma samples were taken at hourly intervals over an 11-h period (08.00–19.00 hours) in order to characterise secretory profiles for 15 Type 1 diabetic patients (eight neuropathic and seven non-neuropathic) and eight non-diabetic control subjects. In the non-diabetic subjects, mean plasma IGF-I levels were stable throughout the 11-h period with a range of 97 g/l–169 g/l. In contrast, mean plasma IGFBP-1 levels declined steadily from a high level of 1.99 g/l at 08.00 hours to approximately one half (0.86 g/l) at 15.00 hours. Comparison of areas under the curves revealed significant negative correlations between IGFBP-1 and glucose (–0.88, p=0.01), IGFBP-1 and insulin (–0.75, p=0.016), and IGFBP-1 and IGF-I (–0.68, p=0.03). A significant positive correlation was found between insulin and IGF-I (+ 0.89, p=0.001). The diabetic patients had markedly elevated plasma IGFBP-1 levels (area under curve, p=0.01) and lower plasma IGF-I levels (p=0.033) even though these patients were hyperinsulinaemic throughout the study period. The neuropathic diabetic patients had grossly elevated IGFBP-1 levels (–X=40 g/l at 08.00 hours) which were significantly higher (area under curve, p=0.05) than in patients without neuropathy (¯X=15 g/l at 08.00 hours). However, plasma levels of insulin and IGF-I in neuropathic and non-neuropathic subjects were similar, suggesting that the regulation of IGFBP-1 is more resistant to insulin in the neuropathic patients. In contrast to the non-diabetic subjects comparison of area under curve values revealed no positive correlation between insulin and IGF-I or negative correlations between IGF-I and IGFBP-1, and IGFBP-1 and glucose. We conclude that in Type 1 diabetes the relationships between plasma glucose, insulin, IGF-I and IGFBP-1 are clearly abnormal, and these abnormalities are more pronounced in patients with peripheral neuropathy.  相似文献   

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体重指数与初诊2型糖尿病代谢状态及慢性并发症的关系   总被引:5,自引:0,他引:5  
目的探讨肥胖程度与糖尿病患者代谢状态及慢性并发症的关系。方法将新诊断的2型糖尿病患者以体重指数分为3组,分别比较空腹血糖及餐后血糖、血压、血脂、胰岛素抵抗指数、空腹C肽水平及大血管/微血管并发症患病率。结果低体重患者主要临床特征为胰岛素分泌水平低下,HbA1C。及空腹血糖增高。超重、肥胖的糖尿病患者主要表现为高血压、胰岛素抵抗、高甘油三酯和低高密度脂蛋白胆固醇血症。超重组易伴发高血压及冠心病等大血管病变,而低体重组微血管病变尤其是视网膜病变较为突出。结论对于初诊的低体重患者,应尽早补充胰岛素并及时筛查视网膜病变等微血管并发症:对于超重患者应强调减肥、降压、调脂等综合治疗。  相似文献   

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目的观察参苓组方对2型糖尿病(T2DM)大鼠胰岛素样生长因子1(IGF-1)代谢途径的影响及胰岛素抵抗(IR)相关指标的改善作用。方法建立T2DM大鼠模型并分组,观察各组大鼠IGF-1、FPG、HbA1c、Fins、TG、TC的变化,比较胰岛素敏感性指数(IAI)、胰岛素抵抗指数(HOMA—IR)。结果参苓组方能升高T2DM大鼠IGF-1水平(P〈0.01),降低FPG,HbA1c、Fins、TG、TC(P〈0.05),使IAI升高,HOMA—IR下降(P〈0.05)。结论参苓组方能改善T2DM大鼠IR和IGF-1水平。  相似文献   

16.
血清von Willebrand因子与糖尿病血管并发症关系的初步研究   总被引:2,自引:1,他引:2  
目的 探讨 2型糖尿病患者血清 von Willebrand因子 (v WF)与微血管、大血管并发症之间的关系。 方法 将 4 0 8例年龄相近的 2型糖尿病患者 ,根据是否合并血管并发症分为 :无并发症组 (1 2 5例 )、大血管并发症组 (1 2 3例 )、大血管和微血管并发症组 (1 6 0例 )。观察不同组患者血清v WF水平 ,并与正常对照组 (1 0 5名 )比较。 结果 血清 v WF水平在正常对照组为 (0 .8± 0 .4 ) U/ml;无并发症组 (1 .2± 0 .5 ) U/ ml;大血管并发症组 (1 .4± 0 .6 ) U/ ml;大血管和微血管并发症组 (1 .6± 0 .6 ) U/ ml;血清 v WF水平随血管并发症增多而上升 ,各组间差异均有非常显著意义 (P<0 .0 1 )。L o-gistic分析表明 ,v WF既与是否合并大血管病变呈显著相关 (回归系数 β=0 .95 6 ,P=0 .0 0 1 ) ,也与是否合并微血管病变呈显著相关 (回归系数 β=1 .783,P=0 .0 1 2 )。多元逐步回归分析表明 ,尿微量白蛋白、年龄、糖尿病病程分别与 v WF呈正相关 (β=0 .32 4 ,P<0 .0 0 1 ;β=0 .2 31 ,P<0 .0 0 1 ;β=0 .1 4 5 ,P<0 .0 5 )。 结论  2型糖尿病患者血清 v WF逐渐升高反映了微血管和大血管并发症的发生和发展  相似文献   

17.
为探讨宫内发育迟缓(IUGR)的发生机制,检测了86例新生儿脐血胰岛素样生长因子-1(IGF-1)、胰岛素样生长因子结合蛋白-3(IGFBP-3)水平,并分析上述指标变化与胎儿期生长的关系。将86例新生儿分为两组,IUGR(即小于胎龄儿)组22例,适于胎龄儿(AGA)组64例,采用竞争性放射免疫分析法(RIA)测定两组脐血IGF-1水平,非竞争性免疫放射分析法(IRMA)测定IGFBP-3水平。结果显示,与AGA组相比,IUGR组脐血IGF-1和IGFBP-3水平显著降低(P<0.001);IGF-1水平随胎龄及出生体重增加而增加(P<0.01);IGFBP-3水平与胎龄及出生体重呈相关(P<0.01);IGF-1与IGFBP-3呈正相关(P<0.01)。认为IUGR与IGF-1及其结合蛋白密切相关,不论何种原因引起的IUGR,其脐血IGF-1、IGFBP-3水平均低,IGF-1水平下降与IGFBP-3下降相伴随;脐血IGF-1、IGFBP-3水平与胎龄及出生体重呈正相关,随着胎龄的增加和出生体重的增长,IGF-1、IGFBP-3水平不断升高。  相似文献   

18.
The possible occurrence of increased non-enzymatic glycosylation of serum insulin-like growth factor binding protein-3 (IGFBP-3) in vivo and the changes that would simultaneously occur in serum levels of IGFBP-3 and insulin-like growth factor-1 (IGF-I) were investigated. We measured levels of IGF-I and IGFBP-3 and the degree of glycation of total serum protein and IGFBP-3, in serum samples obtained from patients with poorly controlled non-insulin-dependent diabetes (type 2) and from age-matched non-diabetic controls. Type 2 diabetic patients had significantly higher glycated serum protein (GlyP) levels. GlyP significantly correlated with age in the control (r = 0.315, P<0.05) but not in the type 2 diabetes group. Control and diabetic subjects had comparable serum IGF-I levels and in both groups IGF-I levels tended to decrease with age (r = –0.567, P<0.001 and r = –0.465, P<0.05 for control and type 2 diabetic subjects, respectively). In the type 2 diabetes group, IGF-I levels showed a negative correlation with serum GlyP values (r = –0.476, P<0.05). Type 2 diabetic and control patients had comparable serum IGFBP-3 levels, which were significantly higher in diabetic patients in the older age subgroups. A negative correlation was found between IGFBP-3 levels and age in the control (r = –0.705, P<0.001) and in the type 2 diabetes groups (r = –0.463, P<0.05). A significant negative correlation was found between IGFBP-3 levels and GlyP in control (r = –0.449, P<0.002) but not in type 2 diabetic subjects. The mean glycated IGFBP-3 (GlyIGFBP-3) levels were higher in the oldest type 2 diabetic patients. In these patients, GlyIGFBP-3 was negatively associated with IGF-I levels (r = –0.447, P<0.05). The IGF-I/IGFBP-3 molar ratio was significantly reduced in the 46–60-year-old type 2 diabetic group, whereas the IGF-I/IGFBP-3 ratio was positively and significantly correlated with GlyP levels only in the control group (r = 0.489, P<0.01). Our results show that: a) increased non-enzymatic glycosylation of IGFBP-3 occurs in vivo; and b) this effect is accompanied by an increase in IGFBP-3 levels. These results suggest that the IGF-I/IGFBP-3 system is another target for the metabolic derangements of type 2 diabetes. Its alterations might play a role in diabetic complications. Received: 22 September 1997 / Accepted in revised form: 30 April 1998  相似文献   

19.
C-反应蛋白与2型糖尿病大血管病变的相关性研究   总被引:10,自引:1,他引:10  
目的 探讨C-反应蛋白(CRP)与糖尿病大血管病变发生的关系。方法 用ELISA方法测定2型糖尿病(T2DM)患者、无糖尿病的大血管病变患者以及正常对照组的CRP水平变化。结果 T2DM伴有或不伴有大血管并发症患者以及无糖尿病的大血管病变患者间血清cRP水平无显著差异;大血管病变患者血清cRP水平较非大血管病变者明显增高。结论 cRP在T2DM大血管病变的发生发展中具有致病作用。  相似文献   

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