冠心病患者胰岛素抵抗与肌钙蛋白I的关系

目的:研究冠心病患者胰岛素抵抗与肌钙蛋白I的关系。方法:用发光免疫法测定空腹胰岛素(FINS)及肌钙蛋白I(TnI),用1/(FINS×FPG)的自然对数作为胰岛素敏感指数(ISI),对ISI与TnI进行相关分析。结果:不稳定型心绞痛组及稳定型心绞痛组的ISI明显低于健康对照组,不稳定型心绞痛组的TnI明显高于其余两组,不稳定型心绞痛组的ISI与TnI呈负相关关系。结论:胰岛素抵抗与心肌损害存在一定内在联系。     

Atherosclerosis,diabetes and lipoproteins

The enormous burden of vascular disease is likely to expand rapidly as sedentary obesity and diabetes increase. Although cholesterol plays a major role in atherosclerosis and LDL is the major carrier of cholesterol in the blood, the importance of the postprandial triglyceride-rich lipoproteins in the development of atherosclerosis is gaining recognition. The role of HDL-cholesterol is also receiving more attention. These changes have been forced upon us by the realization that statins, which primarily lower LDL-cholesterol, only reduce the risk of atherosclerosis by 30%, suggesting that 70% of the risk still has to be explained and treated. In diabetes, abnormality in the metabolism of the triglyceride-rich lipoproteins and the inter-relationship with HDL-cholesterol appears to be of primary importance in atherosclerotic risk. Postprandial studies are difficult to carry out, which is one reason why large studies have not so far been performed. The important new findings in chylomicron metabolism suggest new treatments for the future.     

肥胖与胰岛素抵抗的关系

目的:探讨肥胖类型与胰岛素抵抗(insulinresistance,IR)及β细胞功能的关系。方法:采用稳态模式胰岛素抵抗指数(HOMA-IR)评价胰岛素抵抗,根据亚-太地区成人体重分级建议将研究对象分为非肥胖组、周围型肥胖组、腹型肥胖组,观察三组间血糖、血浆胰岛素水平及HOMA-IR、HOMA-β的差异。结果:(1)本组肥胖的检出率为35.1%(283/807),周围型肥胖、腹型肥胖分别占25.8%及74.2%。(2)非肥胖组、周围型肥胖组、腹型肥胖组IR的检出率分别为12.0%、26.0%、50.0%。(3)与非肥胖组相比,周围型肥胖组及腹型肥胖组的FPG、PG2h、HOMA-IR均明显增高,腹型肥胖组较其他两组具有更高的FIns、PG2h、HOMA-IR,而HOMA-β明显降低。结论:肥胖与IR关系密切,腹型肥胖者具有更严重的IR以及更严重的β细胞功能下降。     

不同人群血清脂联素、瘦素水平与胰岛素抵抗的关系

【目的】研究不同人群（健康人群、肥胖和2型糖尿病患者）血清脂联素（APN）、瘦素（LEP）水平及其与肥胖、胰岛素抵抗的关系。【方法】采用病例对照研究,2型糖尿病（T2DM）伴有肥胖组（DO）42例,T2DM不伴肥胖组（NDO）42例,单纯性肥胖组（OB）37例,正常对照组（NC）28名。检测了4组研究对象血脂、血糖、空腹胰岛素（Fins）、APN、LEP水平,用HOMA模型公式计算胰岛素抵抗指数（HOMAIR）。[结果]NC组的APN水平明显高于其他3组（均P〈0．05）。DO组、OB组的LEP水平明显高于NDO组及NC组（P〈0．05）。相关分析显示：APN与HOMAIR、体质指数（BMI）、腰围（WC）、腰臀比（WHR）、空腹血糖（FBG）、甘油三脂（TG）和Fins呈显著负相关（P〈0．01）;LEP与BMI和体脂百分含量（BFC）呈显著正相关（P〈0．01）,与WC和Fins呈正相关（P〈0．05）;APN与LEP无相关性。多元逐步回归分析显示：APN与Fins呈显著负相关（P〈0．01）,与WHR、FBG呈负相关（P〈0．05）;LEP与BFC呈显著正相关（P〈0．01）。【结论】血清APN水平与2型糖尿病及肥胖相关。血清瘦素水平与2型糖尿病无关,但与肥胖有关。APN与瘦素之间无相关性,APN对于胰岛素抵抗的影响程度明显大于瘦素。     

高血压个体胰岛素抵抗发病状况的研究

目的 :探讨高血压个体胰岛素抵抗的发病状况以及与肥胖、血脂紊乱之间的关系。方法 :对 136例 4 0岁以上住院和门诊高血压病人以及 10 4例保健科健康体检者抽取空腹血糖和血浆胰岛素 ,将前者分为 4个亚组 ,即正常体重单纯高血压亚组、正常体重高血压合并高甘油三脂 (TG) /低高密度脂蛋白胆固醇 (HDL C)亚组、超重 /肥胖单纯高血压亚组及超重 /肥胖高血压合并高TG/低HDL C亚组、用稳态模式评估法的胰岛素抵抗指数 (HOMA IR)评价胰岛素抵抗 ,计算出各组胰岛素抵抗发病率。结果 :校正年龄、性别、体重指数等因素后 ,伴有高TG的各血脂异常亚组的胰岛素抵抗指数升高较明显。结论 :血脂紊乱是导致高血压个体胰岛素抵抗的主要因素     

胰岛素及胰岛素抵抗与糖尿病认知功能障碍

糖尿病导致的学习记忆功能障碍日益受到人们的重视。糖尿病明显增加痴呆的发生风险,包括血管性痴呆和阿尔茨海默病;糖尿病本身也可以导致患者轻、中度认知功能的下降。胰岛素水平不足和胰岛素抵抗可明显导致糖尿病认知功能障碍的发生并加速了认知功能下降的进展。     

实验性胰岛素抵抗综合征大鼠模型

目的:建立胰岛素抵抗综合征大鼠模型.方法:用高脂高糖高盐饲料喂养大鼠八周,观察大鼠饮水量,体重,血压,葡萄糖耐量,血脂,血糖及血胰岛素水平,并算出胰岛素敏感性指数等.结果:与基础饲料组大鼠相比,高脂高糖高盐饲料组大鼠饮水量明显增多(多出47%,P＜0.01);体重明显增加(高出11%,P＜0.01);血压明显升高(高出20%,P＜0.01);葡萄糖耐量明显降低(P＜0.01);血清甘油三酯和胆固醇均明显增高(分别高出49%和57%,二者均P＜0.01);高密度脂蛋白胆固醇明显降低(低出30%,P＜0.05);血糖和胰岛素均明显升高(分别高出12%,P＜0.05和69%,P＜0.01),胰岛素敏感性指数明显降低(P＜0.01).结论:高脂高糖高盐饮食可以造成胰岛素抵抗综合征大鼠模型.     

The putative diabetic plasma marker,soluble CD36, is non‐cleaved,non‐soluble and entirely associated with microparticles

Summary. Background: CD36 is a widely expressed cell surface receptor that binds lipoproteins, and its function has been implicated in many complications of the metabolic syndrome. A cell‐free form of CD36, soluble CD36 (sCD36), has been reported in human plasma, found to be elevated in obesity and diabetes, and claimed as a marker of insulin resistance. Objective: To determine the nature of sCD36; in particular, whether sCD36 is truly soluble or, as hypothesized, is found as a component of circulating microparticles (MPs). Methods: Lipoproteins were fractionated by density gradient centrifugation, and plasma MPs were isolated by ultracentrifugation, size exclusion, and immunoprecipitation with CD36 detected by immunoblotting. MPs from plasma and activated platelets were analyzed by multicolor flow cytometry, with a DyLight‐488 anti‐CD36 conjugate in combination with antibodies against different cellular markers. Results: Cell‐free plasma CD36 was not observed associated with lipoproteins and was not a proteolytic fragment; rather, it was associated with the plasma MP fraction, suggesting that sCD36 in the plasma of normal subjects is a product of circulating MPs. Cytometric and immunoblotting analyses of plasma from normal donors showed that these MPs were derived mainly from platelets. Analysis of in vitro activated platelets also showed that CD36 to be secreted in the form of MPs. Conclusions: sCD36 is not a proteolytic product, but rather is associated with a specific subset of circulating MPs that can readily be analysed. This finding will enable more specific investigations into the cellular source of the increased levels of plasma CD36 found in subjects with diabetes.     

Insulin Resistance and Left Ventricular Mass in Non-Diabetic Hemodialysis Patients

Background

Insulin resistance (IR) is frequently recognized in patients with uremia, and it is thought that IR has a basic role in the pathogenesis of cardiovascular disease.

Objective

To evaluate the effect of IR on cardiovascular risk in non-diabetic patients receiving hemodialysis (HD).

Methods

We performed a cross-sectional observational study that comprised 186 non-diabetic patients receiving HD (95 men; mean [SD] age, 46.4 [10.8] years; age range, 35–60 years) who had been receiving HD for 7.3 (3.5) years. Demographic variables and laboratory values were recorded. Insulin resistance was determined using the Homeostatic Model Assessment (HOMA), and the left ventricular mass index (LVMI) was calculated via echocardiography.

Results

According to HOMA-IR levels, patients were categorized as having IR (HOMA-IR score ≥2.5; n = 53) or not having IR (HOMA-IR score <2.5; n = 133). Insulin resistance was determined in 28.4% of study patients. Compared with the non-IR group, the IR group had been receiving HD longer; had greater body mass index; and had higher serum creatinine, uric acid, triglyceride, insulin, and C-reactive protein concentrations, leukocyte count, and LVMI (P < 0.05). Patients with increased LVMI had significantly higher body mass index, systolic blood pressure, serum cholesterol and C-reactive protein concentrations, and HOMA score. At multivariate analysis, systolic blood pressure (β = 0.22; P = 0.03) and HOMA score (β = 0.26; P = 0.01) affected LVMI.

Conclusions

Insulin resistance and hypertension are independent risk factors for left ventricular hypertrophy in non-diabetic patients with uremia who are receiving HD. Further studies are needed to indicate the benefits of improving IR for cardiovascular mortality in this subgroup of patients with uremia.     

补充维生素D对妊娠期糖尿病孕妇胰岛素抵抗及新生儿胰岛素的影响

目的：探讨补充维生素D（VD）对妊娠期糖尿病（GDM）胰岛素抵抗及新生儿胰岛素的影响。方法：将56名GDM孕妇随机分为VD组26例和对照组30例,VD组在饮食控制的同时口服维生素D,400IU,每日二次,以20名健康孕妇为正常组;比较三组空腹血糖（FBG）、空腹胰岛素（FINS）、血清25-（OH）VD3、胰岛素抵抗指数（HOMA—IRI）和新生儿的胰岛素水平。结果：VD组补充VD一个月后,25-（OH）VD,明显高于饮食控制组（P〈0．05）：三组间的FINS有统计学差异（P〈0．05）;VD组HOMA—IRI明显低于饮食控制组而高于健康孕妇组（P〈0．05）;VD组和饮食控制组的FBG无明显差异,但均显著高于对照组（P〈0．05）。对照组新生儿胰岛素与VD组和饮食控制组有明显差异（P〈0．05）,但VD组和饮食控制组无明显差异（P〉0．05）。结论：VD与GDM发生密切相关,GDM孕妇补充VD后,25-（OH）VD,水平明显升高,胰岛素抵抗明显改善,但却不能恢复至正常孕妇状态：补充VD对GDM孕妇分娩的新生儿胰岛素无明显影响。     

高血压前期动脉弹性与胰岛素抵抗的相关性研究

目的探讨高血压前期大动脉、小动脉弹性与胰岛素抵抗的相关关系。方法选择高血压前期36人、1-2级高血压患者46例、理想血压健康者30人,使用CVProfilorDO-2020动脉弹性功能测定仪检测桡动脉脉搏波形和动脉弹性指数C1和C2,采用HOMA-IR公式计算胰岛素抵抗指数（IR）;比较各组间大动脉、小动脉弹性情况,对高血压前期者动脉弹性与IR进行相关分析。结果校正了年龄和病程后,高血压组与理想血压组、高血压前期组比较,C1和C2均降低（P〈0.05）;高血压前期组与理想血压组比较,C2降低（P〈0.05）,高血压前期组和高血压组与理想血压组比较,HOMA-IR升高（P〈0.05）。C2与HOMA-IR负相关（r=-0.687,P〈0.05）。结论高血压前期者已经存在小动脉弹性的减退及胰岛素抵抗,且两者之间呈负相关。     

糖尿病肾病患者尿微量蛋白与胰岛素抵抗的关系

[目的]探讨2型糖尿病肾病(DN)患者尿微量蛋白(mALB)与胰岛素抵抗(IR)之间的关系.[方法]检测81例2型DN患者mALB及血糖、胰岛素、血脂等生化指标,分析各指标之间的相关性,并根据尿白蛋白量分为正常蛋白尿组与蛋白尿组进行评估.[结果]mALB与尿转铁蛋白(TRF)、尿免疫球蛋白G(IgG)、尿β2-微球蛋白(β2-MG)、尿α1-微球蛋白(α1-MG)呈正相关.蛋白尿组胰岛素敏感指数(ISI)明显低于无蛋白尿组,甘油三酯、空腹胰岛素、2 h胰岛素、TRF、尿IgG、尿β2-MG、尿α1-MG均高于无蛋白尿组,且差异有显著性.[结论]mALB、TRF、尿IgG 、尿β2-MG、尿α1-MG均可作为早期DN检测的指标,且与IR相关.     

不同糖耐量人群胰岛素抵抗的比较

【目的】研究不同糖耐量人群胰岛素抵抗程度的差异。【方法】将412名门诊患者按OGTT分为4组：糖尿病组（NDM，n=180），空腹血糖受损组（IFG，n=35），糖耐量异常组（IGT，n=46），糖耐量正常组（NGT，n=151）。测定血压、血脂（TG和HDL）、体质指数（BMI）；应用胰岛素抵抗（HOMA-IR）及胰岛素作用指数（IAI）对不同糖耐量人群进行测定。【结果】DM、IFG及IGT组均较NGT组IAI下降，HOMA-IR增高，DM组表现得尤为显著；而IFG组与IGT组比较，亦有显著的IAI下降及HOMA-IR增高（P〈0．05）。【结论】不同糖耐量人群随着糖调节不同程度的受损HOMA-IR和IAI均有增幅变化，这两种指标可较准确的评估胰岛素敏感性。IFG与IGT人群胰岛素抵抗的机制可能有所不同。     

盐敏感性高血压患者胰岛素抵抗与脂联素水平的关系

目的：探讨盐敏感性高血压患者胰岛素抵抗与脂联素代谢异常的关系。方法：对100例高血压患者采用急性盐水负荷试验,确定65例为盐敏感性（ss）高血压患者,35例为盐不敏感性（NSS）高血压患者,选定正常人50例为对照组,分别测其胰岛素水平、血脂、血尿酸及脂联素水平。结果：高血压患者存尿酸、胆固醇、甘油三酯水平升高（P〈0．01）,SS组较NSS组的血尿酸、血胆固醇、血甘油三脂增高（P〈0．01）。SS组脂联素[（6．04±2．08）ng／mL],较NSS组[（7．89±3．35）ng／mL（P〈0．01）]降低,且SS组存在胰岛素抵抗,HOMA指数分别为[2．54±0．53,2．21±0．55（P〈0．01）]。血浆脂联素水平与胰岛素抵抗指标存在正相关,r=-0．36,（P〈0．01）。结论：盐敏感性高血压患者存在胰岛素抵抗及脂联素降低,胰岛素抵抗可能是其他代谢异常及脂联素降低的基础。     

罗格列酮对3T3-L1脂肪细胞胰岛素抵抗的作用

【目的】探讨罗格列酮对脂肪细胞胰岛素抵抗的影响。【方法】培养3T3-L1前脂肪细胞,采用地塞米松诱导3T3-L1脂肪细胞建立胰岛素抵抗模型,检测细胞培养基中葡萄糖浓度,同时观察罗格列酮对脂肪细胞葡萄糖转运子4（GLUT4）mRNA表达的影响。【结果】在DMEM高糖培养基中,罗格列酮能明显增加胰岛素抵抗3T3-L1脂肪细胞培养基中的葡萄糖消耗量,并可使GLUT4 mRNA表达升高,增强对胰岛素的敏感性。【结论】罗格列酮明显上调抵抗脂肪细胞GLUT4的表达,改善胰岛素抵抗。     

非诺贝特对高脂饮食诱导的胰岛素抵抗大鼠的影响

目的观察非诺贝特对胰岛素抵抗大鼠（insulin resistance,IR）糖脂代谢和血压的影响,探讨非诺贝特改善IR的机制。方法高脂饮食喂养Wistar大鼠6周后再给予非诺贝特4周,测定体重、附睾脂肪重量、FPG、FINS、FFA和血脂;高胰岛素．正常葡萄糖钳夹技术评价胰岛素敏感性;经颈动脉测量血压。结果非诺贝特治疗后IR大鼠的体重、附睾脂肪重量、FINS、TG、FFA降低（P〈0．01或P〈0．05）,HDL-C和胰岛素敏感性显著增加（P〈0．01）,血压水平也下降明显（SBP和DBP分别下降了19mmHg和21mmHg）,但与HF组比较无统计学差异（P〉0．05）。结论非诺贝特可以明显减轻体重和内脏脂肪重量,改善脂代谢紊乱,提高胰岛素敏感性,并可能降低血压。     

饮食运动对肥胖症患者胰岛素抵抗的影响

目的探讨饮食、运动对肥胖症患者胰岛素抵抗和血脂、血压的影响。方法选取肥胖症患者54例,随机分为两组,干预组进行为期24周的饮食、运动干预。结果接受饮食、运动干预24周后干预组体质量、体质量指数、腰围、腰臀比、血压、空腹血糖、空腹胰岛素、甘油三酯和HOMA-IR指数下降,McAuley指数升高,与对照组比较均有统计学意义(P<0.05)。结论饮食、运动干预可减轻体质量,改善肥胖症患者的胰岛素抵抗、血压和甘油三酯。     

2型糖尿病患者血清脂联素水平与胰岛素抵抗的关系

【目的】探讨2型糖尿病（T2DM）患者血清脂联素（APN）水平与肥胖、胰岛素及胰岛素抵抗的关系。【方法】采用病例对照研究,T2DM伴有肥胖组（DO）42例,T2DM不伴肥胖组（NDO）42例,正常对照组（NC）28名。检测三组对象血脂、血糖、空腹胰岛素（Fins）、APN水平。用HOMA模型公式计算胰岛素抵抗指数（HOMAIR）。【结果JDO组和NDO组的血清APN水平均明显低于NC组[DO组（8．02±3．57）mg／L,NDO组（8．35±2．68）mg／L比NC组（14．04±4．75）mg／L,均P〈O．01],DO组与NDO组APN水平差异无显著性。APN与体质指数（BMI）、腰围（w）、腰臀比（WHR）、空腹血糖（FBG）、甘油三脂（TG）、Fins、HO—MAIR呈显著负相关（P〈0．01）,APN与高密度脂蛋白（HDL-C）呈显著正相关（P〈0．01）。多元逐步回归分析显示HOMAIR和WHR是血清APN浓度的主要影响因素。【结论】脂联素参与了胰岛素抵抗的发生,与2型糖尿病的发生相关。     

血清瘦素及游离脂肪酸在肥胖患者中的致胰岛素抵抗作用

目的研究瘦素及游离脂肪酸(FFA)对肥胖患者胰岛素抵抗(IR)状态形成的作用.方法按体重指数(BMI)将实验对象(82例)分为肥胖组及对照组;测量身高、体重、腰围、臀围,计算体重指数、脂肪百分比(?t)、腰臀比(WHR)及胰岛素敏感指数(ISI);葡萄糖氧化酶法测定血清葡萄糖;化学发光免疫分析法测定血清胰岛素;生化比色法测定血清游离脂肪酸.结果肥胖人群中血清瘦素、FFA水平明显高于对照组(P＜0.01),且升高幅度与反应肥胖度的各项指标(BMI、WHR、?t)呈显著正相关,与ISI呈负相关.结论瘦素及FFA是重要的致IR物质,也是IR存在时重要标志.     

Insulin sensitivity, insulinemia, and coronary artery disease: the Insulin Resistance Atherosclerosis Study

OBJECTIVE: The aim of this study was to evaluate whether low insulin sensitivity (Si) measured using a modified frequently sampled intravenous glucose tolerance test with minimal model analysis is associated with coronary artery disease (CAD) independent of other cardiovascular risk factors. RESEARCH DESIGN AND METHODS: We studied 1,482 women and men, age 40-69 years old, African American (28%), Hispanic (34%), or non-Hispanic white (38%), with normal (45%), impaired (23%), or diabetic (32%) glucose tolerance. CAD defined as confirmed past myocardial infarction, coronary artery bypass graft, coronary angioplasty, or presence of a major Q-wave was found in 91 participants. RESULTS: The odds ratio (OR) for CAD was greatest among individuals in the two lowest quintiles of Si (2.4, 95% CI 1.0-5.6 and 4.7, 2.1-10.7) compared with the highest Si quintile. After adjusting for demographic and cardiovascular risk factors, a decrement from the 75th to 25th percentile in Si was associated with a 56% increase in CAD (P=0.028). Similar increments in fasting or 2-h insulin levels were associated with, respectively, only 15 (NS) and 3% (NS) increases in CAD. The association between Si and CAD was partially mediated by insulin, HDL cholesterol and triglyceride levels, hypertension, diabetes, and obesity, but not LDL cholesterol or cigarette smoking. CONCLUSIONS: Low Si is associated with CAD independently of and stronger than plasma insulin levels. Part of the association is accounted for by dyslipidemia, hypertension, diabetes, and obesity.