胰岛素抵抗指数与PSA的相关性研究

良性前列腺增生症及前列腺癌患者各50例,分别根据不同前列腺特异性抗原(PSA)检测结果分为0～4 ne/ml组、4～10 ng/ml组、>10 ng/nd组.采用放免法测定PSA及空腹胰岛素(FINS)水平,已糖激酶法测定空腹葡萄糖.运用HOMA模型中的胰岛素抵抗计算公式计算胰岛素抵抗指数(IRI).发现PSA 4～10 ng/ml、>10ng/ml良性前列腺增生与前列腺癌患者IRI比较均有统计学差异.认为IRI可能有助于前列腺癌患者早期诊断.     

体型指数与胰岛素抵抗的相关性临床分析

目的 探讨体型指数(figure index,FI)与胰岛素抵抗(IR)的相关性,并与体重指数(BMI)和腰围(WC)进行比较.方法 256研究对象分为2型糖尿病(DM)组、糖调节受损(IGR)组和正常糖耐量(NGT)组,比较FI、WC、BMI与IR的相关性以及相关性在3组的差异.结果 FI、WC、BMI与稳态模型胰岛素抵抗指数均有显著相关性(P＜ 0.01),FI与IR的相关性更强;不同糖代谢各组比较,FI、WC、BMI与各指数间的相关性DM组＞ IGR组＞ NGT组,即与各指数间的相关性随糖调节异常的加重而增强.结论 FI、WC、BMI均是评估IR的良好指标,以FI敏感性最高.     

社区非糖尿病人群血压水平与稳态模型胰岛素抵抗指数及定量胰岛素敏感性指标的相关性研究

目的 探讨社区非糖尿病人群血压测值与稳态模型胰岛素抵抗指数(HOMA-IR)及定量胰岛素敏感性指标(QUICKI)的相关性.方法 2002年8月至2004年3月,在上海交通大学医学院附属仁济医院内分泌科对上海浦东上钢和塘桥社区居民743名(除外糖尿病和糖耐量受损、继发性高血压及有严重肝、肾功能损害者)进行研究检测.以标准法测量血压、身高、体重、腰围和臀围.根据不同血压测值分为非高血压组和高血压组.非高血压组包括(1)理想血压组,收缩压＜120 mm Hg(1 mm Hg=0.133 kPa),舒张压＜80 mm Hg;(2)正常血压组收缩压120～＜130 mm Hg,舒张压80～＜85 mm Hg;(3)正常高值血压组收缩压130～＜140 mm Hg,舒张压85～＜90 mm Hg.高血压组收缩压≥140 mm Hg和(或)舒张压≥90 mm Hg.放免法测定空腹血浆胰岛素,并计算HOMA-IR及QUICKI.采用SPSS 11.5软件进行统计分析.结果 社区743名非糖尿病人群中,正常高值血压组和高血压组与理想血压组之间HOMA-IR及QUICKI比较差异均有显著性意义(P＜0.01).血压值与年龄、体重指数(BMI)、腰围、WHR、空腹胰岛素、血浆总胆固醇、三酰甘油及HOMA-IR呈正相关,与QUICKI呈负相关.在控制年龄及性别之后,HOMA-IR及QUICKI和血压之间仍明显相关(P＜0.001).结论 HOMA-IR和QUICKI指数均是预测正常高值血压人群胰岛素抵抗的独立影响因子.治疗早期高血压,减轻胰岛素抵抗的因素可能更重要.     

我国中老年人群脂肪肝指数与胰岛素抵抗的相关性研究

目的 探讨我国中老年人群脂肪肝指数(FLI)与胰岛素抵抗(IR)的相关性。方法 纳入南京市鼓楼区45岁以上社区自然人群3592例，根据胰岛素抵抗指数(HOMA-IR)分为IR组1938例和无IR组1654例；根据FLI分为FLI＜30组2221例、30≤FLI＜60组911例、FLI≥60组460例，比较不同亚组的一般资料、生化指标、血糖及胰岛素相关指标。采用Spearman非参数相关性分析评估FLI与HOMA-IR及胰岛β细胞功能相关指标的相关性；采用受试者工作特征(ROC)曲线评估FLI对IR的预判能力；采用多因素logistic回归分析评估FLI与IR的关系。结果IR组男性比例、年龄、血压、血脂、肝功能、OGTT各时间点血糖和胰岛素、FLI、胰岛β细胞功能指数(HOMA-β)、早期胰岛素分泌指数(ΔI0-30/ΔG0-30)及HOMA-IR均高于无IR组，血肌酐和Matsuda ISI 均低于无IR组(P＜0.05或P＜0.001)。不同FLI亚组血压、生化指标、血糖及胰岛素相关指标比较差异均有统计学意义(P<0.001)。Spearman非参数相关分析结果显示，FLI与HONA-IR呈正相关(P＜0.001)，与Matsuda ISI呈负相关(P<0.001)。ROC曲线分析结果显示，依据FLI判断IR的ROC曲线下面积(AUC)为0.670(95%CI 0.653～0.688)。多因素logistic回归分析结果显示，FLI为IR的危险因素之一，可使IR的发生风险增加1.021倍(P<0.001)。结论 在我国中老年人群中，FLI与IR相关，FLI可作为评估IR的简单易行的指标。     

再论胰岛素抵抗和胰岛素敏感性指数

再论胰岛素抵抗和胰岛素敏感性指数纪宝华近年，临床医师对高血压、糖尿病、异常脂蛋白血症有了进一步认识。内科医师治疗高血压时会考虑到其他经常合并存在的糖耐量异常、异常脂蛋白血症、肥胖、血小板和凝血机制异常等心脑血管疾病的危险因素，糖尿病医师对糖尿病的治疗...     

高血压前期与胰岛素抵抗相关性研究进展

研究证实高血压前期与胰岛素抵抗之间密切相关,高血压前期常伴有胰岛素抵抗,表现为代谢综合征和其他胰岛素抵抗指标升高,且常伴随与胰岛素抵抗相关的其他代谢异常。同样,胰岛素抵抗个体比胰岛素敏感性正常的个体面临更大的血压升高风险,故需对高血压前期患者或胰岛素抵抗个体加强监测和治疗干预以预防心血管事件的发生。现重点介绍高血压前期与胰岛素抵抗的相互关系及可能的作用机制。     

非糖尿病人群肥胖相关指数与胰岛素抵抗的关联

青岛市区30-74岁的居民724名（NGT者447名，IGT者277名）。WC、WHR及BMI同胰岛素抵抗指数的相关性（分别为0．45、0．33、0．47），与WC、WHR及BMI同Fins的相关性（分别为0．44、0．33、0．45）几乎完全一致。     

胰岛素抵抗与良性前列腺增生的相关性研究

目的 探讨胰岛素抵抗与良性前列腺增生间(BPH)的关系. 方法 选取在我院行健康体检老年男性200例,根据前列腺体积(PV)分为对照组(PV≤20 ml)100例,BPHl组(PV 21～49ml)50例,BPH2组(PV≥50 ml)50例.采用己糖激酶法测定空腹血糖(FPG),放免法测定空腹胰岛素(FSI)水平,运用HOMA模型计算胰岛素抵抗指数(IRI);测量身高和体质量,并计算体质指数.结果 BPH1组IRI(1.10±0.18)和体质指数(22.0±3.0)与对照组(1.18±0.21和21.8±2.7)比较,差异无统计学意义(均P＞0.05);BPH2组IRI(1.31±0.19)和体质指数(24.8±3.29)较对照组明显增高(P=0.01,0.03).高血糖所占比例BPH组(25%)高于对照组(5%)(P=0.00),其中BPH2组高血糖所占比例更高(36%)(P=0.01);BPH2组高血糖组IRI(1.47±0.21)较对照组(1.34±0.18)明显增高(t=3.92,P=0.00),但体质指数(25.8±4.3)kg/m2与对照组(24.3±2.7)kg/m2比较,差异无统计学意义(t=0.06,P=0.95). 结论 高血糖和胰岛素抵抗与重度前列腺增生存在相关性,且胰岛素抵抗的存在不依赖于体质指数的改变.     

HOMA2-IR是个较好的胰岛素抵抗指数

本文复习了HOMA2IR的由来及应用范围,认为在流行病学较大样本的研究中,它是一个较好的IR指数。     

胰岛素抵抗与良性前列腺增生的相关性研究

Objective To investigate the correlation of insulin resistance (IR) and benign prostate hyperplasia (BPH). Methods The 200 health examination men were divided into three groups according to the prostate volume (PV). There were 100 healthy subjects as control group (PV≤20 ml), 50 cases in BPH1 group (20 ml＜PV＜50 ml) and 50 cases in BPH2 group (PV≥50 ml).The fasting blood glucose (FBG) and fasting serum insulin (FSI) were determined using hexokinase method and radioimmunoassy, respectively. The IR index (IRI) and body mass index (BMI) were calculated according to the formula in HOMA model. Results There were no statistical differences between BPHl group and healthy control group in IRI (1.10±0. 18 vs. 1.18±0.21) and BMI (22. 0±3.0vs. 21.8±2.7) (t=0.74, 0.18, both P＞0. 05), but the IRI (1.31±0.19) and BMI (24. 8±3.29) increased in BPH2 group (P=0. 01, 0.03). The percentage of hyperglycosemia was higher in BPH patients than in normal controls (25% vs. 5%, P = 0. 00). Of them, the percentage of hyperglycosemia was the highest in BPH2 group (36%, P = 0. 01 ), their IRI ( 1.47 ± 0.21 ) was higher than in euglycemia patients (t=3.92, P=0.00), but the BM1 was unchanged compared with the control group ( 25.8 ± 4.3 vs. 24.3 ± 2.71, P = 0. 95 ). Conclusions There is a positive correlation of IR and hyperglycosemia with severe BPH, and the IR in severe BPH is independent of BMI.     

Lung function,insulin resistance and incidence of cardiovascular disease: a longitudinal cohort study

OBJECTIVES: To explore whether a reduced lung function is a risk factor for developing diabetes and insulin resistance (IR), and whether such relationship contributes to the largely unexplained association between lung function and incidence of cardiovascular disease (CVD). DESIGN: Forced vital capacity (FVC) was assessed at baseline. Incidence of diabetes and IR [according to the homeostasis model assessment (HOMA) model] was assessed in a follow-up examination after 13.9 +/- 2.6 and 9.4 +/- 3.6 years for men and women, respectively. After the follow-up examination, incidence of CVD (stroke, myocardial infarction or cardiovascular death) was monitored over 7 years. SETTING: Populations-based cohort study. SUBJECTS: Initially nondiabetic men (n = 1436, mean age 44.6 years) and women (n = 896, mean age 49.8 years). RESULTS: Prevalence of IR at the follow-up examination was 34, 26, 21 and 21%, respectively, for men in the first (lowest), second, third and fourth quartile of baseline FVC (P for trend <0.0001). The corresponding values for women were 30, 29, 25 and 17%, respectively (P for trend <0.001). Adjusted for potential confounders, the odds ratio (OR) for IR (per 10% increase in FVC) was 0.91 (CI: 0.84-0.99) for men and 0.89 (CI: 0.80-0.98) for women. FVC was similarly significantly associated with the incidence of diabetes (OR = 0.90, CI: 0.81-1.00), adjusted for sex and other confounders. The incidence of CVD after the follow-up examination was significantly increased only amongst subjects with low FVC who had developed IR (RR = 1.7, CI: 1.02-2.7). CONCLUSION: Subjects with a moderately reduced FVC have an increased risk of developing IR and diabetes. This relationship seems to contribute to the largely unexplained association between reduced lung function and incidence of CVD.     

Adverse endothelial function and the insulin resistance syndrome

Type 2 diabetes is characterized by impaired endothelial dependent vasodilatation which may contribute to the high prevalence of vascular disease in such patients. Although hyperglycaemia, dyslipidaemia and hypertension can all independently cause a similar defect, recent data suggest that endothelial dysfunction may be intrinsic to the insulin resistance syndrome that commonly precedes type 2 diabetes. Such abnormalities in endothelial function could represent the impact of subclinical disturbance of metabolism or alternatively the presence of a common cellular defect that influences both nitric oxide bioavailability and insulin mediated glucose disposal. Resolution of this puzzle is likely to lead to important advances in our knowledge and ultimately treatment of vascular disease.     

老年2型糖尿病患者微量白蛋白尿与胰岛素抵抗的关系

目的了解老年２型糖尿病患者的微量白蛋白尿（ＭＡＵ）与胰岛素抵抗的关系。方法对血压正常的３０例老年２型糖尿病合并ＭＡＵ患者与２６例未合并ＭＡＵ患者的空腹血糖、胰岛素、胰岛素敏感性指数（ＩＳＩ）和血脂等进行比较分析,并对所有患者的尿白蛋白排泄率（ＵＡＥＲ）与有关因素进行多元回归分析。结果２型糖尿病合并ＭＡＵ组ＩＳＩ（－４．９９±０．４８）显著低于未合并ＭＡＵ组（－４．７６±０．４８,Ｐ＜０．０５）,而且ＩＳＩ与ＵＡＥＲ呈独立相关〔标准偏回归系数（β）＝－０．３９７,Ｐ＜０．０１〕。结论在血压正常的老年２型糖尿病患者中,胰岛素抵抗是ＭＡＵ的独立危险因素。     

The relationship between insulin resistance and dyslipidaemia in cigarette smokers

AIM: Considerable evidence shows that cigarette smokers tend to have the dyslipidemic pattern of high plasma triglyceride (TG) and low high-density lipoprotein cholesterol (HDL-C) concentrations, a highly atherogenic lipoprotein profile also typical of the insulin-resistant state even in the absence of cigarette smoking. However, because cigarette smokers are frequently insulin resistant, it is unclear if this dyslipidaemia is secondary to smoking, per se, or simply to the fact that smokers tend to be insulin resistant. The present study was initiated to determine whether this dyslipidaemia prevalent in cigarette smokers and characteristic of insulin-resistant individuals is a function of cigarette smoking or of insulin resistance. METHODS: As measured using vertical auto profile-II methodology, the lipid and lipoprotein concentrations were compared in 34 cigarette smokers divided into insulin-sensitive and insulin-resistant subgroups. The two groups were similar in age and body mass index, differing only in their insulin-mediated glucose uptake as quantified by the steady-state plasma glucose concentration determined during the insulin suppression test. RESULTS: While levels of TG and very low-density lipoprotein cholesterol (VLDL-C) were significantly elevated in insulin-resistant cigarette smokers, total cholesterol (C), low-density lipoprotein cholesterol (LDL-C), narrow-density (ND) LDL-C, intermediate-density lipoprotein-C (IDL-C), HDL-C and non-HDL-C were not different in the two groups. The insulin-resistant smokers also had a preponderance of small, dense LDL particles, while the reverse was true of the insulin-sensitive cigarette smokers. CONCLUSIONS: These data suggest that the dyslipidaemia previously attributed to smoking occurs primarily in those smokers who are also insulin resistant.     

非酒精性脂肪肝与胰岛素抵抗

目的探讨非酒精性脂肪性肝病（NAFLD）与胰岛素抵抗（IR）的关系。方法NAFLD组52例,非NAFLD组50例,比较两组间BMI、WHR、TC、TG、CRP、HDL-C、LDL-C、ALT、Cr、FBG、FINS和HOMA-IR的差异,并进行Logistic回归分析。结果NAFLD组与非NAFLD组在BMI（26.7±2.3与22.4±2.5,P〈0.01）、WHR（0.94±0.06与0.83±0.05,P〈0.01）、TG（2.4±0.6与1.8±0.6,P〈0.01）、ALT（37.3±8.3与28.1±7.2,P〈0.05）、FBG（6.2±1.4与5.2±0.7,P〈0.01）、FINS（23.6±13.6与8.6±3.5,P〈0.01）、HOMA-IR（6.7±4.7与2.0±1.6,P〈0.01）的差异有统计学意义,Logistic回归分析显示BMI（P〈0.01）、WHR（P〈0.01）、TG（P〈0.01）、ALT（P〈0.05）、HOMA-IR（P〈0.01）是NAFLD的独立影响因素。结论BMI、WHR、TG、ALT、HOMA-IR是NAFLD的独立影响因素。     

抵抗素与肝脏胰岛素抵抗的关系

抵抗素是一种脂肪细胞因子,研究发现高抵抗素水平可诱导肝脏胰岛素抵抗发生,其机制可能是抑制腺苷酸活化蛋白激酶(AMPK)磷酸化,上调糖异生关键酶PEPCK和G6Pase的表达促进糖异生,从而使肝糖输出增多。肝脏是胰岛素作用的重要靶点,也是机体代谢的关键器官。肝脏胰岛素抵抗时,糖脂代谢紊乱加重机体胰岛素抵抗,促进2型糖尿病的发生。AMPK是物质代谢的关键激酶,通过磷酸化作用调节糖脂代谢相关酶的活性以及调节机体的能量平衡。抵抗素通过AMPK调节肝糖代谢这一观点为探讨抵抗素在胰岛素抵抗中的作用提供了新的思路。     

老年慢性阻塞性肺疾病患者血清瘦素水平与炎症及胰岛素抵抗的研究

目的分析老年慢性阻塞性肺疾病（COPD）患者血清瘦素水平与C反应蛋白（CRP）、空腹血糖（FBG）、胰岛素抵抗及体质量指数（BMI）的关系。方法选取住院的老年COPD患者60例,按病程分为急性加重期和临床稳定期,在不同时期测定空腹血清瘦素、CRP、FBG、胰岛素（FINS）、动脉血氧分压（PaO2）,测量身高、体质量,计算BMI、胰岛素抵抗指数（HOMA-IR）。选择同期健康老年人50例作为对照。结果 （1）COPD急性加重期血清瘦素、CRP、FBG、FINS、HOMA-IR均显著高于临床稳定期及对照组（P〈0.01）。（2）COPD临床稳定期FINS和HOMA-IR显著高于对照组（P〈0.05）。（3）各组中瘦素与FBG、FINS、HOMA-IR、BMI均呈显著正相关（P〈0.05或P〈0.01）;在急性加重期,瘦素还与CRP呈显著正相关（P〈0.01）,均衡FBG、FINS、HOMA-IR、BMI后进行偏相关分析,瘦素与CRP的相关性不再显著（P〉0.05）。结论老年COPD急性加重期患者血清瘦素、CRP水平升高并伴一定的胰岛素抵抗,瘦素与CRP、FBG、胰岛素抵抗及BMI存在一定的相关性,瘦素可能参与COPD急性加重期的炎症反应。