急性脑血管病患者胰岛素抵抗和血清胰岛素抗体水平的临床观察

目的观察急性脑血管病患者胰岛素抵抗(IR)和血清胰岛素抗体(IAb)水平变化,并分析其临床意义。方法采用放射免疫法测定36例急性脑梗死(ACI)、32例急性脑出血(ACH)、30例急性脑血管病恢复期患者(简称恢复组)及30名健康对照者的空腹血胰岛素和IAb水平,同时检测空腹血糖、血脂水平,计算胰岛素敏感指数(ISI)。结果 ACI组及ACH组血胰岛素和IAb水平显著高于恢复期及健康对照组(P0.05),而ISI值显著低于恢复组和健康对照组(P0.01);ACH组ISI高于ACI组(P0.05).而两组间血胰岛素和IAb水平无统计学差异(P0.05)。结论 IR及IAb可能参与了急性脑血管病的发病过程。IR参与脂质代谢紊乱过程,可能是脑卒中的独立危险因素之一。     

脑血管病患者血浆抵抗素水平与胰岛素抵抗的相关性研究

目的　探讨脑血管病患者血浆抵抗素水平与胰岛素抵抗(IR)之间的关系。方法　采用酶联免疫方法(ELISA)测定50例动脉粥样硬化性血栓性脑梗死(ACI)、36例腔隙性脑梗死(LI)、36例脑出血(ICH)患者及46名健康对照者的空腹血浆抵抗素、胰岛素(INS)水平,同时检测空腹血糖、血脂、血压、身高和体质量,计算体质量指数(BMI)和INS敏感指数(QUICKI)。结果　ACI和ICH组空腹INS水平均明显高于对照组(P<0 .05,P< 0 .01 ),QUICKI值均显著低于对照组(P< 0 .05,P< 0. 01 );ICH组血浆抵抗素水平[ (7. 47±4. 60)ng/ml]与对照组[ (5. 32±2. 15)ng/ml]相比明显升高(P<0 .05 );ACI、LI组血浆抵抗素水平与对照组差异均无显著性(均P>0. 05)。血浆抵抗素水平与QUICKI呈负相关(r=-0 188,P<0 .05)。结论　脑血管病患者存在IR,血浆抵抗素水平可能与IR密切相关。     

胰岛素抗体和胰岛素抗性对脑梗死影响的临床研究

目的　为了探讨脑梗死 (CI)患者与胰岛素抗体 (IAb)及胰岛素抗性 (IR)的关系。方法　采用放射免疫法 ,测定 50例脑梗死与 30例脑动脉硬化 (AS)及正常对照组血浆IAb及IR。结果　CI及AS血浆IAb阳性率明显高于对照组 ,且脑梗死伴高血压者血浆IAb明显高于单纯脑梗死组。CI、AS患者存在明显胰岛素抵抗 ,且脑梗死伴高血压组与单纯脑梗死比较 ,其IR更明显。结论　IAb、IR参与了CI、AS的发病过程 ,IR可能是CI及AS的独立危险因素     

脑梗死患者的胰岛素抵抗与血浆组织型纤溶酶原激活物抑制物-1活性相关性的研究

目的　探讨动脉硬化性脑梗死 (ACI)患者急性期和恢复期的胰岛素抵抗 (IR)与血浆组织型纤溶酶原激活物 (t PA)抑制物 1(PAI 1)活性的关系。方法　分别测定 91例ACI患者急性期和恢复期血糖、胰岛素水平和血浆t PA和PAI 1的活性。血糖与胰岛素乘积之倒数的自然对数作为胰岛素敏感性指数 (ISI) ,并与4 0名健康同龄人对照。结果　ACI患者急性期和恢复期的血糖、胰岛素水平及PAI 1活性显著高于对照组(P <0 0 1～ 0 0 5 ) ,ISI和t PA活性显著低于对照组 (P <0 0 1～ 0 0 5 ) ;PAI 1活性与胰岛素水平显著正相关(r=0 .6 7,r=0 .6 6 ,均P <0 0 1) ,与ISI显著负相关 (r=- 0 .85 ,r=- 0 .6 6 ,均P <0 0 1) ;t PA活性与这些参数不相关 ;脑梗死体积与ISI负相关 (r=- 0 .19,P <0 .0 5 ) ,与PAI 1活性正相关 (r=0 .5 6 ,P <0 .0 5 ) ;体重指数与ISI负相关 (r=- 0 .4 9,P <0 .0 5 ) ,与PAI 1活性正相关 (r=0 .5 3,P <0 .0 5 )。结论　IR提高ACI患者的血浆PAI 1活性 ,IR的个体处于脑血栓形成的危险之中     

餐后高甘油三酯血症与胰岛素抵抗关系分析

目的:探讨高甘油三酯血症与胰岛素抵抗(IR)的关系。方法:56例青年男性分为试验组和对照组(各28例),试验组行脂肪耐量试验。两组于空腹、餐后3、8h分别采血,测定甘油三酯(TG)、高密度脂蛋白-胆固醇(HDL-C)、血糖(GLU)、胰岛素(INS)水平,并计算3个时间点胰岛素敏感性指数(ISI,=log(1/GLU.INS))。结果:试验组有4/28存在富含甘油三酯脂蛋白(TRL)清除延迟。3/4TRL清除延迟者餐后8h,ISI均值低于试验组餐后3h均值;试验组在餐后3h高TG/低HDL-C应答同时,ISI降低(与空腹及对照组相比P<0.01)。提示产生胰岛素抵抗(IR)现象。结论:餐后高TG/低HDL-C/TRL清除延迟是一组动脉粥样硬化相关脂蛋白表型;可导致胰岛素抵抗。合理膳食、防治高TG血症是解决这些问题的根本措施。提出甘油三酯代谢紊乱综合征的概念,认为甘油三酯代谢紊乱综合征是代谢水平脂质紊乱和多种动脉粥样硬化相关危险因素的病理基础。     

脑卒中患者胰岛素抵抗的临床分析

目的 对脑卒中患者的胰岛素抵抗(IR)进行分析研究,探讨二者关系。方法 56例脑卒中患者脑梗死30例、脑出血26例,分别测定急性期及恢复期空腹血糖、C-肽、胰岛素浓度,计算其胰岛素敏感指数(ISI),并与对照组进行对比研究。结果 脑卒中患者急性期普遍存在胰岛素抵抗,而在恢复期脑梗死组的ISI显著低于对照组(P<0.05),脑出血组的ISI与对照组无显著性差异。结论 胰岛素抵抗在脑卒中的发病中可能发挥一定作用,且与卒中类型有关。     

脑梗死患者血脂代谢紊乱与胰岛素抵抗

目的 探讨脑梗死患者血脂代谢紊乱与胰岛素抵抗相关关系。方法 选取脑梗死患者40例及健康对照者30例为研究对象,测定总胆固醇(CH)、甘油三脂(TG)、高密度脂蛋白(HDL-C)、低密底脂蛋白(LDL-C)、血糖(G)、胰岛素(INS)含量,同时采用李光伟等提出的胰岛素敏感指数(ISI)方法进行计算。结果 脑梗死患者CH、TG、LDL-C显著高于对照组(P<0.01)而HDL-C明显低于对照组(P<0.01);INS显著高于对照组(P<0.01),而ISI显著低于对照组(P<0.01)。结论 脑梗死患者血脂代谢紊乱与胰岛素抵抗呈正相关,两者共同参与脑梗死发生及发展。     

高血糖、胰岛素抵抗与脑缺血性损伤

目的:探讨急性脑梗死后高血糖与胰岛素抵抗的作用及相互关系。方法:选取我院非腔隙性脑梗死住院病人50例作为实验组,依据血糖水平将其分为A组22例(单纯性高血糖)及B组(血糖正常)28例。分别在起病24h内、48h、72h、5d及9d测定患者血清中的神经元特异性烯醇酶(NSE)作为脑缺血损伤的生化标志;同时在急性期和恢复期测定空腹血糖(FPG)及空腹胰岛素(FINS),分别计算胰岛素敏感指数(ISI)及NSE释放曲线下面积。结果:实验组NSE呈动态升高,ISI值明显降低,而A组ISI值降低更明显;A组与B组相比,NSE高峰后移及峰值加大;NSE曲线下面积主要与升高的血糖有关,而与血中胰岛素水平及ISI相关性不显著。结论:高血糖加重脑缺血性损伤:胰岛素抵抗是脑梗死的危险因素,但对脑损伤的作用不明显。     

伴颈动脉粥样硬化的急性脑梗死患者胰岛素抵抗与TNF-α关系的临床研究

目的探讨肿瘤坏死因子α(TNF-α)与胰岛素抵抗(IR)在伴颈动脉粥样硬化(CAS)的急性脑梗死中的作用机制及二者之间的关系。方法比较44例伴CAS的急性脑梗死患者与80例健康对照组中空腹血糖(FPG)、空腹血清胰岛素(FINS)、胰岛素敏感指数(ISI)、胰岛素抵抗指数(HOMA-IR)、TNF-α、体重指数(BMI)等6个因素之间有无差异,并了解IR与TNF-α的相关性。结果伴CAS的急性脑梗死组与对照组相比,FPG、FINS、HOMA-IR、TNF-α明显高于对照组,ISI明显低于对照组(P<0.01或P<0.05);脑梗死组中,ISI与TNF-α呈显著负相关(r=-0.494,P<0.01)。结论在伴有CAS的急性脑梗死中同时存在IR及TNF-α升高,IR程度与TNF-α呈正相关。     

胰岛素抵抗与脑卒中关系的临床研究

目的　探讨胰岛素抵抗 (IR)与脑卒中的关系。方法　 94例脑卒中患者分为动脉粥样硬化血栓性脑梗死组 (ATI,34例 ) ,腔隙性脑梗死组 (LI,2 5例 ) ,脑出血组 (ICH,35例 ) ;测定其空腹血糖 (FPG)和餐前、餐后C 肽及胰岛素浓度 ,计算其胰岛素敏感性指数 (ISI) ,并与对照组对比研究。结果　ATI组及LAC组的ISI显著低于对照组 (P<0 0 5 ) ,ICH组的ISI与对照组无显著性差异 (P >0 0 5 )。脑卒中的IR主要见于肥胖或甘油三脂 (TG)、低密度脂蛋白胆固醇 (LDL C)、尿酸 (UA)、载脂蛋白B(APO B)、高密度脂蛋白 (HDL)等生化指标中有三项以上异常的患者 (占39 4 % )。结论　IR与脑卒中有密切关系 ,提示通过饮食、运动、药物等方法在大宗人群进行降低IR的早期干预 ,不仅对现代常见代谢病 ,而且对脑卒中会有积极的预防作用。     

血脂、血尿酸及凝血功能与急性脑梗死 和脑出血的相关性

目的 探讨血脂、血尿酸（UA）及凝血功能与急性脑梗死（ACI）和脑出血（ICH）的相关性。 方法 测定同期住院的62例ACI和50例ICH患者的血脂、UA及凝血功能等指标，并以同期住院的50例非 脑血管病患者为对照进行相关分析。 结果 ACI组总胆固醇（TC）、甘油三酯（TG）水平显著高于对照组（P＜0.01），载脂蛋白A1（ApoA1）水平 显著低于对照组（P＜0.01）；高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C）、载脂蛋 白B（ApoB）水平与对照组比较差异无统计学意义（P＞0.05）。ACI组血UA、纤维蛋白原（Fib）显著高于对 照组和ICH组（P＜0.01）；ICH组血脂指标、血UA、Fib与对照组比较差异无统计学意义（P＞0.05）。 结论 血脂代谢紊乱、高尿酸血症、高纤维蛋白原血症与脑梗死明显相关，是脑梗死的危险因素，与 ICH则无明显相关性。     

Alzheimer disease and vascular dementia: relationships with fasting glucose and insulin levels

Cerebrovascular disease and Alzheimer disease are the leading causes of dementia in elderly subjects. In spite of it, relatively little is known about the pathogenesis and risk factors for dementia. We evaluated fasting plasma glucose and insulin, albumin, lipids, Lp(a) and uric acid levels in nondiabetic patients of both sexes affected by vascular dementia (VD) and senile dementia of the Alzheimer type (SDAT) as well as in a control group of age-matched nondemented subjects. Following a covariance analysis by gender, body mass index, albumin levels and prevalence of arterial hypertension, total and LDL cholesterol as well as HDL cholesterol levels were not significantly different among the three groups. Fasting glucose (p < 0.001 and p < 0.005, respectively) and insulin levels (p < 0.05 for both differences) were higher in patients with VD and SDAT than in control subjects. Our data show that nondiabetic patients with VD or SDAT have higher fasting glucose and insulin levels than healthy control subjects. These metabolic characteristics were not influenced by differences in gender, adiposity, nutritional status, lipids or presence of arterial hypertension.     

合并OSAHS的老年急性脑梗死患者同型半胱氨酸和胰岛素抵抗临床分析

目的研究合并阻塞性睡眠呼吸暂停综合征(OSAHS)的老年急性脑梗死(ACI)患者血清同型半胱氨酸(Hcy)及稳态模型胰岛素抵抗指数(HOMA-IR)水平,分析老年ACI患者OSAHS、Hcy和HOMA-IR相互关系。方法根据年龄和睡眠呼吸监测数据,将患者分为老年ACI+OSAHS组(n=21)、老年ACI组(n=30)、中年ACI+OSAHS组(n=28)和中年ACI组(n=34),检测并比较各组血清Hcy、胰岛素抵抗指数(HOMA-IR)等各指标。结果老年ACI+OSAHS组较其余3组的Hcy和HOMA-IR均升高,差异有统计学意义(P0.05);中年ACI+OSAHS组较中年ACI组Hcy和HOMA-IR增高,差异有统计学意义(P0.05)。Hcy与年龄、AHI、平均腰围、BMI、HOMAIR均呈正相关;多元线性回归分析显示AHI与年龄、Hcy、HOMA-IR、BMI呈正相关。结论随年龄的增加,合并OSAHS的急性脑梗死患者Hcy和HOMA-IR水平随之升高;OSAHS可能通过升高Hcy及增加胰岛素抵抗导致ACI。     

脑白质疏松与胰岛素抵抗和单核细胞趋化蛋白-1的关系

目的探讨脑白质疏松患者胰岛素抵抗(IR)与血浆单核细胞趋化蛋白-1(MCP-1)水平的关系。方法选择48例脑白质疏松患者,以30例健康者作为对照组。采用放射免疫法测定两组的空腹血胰岛素(FINS)水平,同时检测空腹血糖(FBG)、血脂,以稳态模型评估法(HOMA)评价胰岛素抵抗(HOMA-IR)。采用ELISA法测定血清MCP-1水平。结果脑白质疏松组的MCP-1水平高于健康对照组(P<0.01);脑白质疏松组FINS、HOMA-IR均高于健康对照组(P<0.01)。相关性分析显示脑白质疏松患者血清MCP-1水平与FPG、TC、LDL-C、血清胰岛素、HOMA-IR呈明显正相关(P<0.01)。结论脑白质疏松患者存在胰岛素抵抗,MCP-1与胰岛素抵抗密切相关。     

Glucose tolerance in amyotrophic lateral sclerosis

Blood glucose and plasma insulin during an oral glucose tolerance test were determined in 21 patients with amyotrophic lateral sclerosis and in 10 control patients matched for age, obesity and physical activity. In addition, 125I-insulin binding to circulating erythrocytes were studied in a subgroup of 4 ALS patients and 8 controls. Both impaired glucose tolerance and diabetes mellitus were evenly distributed between the study groups, and no difference in mean blood glucose levels during the OGTT was found between ALS and control patients. Fasting plasma immunoreactive insulin concentration was significantly higher in ALS patients as compared to controls, but plasma IRI increments to the glycemic stimulus were similar in the 2 groups. The number of insulin binding sites per cell appeared lower in patients with ALS, but the difference in receptor concentration was not statistically significant. In addition, the specific bound fraction of 125I-insulin showed no difference between ALS and control patients. In conclusion, we were unable to demonstrate any marked deterioration of glucose tolerance or increase in insulin resistance in patients with ALS.     

胰岛素抵抗与正常血压脑出血及脑梗塞关系的探讨

为研究胰岛素抵抗与脑出血、脑梗塞的关系,测定了正常血压脑出血41例、正常血压脑梗塞51例及对照组39例的血清胰岛素与血糖比值I/G,结果显示:三组I/G分别为6.3098±8.3268,5.1867±3.0069和2.4091±1.1374(means±SD)。正常血压脑出血组与对照组比较P<0.01。正常血压性脑梗塞组与对照组比较P<0.05。认为胰岛素抵抗是脑出血、脑梗塞的危险因素。     

多囊卵巢综合征骨骼肌胰岛素抵抗大鼠模型的建立

背景：研究表明胰岛素抵抗在多囊卵巢综合征的发生与发展过程中起重要作用,建立理想的多囊卵巢综合征骨骼肌胰岛素抵抗动物模型是研究该疾病的基础。 目的：探讨建立较为理想的多囊卵巢综合征骨骼肌胰岛素抵抗大鼠模型的方法。 方法：将八九周龄SD雌性大鼠随机分为模型组和对照组。模型组给予胰岛素联合人绒毛膜促性腺激素皮下注射,并以高脂饲料和50 g/L葡萄糖水喂养,对照组皮下注射生理盐水,常规饮食喂养。 结果与结论：造模6周后,模型组大鼠卵巢体积明显增大,且呈多囊性改变;血清睾酮、黄体生成素、空腹血糖和胰岛素水平高于对照组;骨骼肌组织中葡萄糖转运蛋白4表达明显低于对照组,且其葡萄糖转运蛋白4阳性颗粒靠近骨骼肌细胞膜边缘者较少。可见胰岛素联合人绒毛膜促性腺激素皮下注射,并饲以高脂饲料和50 g/L葡萄糖水是建立多囊卵巢综合征骨骼肌胰岛素抵抗大鼠模型较为理想的方法。     

Differential effects of intranasal insulin and caffeine on cerebral blood flow

Insulin is an important modulator of brain functions such as memory and appetite regulation. Besides the effect on neuronal activity, it is also possible that insulin has a direct vasodilatory effect on cerebral blood flow (CBF). We investigated the impact of increased insulin levels in the central nervous system on basal and task-induced CBF as well as blood oxygenation level-dependent (BOLD) response in the visual cortex using pulsed arterial spin-labeling MRI. An intranasal insulin application was used to avoid peripheral hyperinsulinaemia, which would lead to a cascade of hormonal changes. In a control experiment, caffeine was applied due to its well-known impact on the vasculature of the brain leading to a reliable reduction of CBF. Eight lean subjects were included in the study. On 2 separate days, intranasal human insulin or caffeine tablets were given to the subjects after fasting over night. On each day, basal CBF and task-induced CBF were measured before and 30 min after application of insulin or caffeine in each subject. During the task condition, a flickering checkerboard was presented. Insulin had no effect on basal CBF and task-induced CBF in comparison with drug-free baseline measurement in the visual cortex and control regions. After caffeine application, however, there was a significant decrease of CBF during stimulation in the visual cortex. The BOLD response was not altered by insulin or caffeine between pre- and postdose measurements. In conclusion, we found no evidence for a direct vasodilatory effect of intranasal insulin on the cerebral vascular system in this study.     

Serum insulin and leptin levels in valproate-associated obesity

PURPOSE: Weight gain is an important adverse effect of valproate (VPA) therapy, and it is associated with hyperinsulinemia and hyperandrogenism in women with epilepsy. Leptin is considered a signaling factor regulating body weight and energy metabolism. In human subjects, obesity is in general associated with elevated serum leptin levels, suggesting decreased sensitivity to leptin. The present study aimed at evaluating the role of insulin and leptin in VPA-related obesity. METHODS: Body mass index (BMI) was calculated, and serum insulin and leptin levels were measured in 81 patients with epilepsy taking VPA and in 51 healthy control subjects. RESULTS: Forty (49%) of the patients taking VPA and 25 (49%) of the control subjects were obese. The mean insulin levels were higher in VPA-treated patients than in the control subjects despite similar BMI values, when all subjects were included in the comparison. Both obese male and female patients taking VPA had higher serum insulin levels than the respective control subjects with similar BMI values. Serum insulin levels also were higher in lean male and lean female patients compared with the lean control subjects of same sex. Serum leptin levels did not differ between the VPA-treated patients and the control subjects. CONCLUSIONS: Both obese and lean patients taking VPA for epilepsy have hyperinsulinemia, suggesting development of insulin resistance. This may be one of the factors leading to weight gain during VPA treatment. However, the results of the present study do not suggest an independent role for leptin in the pathogenesis of VPA-related obesity.