脑血管病与胰岛素抵抗的关系探讨

目的 研究胰岛素抵抗(IR)与脑卒中之问的关系。方法 选取急性脑卒中患作为研究对象，测定血糖(FPG)、胰岛素水平(FINS)、总胆固醇(CH)、甘油三酯(TG)，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 急性脑卒中患FINS显高于对照组(P＜0.01)，其ISI较对照组显降低(P＜0．01)。脑梗死组FINS显高于脑出血组(P＜0．05)，其ISI较脑出血组显降低(P＜0．05)。结论 急性脑卒中患存在IR，IR为其重要的危险因素，尤其是脑梗死患IR比脑出血患更为敏感。     

胰岛素抵抗与高血压性脑出血关系的初步研究

探讨高血压性脑出血（HIH）患者是否存在胰岛素抵抗（IR）与高胰岛素血症（HIS）,以及IR与患者病情、预后的关系。方法测定了56例HIH患者及37例原发性高血压（EH）患者、49例健康人的血糖（FPG）与血清胰岛素水平（FINS）,同时采用李光伟等提出的胰岛素敏感性指数（ISI）方法进行计算,3个月后随访HIH患者,进行日常生活能力（ADL）Barthel指数评分。结果HIH患者FPG及FINS均明显高于对照组（P＜0．001,P＜0．001）,其ISI较对照组明显减低（P＜0．001）。HIH患者轻型组与重型组的FPG、FINS、ISI比较也存在显著性差异（P＜0．001,P＜0．05,P＜0．001）。随访HIH患者轻型组ADL评分明显高于重型组。结论HIH患者存在IR及HIS,其胰岛素水平及IR程度与患者病情、预后有关。建议对HIH患者的血糖水平升高与IR及ISI下降者应积极使用改善胰岛素敏感性的药物治疗。     

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。     

脑梗死急性期血清胰岛素测定及意义

检查30例脑梗死急性期患者和20例正常人的血清胰岛素和血糖含量。结果,脑梗死组血清胰岛素显著高于对照组（P＜0．01）,而血糖与对照组比较无显著差异（P＜0．05）。提示脑梗死急性期患者血清胰岛素升高,存在高胰岛素血症及胰岛素抵抗。胰岛素抵抗可能为脑梗死发病的独立危险因素。     

脑出血患者血清瘦素浓度及意义

目的 分析脑出血患者血清瘦素浓度的变化,探讨瘦素与脑出血的关联。方法 对86例脑出血患者和58例对照者进行瘦素、空腹胰岛素等的检测,并进行比较。结果 （1）脑出血组与对照组相比胰岛素敏感指数（ISI）降低（P〈0．01）,男性患者瘦素水平高于对照组（P〈0．01）。（2）脑出血组与对照组相比收缩压和舒张压水平均升高（P〈0．01）。（3）脑出血患者血清瘦素水平与ISI呈负相关（P〈0．05）。（4）男性患者中高瘦素-高血压水平（收缩压或舒张压）的联合作用与增加脑出血的危险强烈相关。结论 脑出血患者存在胰岛素抵抗;男性脑出血患者的瘦素水平升高,高瘦素-高血压水平的联合作用增加发生脑出血的危险。     

梗死面积及出血量不同的急性脑血管病患者血浆D—二聚体水平及其临床意义

目的 探讨梗死面积及出血量不同的脑血管病（CVD）患者血浆D－二聚体（D－D）水平及其临床意义。方法 对206例急性CVD患者进行血浆D－D含量测定,并与对照组比较。结果 （1）脑梗死、腔隙性脑梗死、大量及小量脑出血患者血浆D－D水平显著高于对照组（P＜0．01）。（2）脑梗死组血浆D－D含量显著高于腔隙性脑梗死组（P＜0．05）。（3）大量脑出血与小量脑出血组、脑梗死与大量脑出血之间血浆D－D水平比较均无显著性差异（P＞0．05）。（4）小时脑出血患者血浆D－D含量显著高于腔隙性脑梗死组（P＜0．05）。结论 D－D可作为急性CVD一个比较特异的指标,对临床鉴别小量出血与腔隙性脑梗死有一定的帮助。     

脑梗死与胰岛素抵抗关系的实验研究

目的 对胰岛素抵抗与脑梗死之间的关系进行探讨。方法 分别对62例单纯性脑梗死患者和35例健康对照组进行空腹血糖(FBG)、空腹破岛素(FINs)、胆固醇(Tc)、甘油三酯(TG)，计算胰岛素敏感指数(ISI)，并与神经功能缺失评分和梗死灶面积进行直线相关分析。结果 脑梗死患者组FB6、FINS、TC、TG显著高于对照组(尸＜0．05)；ISI显著低于对照组。脑梗死轻型组与脑梗死重型组之间FINS和IsI也存在显著差异。IsI与梗死灶面积、神经功能缺失评分呈负相关。结论 破岛素抵抗与脑梗死有密切关系，可能是脑梗死的一个重要危险因素，它参与了脑梗死的发生发展。     

胰岛素抵抗、血脂异常与高血压合并脑梗死关系的研究

目的　研究胰岛素抵抗 (IR)、血脂异常与高血压合并脑梗死之间的关系。方法　测定 6 7例高血压合并脑梗死患者 (脑梗死组 33例 ,腔隙性脑梗死组 34例 )的血脂、血糖、血清胰岛素以及胰岛素敏感指数(ISI) ,并与 30名健康对照者进行比较。结果　高血压合并脑梗死患者血脂、血糖、胰岛素、ISI与对照组比较均有显著性差异 (均P <0 .0 1) ,其中腔隙性脑梗死组胰岛素明显高于脑梗死组 (P <0 .0 5 ) ,而ISI较脑梗死组明显减低 (P <0 .0 5 )。结论　高血压合并脑梗死存在IR ,IR可能是其独立危险因素之一。尤其腔隙性脑梗死可能与IR关系更密切     

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。     

急性脑梗死与胰岛素抵抗及胰岛素抗体水平相关性分析

目的 探讨急性脑梗死(ACI)与胰岛素抵抗(IR)及胰岛素抗体(IAb)水平之间的相关性.方法 采用放射免疫法测定34例ACI组,28例ACI恢复期组及30名健康对照者的空腹血胰岛素(INS)、IAb水平,同时检测空腹血糖(FBG)、血脂,计算胰岛素敏感指数(ISI).结果 ACI组INS、IAb显著高于恢复期组及对照组;ISI较对照组显著降低.结论 ACI患者存在明显IR,血IAb水平亦显著增高,IR及IAb可能参与了ACI的发病过程.     

Centrally mediated hypoglycemic effect of insulin: apparent involvement of specific insulin receptors

We have studied the involvement of central nervous system (CNS) insulin receptors in mediating the central hypoglycemic effect of insulin by using insulin derivatives modified at regions of the hormone necessary for receptor reactivity and peripheral bioactivity. Acetylation or succinylation of the 3 free amino groups of insulin at positions A1, B1 and B29 resulted in a corresponding decrease in lipogenic activity in isolated rat adipocytes, with concentrations of hormone required to produce half the maximal effect (ED₅₀) being 0.15 ng/ml, 3 ng/ml and 50 ng/ml for native insulin, acetyl₃ insulin and succinyl₃ insulin, respectively. Moreover, the modified insulins exhibited diminished hypoglycemic effect following central administration in mice, with the doses needed for suppresion of plasma glucose to 50% of basal levels being 1 μg, 10 μg and 25 μg for native insulin, acetyl₃ insulin and succinyl₃ insulin, respectively. Because binding of insulin derivatives to CNS receptors can be predicted from their peripheral bioactivity, the present finding of parallel decrements in lipogenic activity in vitro and central hypoglycemic effect in vivo, following modification of insulin at regions implicated in receptor activation, is consistent with the view that insulin exerts its central effect on plasma glucose by interacting with specific CNS receptor sites which are closely related to the peripheral insulin receptors.     

Effect of diet-induced obesity and experimental hyperinsulinemia on insulin uptake into CSF of the rat

We examined the hypothesis that the uptake of plasma insulin into cerebrospinal fluid (CSF) is saturable in two rat models. Dietary obese and control female Osborne Mendel rats received 24-h infusions of vehicle or insulin. CSF insulin levels in cafeteria- and chow-fed rats were comparable at all levels of plasma insulin (4.5 ± 2.8, 7.6 ± 2.4, and 23.9 ± 6.4 μU/ml in cafeteria diet vs. 4.5 ± 0.9, 6.8 ± 1.1, and 17.0 ± 4.0 μU/ml in chow rats). CSF insulin uptake as a percentage of plasma insulin decreased with increased plasma insulin in both groups. A similar relationship was observed in Wistar rats receiving 6-day infusions of vehicle or insulin (plasma insulin = 55 ± 12 vs. 365 ± 98 μU/ml; CSF/plasma insulin ratio = 0 ± .007 vs. 0.013 ± .006, respectively). Hyperinsulinemic Wistar rats did not demonstrate decreased brain capillary insulin binding vs. vehicle-infused controls. The results suggest that a saturable transport process contributes insulin transport into CSF in normal rats and that this process is not altered by moderate diet-induced obesity or hyperinsulinemia per se.     

运动神经元病患者血浆胰岛素样生长因子-1的变化

目的 探讨运动神经元病（ＭＮＤ）患者血浆胰岛素生长因子－１（ＩＧＦ－１）变化的临床意义。方法 应用放射免疫法测定２１例ＭＮＤ患者血浆ＩＧＦ－１水平,同时测定其血清胰岛素和空腹血糖水平,并设立正常对照组。结果 与正常对照组比较,ＭＮＤ患者血浆ＩＧＦ＿１水平显著下降,虽然两组血糖水平无明显差异,但口才组血浆胰钫 水平明显下降。结论 ＩＧＦ－１系统参与了ＭＮＤ的发病机理,神经营养支持的缺乏是导致髓运动元     

难治性抑郁症患者血清胰岛素和神经内分泌激素的对照研究

目的研究难治性抑郁症患者治疗前后血清胰岛素和神经内分泌激素变化。方法难治性抑郁症患者(TRD组)、非难治性抑郁症患者(NTRD组)、健康者(正常对照组)各60例为研究对象,使用HAMD量表评估患者的临床症状,检测患者血清胰岛素、皮质醇(CORT)、促肾上腺皮质激素(ACTH)、三碘甲状腺原氨酸(T3)、游离三碘甲状腺原氨酸(FT3)、甲状腺素(T4)、游离甲状腺素(FT4)、促甲状腺激素刺激激素(TSH)等神经内分泌激素水平,并进行治疗前后各组上述指标的统计学处理。结果 TRD组血清胰岛素、CORT、ACTH、T3、FT3、T4、FT4、TSH与正常对照组存在显著差异,血清胰岛素、CORT、ACTH、FT4与NTRD组存在显著差异;NTRD组血清CORT、ACTH、T3、FT3、T4、FT4、TSH等与正常对照组存在显著差异(P0.05);治疗后,TRD组胰岛素、CORT、ACTH、FT3、FT4、TSH与对照组存在显著差异,而NTRD组CORT与对照组存在显著差异(P0.05)。结论 TRD患者HPA轴功能亢进、HPT轴功能低下等较NTRD患者更为严重,药物治疗后仍存在显著差异。     

Valproate modulates glucose metabolism in patients with epilepsy after first exposure

Valproate (VPA) treatment has been reported to be associated with weight gain and metabolic changes, such as hyperinsulinemia. The question of whether hyperinsulinemia and other metabolic changes are consequences of increased weight, or are instead direct results of VPA treatment, remains a matter of debate. The aim of the current study was to explore the influence of VPA treatment on glucose and insulin levels during the oral glucose tolerance test (OGTT) directly following the first intravenous (IV) administration. Sixteen patients (18–46 years old) with newly diagnosed epilepsy underwent an OGTT with 75 g glucose prior to the start of VPA treatment, as well as directly following the first IV VPA administration. We observed that plasma glucose levels during the 120 min of OGTT session following infusion of VPA were significantly lower than those measured during OGTT without VPA treatment (mean ± standard deviation [SD] 4.28 ± 0.94 mmol/l vs. 4.75 ± 1.09 mmol/l respectively, p = 0.038). However, blood concentrations of insulin and C‐peptide did not differ significantly between the two measurements. This is the first study to show a potential acute glucose‐lowering effect of VPA during OGTT in patients with newly diagnosed epilepsy.     

胰岛素与颅脑损伤

胰岛素是人体正常生理状态不可缺少的激素,在生理状态下由血液中代谢底物水平的升高刺激胰腺胰岛β细胞分泌,参与单糖、脂肪酸和氨基酸的摄取并转化为糖原、甘油三酯和蛋白质.随着其在颅脑损伤中作用及机理的不断研究,临床应用也逐渐受到重视.     

氯氮平对胰岛素敏感性的影响

目的：了解氯氮平对胰岛素敏感性的影响。探讨药源性肥胖的可能成因。方法；对24例首发精神分裂症及分裂样精神病患者予氯氮平治疗18周，监测治疗前后胰岛素敏感性指数（ISI），体重变化。结果：治疗前患者ISI与正常对照组相似。经氯氮平治疗后，患者体重均有增加；ISI显著低于治疗前及正常对照者，治疗前后ISI差值与氯氮平剂量，体重变化无显著相关性。结论：氯氮平可降低胰岛素敏感性，胰岛素阻抗（IR）可能是药源性肥胖的重要原因之一。     

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。     

Insulin induces tyrosine phosphorylation of the insulin receptor and SHC, and SHC/GRB2 association in cerebellum but not in forebrain cortex of rats

A growth-related branch of the insulin-signaling pathway was studied in the forebrain cortex and cerebellum of Wistar rats. Anesthetized rats received a bolus injection of saline or insulin through the cava vein after which fragments of cerebellum and forebrain cortex were excised and immediately homogenized. Insulin receptor and p46SHCA phosphorylation, and p46SHCA/GRB2 association were detected by immunoprecipitation and blotting with specific antibodies. Insulin stimulated the rapid phosphorylation of its receptor in cerebellum, followed by p46SHCA phosphorylation and GRB2 recruitment. The optimal insulin dose for the induction of p46SHCA/GRB2 binding was 60 microg, and time-course experiments showed that maximum phosphorylation/binding occurred 2-3 min after stimulation. Although insulin receptors and SHC were present in forebrain cortex, there was no increase in their phosphorylation, nor was there any recruitment of GRB2 following stimulation with insulin. Thus, although elements involved in the early intracellular response to insulin are present in the central nervous system, differences in their activation/regulation may account for the functional roles of insulin in these tissues.