胰岛素抵抗,血脂异常与缺血性脑血管病关系的动态研究

目的 研究胰岛素抵抗（ＩＲ），血脂异常与缺血性脑血管病之间的关系。方法 测定不同病程脑梗死患者的血脂，胰岛素，血糖及ｃ－肽（ｃ－ｐ）等，并与健康对照组（２９例）比较。结果 在脑梗死的不同发展阶段，血脂，血糖，ｃ－ｐ及胰岛素敏感指数（ＩＳＩ）与对照组相比均有显著性差异（Ｐ〈０．０５），ＩＳＩ在恢复期组与甘油三酯和ａｐｏＢ有显著负相关（Ｐ〈０．０５），在其他各组均无相关。结论 在脑梗死发病的全过程中Ｉ     

中枢神经系统感染患者血浆与脑脊液中内皮素变化的研究

目的探讨中枢神经系统感染（ＣＮＳＩ）时血浆与脑脊液（ＣＳＦ）中内皮素（ＥＴ）的变化。方法采用放射免疫法测定６６例ＣＮＳＩ患者血浆和ＣＳＦ中的ＥＴ－１水平。结果ＣＮＳＩ患者ＣＳＦ中的水平较对照组高，对照组与病毒脑、结脑组相比有显著性差异（Ｐ分别＜０．００１、０．０５），与化脑组相比无显著性差异（Ｐ＞０．０５），血浆中的水平与ＣＮＳＩ关系不明显（Ｐ＞０．０５）；ＣＮＳＩ伴重度脑功能障碍者ＣＳＦ和血浆中ＥＴ－１水平明显高于伴轻中度脑功能障碍者（Ｐ＜０．００１）或无脑功能障碍者（Ｐ＜０．００１），轻中度脑功能障碍又明显高于无脑功能障碍者（Ｐ＜０．００１）。结论ＣＳＦ和血浆中ＥＴ－１水平与ＣＮＳＩ的病种无关，而与脑损伤的程度有关，其含量增高可作脑实质损伤的重要指标，ＥＴ－１可能是脑实质损伤的重要因素     

脑梗死患者血浆β—TG,PF4的检测及意义

目的 观察血浆β－ＴＧ,ＰＦ在急性脑梗死（ＡＣＩ）和多灶性脑梗死（ＭＦＣＩ）中有浓度变化及意义。方法 采用酶标免疫测定法测定４０例ＡＣＩ于发病６￣７２ｈ,７天,。与３３例ＭＦＣＩ患者及３０例对照组血浆β－血浆ＰＦ４无高于对照组（Ｐ〈０．００１）,且ＡＣＩ组治疗７天后ＰＦ４较发病６￣７２ｈ显著下降（Ｐ〈０．００１）,但仍高于对照组（Ｐ〈０．００１）;ＡＣＩ组治疗７天后β－ＴＧ与ＭＦＣＩ组,对照组均无     

53例病毒性脑炎脑脊液可溶性白细胞介素II受体的检测

本文采用单抗体与多抗体夹心法检测了５３例急性病毒性脑炎（简称疾脑）患儿脑脊液（ＣＳＦ）中可溶性白细胞介素Ⅱ受体（ｓＩＬ－２Ｒ）的水平，并对其中的２８例进行了恢复期ＣＳＦ的检测，结果表明，急性期病脑ＣＳＦ中的ｓＩＬ－２Ｒ较正常对照组显著增高（Ｐ〈０．００１），至恢复期，ＣＳＦ中的ｓＩＬ－２Ｒ显著下降，与急性期比较差异显著（Ｐ〈０．００１）。     

脑血栓形成者血清胰岛素及与PAI-1关系的探讨

目的探讨脑血栓形成者是否存在胰岛素抵抗（ＩＲ）,并进一步探讨其与血浆纤溶酶原激活物-１（ＰＡＩ－１）活性的关系。方法选择６７例无糖尿病病史的ＣＴＢ患者,根据梗死面积分为大中病灶组（４３例）和小灶组（２４例）、另取２８例健康成人作对照组。分别用发色底物法和放免法测定血浆ＰＡＩ－１活性、ＩＳ、Ｃ肽水平。结果（１）ＣＴＢ组ＰＡＩ－１活性、ＩＳ、Ｃ肽水平明显高于对照组（Ｐ均＜０．０１）;但两不同梗死面积组间无显著差别：（２）ＣＴＢ组ＰＡＩ－１与ＩＳ、Ｃ肽及ＩＳ与Ｃ肽间呈显著正相关（Ｐ均＜０．００１）,有极显著性差异。结论（１）ＩＲ和／或ＨＩ可能参与了ＣＴＢ的发生;（２）血浆ＰＡＩ－１活性增高与ＩＳ及Ｃ肽有关．ＰＡＩ－１活性增高致血浆纤溶活性降低．可能是ＩＲ与ＣＴＢ的中间环节。     

53例病毒性脑炎脑脊液可溶性白细胞介素Ⅱ受体的检测

本文采用单抗体与多抗体夹心法检测了５３例急性病毒性脑炎（简称病脑）患儿脑脊液（ＣＳＦ）中可溶性白细胞介素Ⅱ受体（ｓＩＬ－２Ｒ）的水平，并对其中的２８例进行了恢复期ＣＳＦ的检测，结果发现：急性期病脑ＣＳＦ中的ｓＩＬ－２Ｒ较正常对照组显著增高（Ｐ＜０．００１），至恢复期，ＣＳＦ中的ｓＩＬ－２Ｒ显著下降，与急性期比较差异显著（Ｐ＜０．００１）。     

高血压合并急性离出血管病的心率变异性改变

对原发性高血压（ＥＨ）合并急性脑血管病（ＡＣＶＤ）患者３０例进行２４小时动态心电图心率变异性（ＨＲＶ）测定，并与３０例无ＡＣＶＤ的ＥＨ患者进行对比。结果显示，合并ＡＣＶＤ组最小心率及平均心率明显高于对照组（Ｐ〈０．０１、〈０．００１）；ＳＤＮＮ、ｒＭＳＳＤ、ＰＮＮ５０比对照组明显减低（Ｐ〈０．００１、〈０．０１、〈０．００１）。提示合并ＡＣＶＤ的ＥＨ患者ＨＲＶ减低，其主要原因可能是自主神经中枢损害     

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。     

髓鞘碱蛋白对脑梗死和多发性硬化的诊断价值

目的探讨髓鞘碱蛋白（ＭＢＰ）对脑梗死（ＣＩ）和多发性硬化（ＭＳ）的诊断价值。方法对１１４例ＣＩ患者、２８例ＭＳ患者、２４名正常者血清以及部分患者脑脊液（ＣＳＦ）的ＭＢＰ进行了检测。结果ＣＩ、ＭＳ患者血清和ＣＳＦ的ＭＢＰ均显著高于正常对照组（Ｐ〈０．０１）,ＭＳ组又高于ＣＩ组（Ｐ〈０．０１）;ＭＳ组中病情活动期患者ＭＢＰ又高于缓解期。结论血清和ＣＳＦ的ＭＢＰ检测对ＭＳ和ＣＩ的鉴别诊断,以及判断ＭＳ病     

胰岛素抵抗与脑梗塞关系的研究

检测６１例高血压并脑梗塞、２９例单纯脑梗塞患者和２０名正常人的血糖（ＢＳ）、血浆胰岛素和促肾上腺皮质激素（ＡＣＴＨ），计算胰岛素敏感性指数，并与神经功能缺损评分和脑梗塞面积进行直线相关分析。结果：两组脑梗塞患者血浆胰岛素显著高于对照组（Ｐ＜０．０１）；胰岛素敏感性指数降低，与对照组比较均Ｐ＜０．０１。而ＢＳ、ＡＣＴＨ与对照组比较无显著差异。胰岛素敏感指数与神经功能缺损评分和梗塞面积呈负相关（ｒ＝－０．７１和－０．６４，Ｐ＜０．０１）。复查时血浆胰岛素水平虽有降低，但仍高于对照组。提示脑梗塞患者存在胰岛素抵抗，并可能为脑梗塞的一个独立危险因素     

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.     

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。     

胰岛素抵抗与脑卒中的关系探讨

目的 研究胰岛素抵抗（IR）与脑卒中之间的关系。方法 选取急性脑卒中患者作为研究对象,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 急性脑卒中患者FINS显著高于对照组（P＜0．01）,其ISI较对照组显著降低（P＜0．01）。脑梗死组FINS显著高于脑出血组（P＜0．05）,其ISI较脑出血组显著降低（P＜0．05）。结论 急性脑卒中患者存在IR,IR为其重要的危险因素,尤其是脑梗死患者IR比脑出血患者更为敏感。     

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。     

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。     

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.     

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.     

葡萄糖及胰岛素对高血压大鼠脑梗塞的影响

目的　为研究葡萄糖、胰岛素对高血压大鼠脑梗塞的不同影响。　　方法　采用易卒中型肾血管性高血压大鼠 ,在单侧大脑中动脉闭塞术前半小时分别腹腔注射葡萄糖、胰岛素和生理盐水 ,术后 2 4小时观察动物神经症状并处死动物 ,用光镜进行脑组织病理观察。　　结果　葡萄糖组脑缺血和脑水肿较对照组严重 ,并且伴有皮层下白质出血 ;而胰岛素组脑缺血和脑水肿较对照组轻微 ,未见皮层下白质出血现象。　　结论　葡萄糖可加重脑缺血性损害 ,而胰岛素具有防治脑缺血性损害的作用。