葛根与丹参对2型糖尿病大鼠模型胰岛素抵抗的影响

观察中药葛根、丹参对实验性2型糖尿病大鼠胰岛素抵抗的作用。用高热量饲料加小剂量链脲佐菌素(STZ)(30 mg/kg)注射复制2型糖尿病大鼠模型,经葛根、丹参治疗6周,测定大鼠空腹血糖、血脂、血清胰岛素等含量,并计算出胰岛素敏感指数;葛根能显著降低糖尿病大鼠空腹血糖、血脂的含量,提高胰岛素敏感指数;葛根通过改善糖脂代谢,提高胰岛素的敏感性,具有改善实验性2型糖尿病大鼠胰岛素抵抗的作用。     

2型糖尿病脂代谢紊乱及胰岛素抵抗与视网膜病变的关系

测定了80例2型糖尿病和30例正常对照组的血脂谱、空腹血糖（FBG）、糖化血红蛋白（HbAlc）、空腹胰岛素（FISN）、胰岛素敏感指数（ISI）等指标并进行比较分析,将糖尿病患者分为：非糖尿病视网膜病变组（NDR）、背景期DR（BDR）及增殖期DR（PDR）。结果表明：与正常对照组比较,糖尿病各组HbAlc、FINS、FBG、甘油三酯（TG）、总胆固醇（TC）、低密度脂蛋白（LDL）、载脂蛋白-B（Apol-B）、载脂蛋白-A／B显著升高（P〈0．05或0．01）,ISI、高密度脂蛋白（HDL-C）则明显降低（P〈0．05或0．01）,各组之间载脂蛋白-Al（Apol-Al）含量无显著性差异（P〉0．05）;糖尿病各组间进行两两比较,TG、HbAlc在NDR组、BDR组、PDR组中逐渐升高,ISI则依次降低（P〈0．05）,BDR组、PDR组FINS明显高于NDR组（P〈0．05）．但PDR组和BDR组之间差异无显著性（P〉0．05）,各糖尿病组间的FBG、TC、LDL、Apol-B、Apol-A／B无显著性差异（P〉0．05）。说明脂代谢紊乱及胰岛素抵抗可能与2型糖尿病视网膜病变关系密切。     

运动对2型糖尿病胰岛素抵抗相关因子的影响研究

通过分析运动对2型糖尿病胰岛素抵抗的相关因子的影响,发现2型糖尿病主要是胰岛素抵抗和胰岛素分泌受损所导致.因此,只要了解胰腺β细胞的胰岛素抵抗程度,就可以加以弥补,使葡萄糖耐受性维持正常.     

2型糖尿病对动脉粥样硬化的影响机制

2型糖尿病的主要特征是胰岛素抵抗和胰岛素分泌相对不足,研究表明胰岛素具有抗炎的功能,胰岛素抵抗或胰岛素分泌相对不足会促进炎症反应。动脉粥样硬化是一种动脉壁炎症性疾病,包括内皮功能异常,单核细胞募集,白细胞粘附及迁移,氧化型低密度脂蛋白(ox-LDL)被巨噬细胞摄取,泡沫细胞形成,最终形成粥样斑块。2型糖尿病对动脉粥样硬化的影响是多方面的,包括加剧炎症反应、糖基化终末产物的增加和糖脂代谢紊乱等。本文主要从炎症角度分析,阐明炎症反应与胰岛素抵抗互作的机理,对于2型糖尿病和动脉粥样硬化的预防及治疗具有十分重要的意义。     

壳寡糖胍对胰岛素抵抗及相关蛋白的作用

针对壳寡糖胍(COSG)对动物体内胰岛素抵抗治疗效果及相关机制尚不明确的问题,建立高脂高糖饮食联合链脲佐菌素诱导的2型糖尿病(T2DM)大鼠模型,并进行COSG灌胃给药治疗8周,研究COSG对T2DM大鼠体内胰岛素抵抗及相关信号通路的影响.结果显示,COSG可明显降低T2DM大鼠血清中总胆固醇(TC)、甘油三酯(TG)和低密度脂蛋白(LDL)水平并提高血清中高密度脂蛋白(HDL)水平;此外,COSG可下调T2DM大鼠的空腹血糖(FBG)和空腹胰岛素(FINS)含量,并减小T2DM大鼠胰岛素抵抗指数(HOMA-IR).进一步研究相关蛋白发现,COSG可抑制骨骼肌中p38丝裂原活化蛋白激酶(p38 MAPK)的磷酸化以及提高胰岛素受体底物-1(IRS-1)酪氨酸位点的磷酸化,并提高蛋白激酶B(AKT)的磷酸化水平和促进葡萄糖转运蛋白4(GLUT4)转移至细胞膜,从而促进细胞对葡萄糖的摄取;另外,COSG还可以降低磷酸烯醇式丙酮酸羧激酶(PEPCK)和肌糖原水平,进而抑制糖异生.从而,COSG达到改善胰岛素抵抗的作用.总之,COSG可改善T2DM大鼠胰岛素抵抗,具有良好的应用前景.     

糖尿病家系人群脂代谢紊乱和胰岛素抵抗调查

探讨2型糖尿病家系成员血脂水平和胰岛素抵抗的相互关系.选取重庆地区2型糖尿病家系中153例非糖尿病一级亲属为研究对象,进行标准75 g葡萄糖耐量(OGTT)试验,排除诊断符合1997年美国糖尿病协会标准的糖尿病患者,研究中脱落及资料不全28人,最后纳入非糖尿病一级亲属125例.通过观察和评估得出: ①评价胰岛素抵抗的HOMA-IR,高血脂组明显高于血脂正常组,P<0.01;②高血脂组HOMA-IR和TC、TG、LDL-C呈显著正相关,其中TG的相关性最强,P<0.01.HOMA-IR和HDL-C无显著相关性.从而验证了糖尿病高危人群中脂代谢紊乱和胰岛素抵抗有密切关系.     

青蒿素治疗胰岛素抵抗和2型糖尿病“异病同治”作用机制的网络药理学探析

目的:探讨青蒿素治疗胰岛素抵抗(IR)和2型糖尿病(T2D)的潜在分子机制。方法:运用Swiss Target Prediction平台数据库、Pubchem数据库、UniProt数据库筛选出青蒿素的药物作用靶点基因,然后用GenCards、STRING、DAVID数据库和Cytoscape3.7.1软件对青蒿素进行网络药理学分析,然后将青蒿素与核心靶点用AutoDock4.5.6和AutoDock vina进行分子对接验证。结果:青蒿素-IR和青蒿素-T2D的共同靶点分别为2207个和3245个。青蒿素-IR共同靶点的PPI网络共包含节点46个、边140条。青蒿素-T2D共同靶点的PPI网络共包含节点47个、边143条。青蒿素-IR共同靶点共富集到GO功能条目185条,KEGG信号通路120条(P<0.05)。青蒿素-T2D共同靶点富集到GO功能条目178条,KEGG信号通路127条(P<0.05)。青蒿素治疗胰岛素抵抗可能是通过EGFR、HSP90AA1等核心靶点基因,作用于MAPK信号通路、癌症途径等多条关键信号通路来实现的;青蒿素治疗2型糖尿病可能是通过EGFR、C...     

PPARγ及与胰岛素抵抗的研究进展

综述了近年来PPARγ受体分型、结构及在糖尿病发病机制中的作用     

甘丙肽拮抗剂M35对糖尿病大鼠胰岛素抵抗的影响

探讨甘丙肽拮抗剂（Galantide）M35对运动糖尿病大鼠胰岛素抵抗的影响。糖尿病大鼠随机分为4组：糖尿病安静组、糖尿病运动组、糖尿病安静M35组、糖尿病运动M35组。用药组腹腔注射甘丙肽拮抗剂M35,对照组腹腔注射同剂量的生理盐水。用正糖钳方法、血浆胰岛素浓度和骨骼肌葡萄糖转运蛋白4（GLUT4）含量来了解胰岛素抵抗水平。糖尿病M35组实验前血浆胰岛素浓度和实验后相比,呈非常显著性降低;糖尿病安静M35组骨骼肌葡萄糖输注速率、GLUT4蛋白含量比糖尿病运动M35组均降低。甘丙肽拮抗剂降低了糖尿病运动大鼠的胰岛素敏感性,其机理可能是抑制GLUT4的活性或降低GLUT4的转位实现的。     

Mechanisms linking obesity to insulin resistance and type 2 diabetes

Obesity is associated with an increased risk of developing insulin resistance and type 2 diabetes. In obese individuals, adipose tissue releases increased amounts of non-esterified fatty acids, glycerol, hormones, pro-inflammatory cytokines and other factors that are involved in the development of insulin resistance. When insulin resistance is accompanied by dysfunction of pancreatic islet beta-cells - the cells that release insulin - failure to control blood glucose levels results. Abnormalities in beta-cell function are therefore critical in defining the risk and development of type 2 diabetes. This knowledge is fostering exploration of the molecular and genetic basis of the disease and new approaches to its treatment and prevention.     

Serum retinol binding protein 4 contributes to insulin resistance in obesity and type 2 diabetes

In obesity and type 2 diabetes, expression of the GLUT4 glucose transporter is decreased selectively in adipocytes. Adipose-specific Glut4 (also known as Slc2a4) knockout (adipose-Glut4(-/-)) mice show insulin resistance secondarily in muscle and liver. Here we show, using DNA arrays, that expression of retinol binding protein-4 (RBP4) is elevated in adipose tissue of adipose-Glut4(-/-) mice. We show that serum RBP4 levels are elevated in insulin-resistant mice and humans with obesity and type 2 diabetes. RBP4 levels are normalized by rosiglitazone, an insulin-sensitizing drug. Transgenic overexpression of human RBP4 or injection of recombinant RBP4 in normal mice causes insulin resistance. Conversely, genetic deletion of Rbp4 enhances insulin sensitivity. Fenretinide, a synthetic retinoid that increases urinary excretion of RBP4, normalizes serum RBP4 levels and improves insulin resistance and glucose intolerance in mice with obesity induced by a high-fat diet. Increasing serum RBP4 induces hepatic expression of the gluconeogenic enzyme phosphoenolpyruvate carboxykinase (PEPCK) and impairs insulin signalling in muscle. Thus, RBP4 is an adipocyte-derived 'signal' that may contribute to the pathogenesis of type 2 diabetes. Lowering RBP4 could be a new strategy for treating type 2 diabetes.     

Leptin reverses insulin resistance and diabetes mellitus in mice with congenital lipodystrophy.

Congenital generalized lipodystrophy (CGL) is a rare autosomal recessive disorder characterized by a paucity of adipose (fat) tissue which is evident at birth and is accompanied by a severe resistance to insulin, leading to hyperinsulinaemia, hyperglycaemia and enlarged fatty liver. We have developed a mouse model that mimics these features of CGL: the syndrome occurs in transgenic mice expressing a truncated version of a nuclear protein known as nSREBP-1c (for sterol-regulatory-element-binding protein-1c) under the control of the adipose-specific aP2 enhancer. Adipose tissue from these mice was markedly deficient in messenger RNAs encoding several fat-specific proteins, including leptin, a fat-derived hormone that regulates food intake and energy metabolism. Here we show that insulin resistance in our lipodystrophic mice can be overcome by a continuous systemic infusion of low doses of recombinant leptin, an effect that is not mimicked by chronic food restriction. Our results support the idea that leptin modulates insulin sensitivity and glucose disposal independently of its effect on food intake, and that leptin deficiency accounts for the insulin resistance found in CGL.     

植物抗旱机制研究进展

干旱影响了植物的正常生长发育,导致植被减少和草地退化等现象。通过微观角度,阐述了形态指标、生长指标、生理生化指标以及其他酶类与抗旱机制之间的关系并进行了较为全面的综述,对植物抗旱机制的研究现状及发展进行了探讨。     

梁-柱节点抗连续倒塌性能研究进展

结构的连续性倒塌一直是土木工程领域关注的焦点,而梁柱节点作为结构体系传递荷载的关键部位,其一旦遭受破坏,就可能造成结构连续性的倒塌倾覆,进而造成无法估量的损失。本文简要介绍了整体结构的两种不同的连续倒塌的形式以及四类主要的抗倒塌设计方法,结合已有研究成果从抗连续倒塌模式、抗连续倒塌机制以及抗连续倒塌性能三个方面总结了节点破坏导致的连续性倒塌研究现状。结合应用及研究热点,从试验研究和数值分析角度分别对装配式梁柱节点和自复位梁柱节点的研究进展进行了阐述。最后提出一种基于超弹性形状记忆合金的新型自复位梁柱节点,并对设计方法、抗倒塌性能以及抗震性能的研究进行了探讨。     

CO_2增稠剂研究述评

在液体CO2压裂和CO2驱提高采收率中,都要使用稠密的CO2。由于其黏度较低,导致压裂施工时支撑剂沉降过快、砂比较小、滤失较大;CO2驱时极易沿高渗带窜流,严重影响其波及效率。为了解决这一难题,在稠密CO2中加入增稠剂,可以提升悬砂效果,降低滤失,增大波及体积。目前国内CO2稠化研究进展缓慢。基于对国内外CO2增稠剂研究的梳理总结,对研发过程中的主要问题进行分析,并在此基础上,展望CO2增稠剂的未来研究方向,以期推动国内CO2稠化剂的研究。     

TiO2光催化剂的研究进展

TiO2作为光催化剂在废水废气净化、抗菌环保等领域有着广泛的应用.对TiO2光催化剂的的性质、制备方法、表面改性及其作为光催化剂时的应用领域进行了详细的评述.     

Remission in models of type 1 diabetes by gene therapy using a single-chain insulin analogue

A cure for diabetes has long been sought using several different approaches, including islet transplantation, regeneration of beta cells and insulin gene therapy. However, permanent remission of type 1 diabetes has not yet been satisfactorily achieved. The development of type 1 diabetes results from the almost total destruction of insulin-producing pancreatic beta cells by autoimmune responses specific to beta cells. Standard insulin therapy may not maintain blood glucose concentrations within the relatively narrow range that occurs in the presence of normal pancreatic beta cells. We used a recombinant adeno-associated virus (rAAV) that expresses a single-chain insulin analogue (SIA), which possesses biologically active insulin activity without enzymatic conversion, under the control of hepatocyte-specific L-type pyruvate kinase (LPK) promoter, which regulates SIA expression in response to blood glucose levels. Here we show that SIA produced from the gene construct rAAV-LPK-SIA caused remission of diabetes in streptozotocin-induced diabetic rats and autoimmune diabetic mice for a prolonged time without any apparent side effects. This new SIA gene therapy may have potential therapeutic value for the cure of autoimmune diabetes in humans.     

增强不锈钢表面耐蚀性的研究进展

不锈钢是使用范围广泛且环保的一种耐蚀材料,但不锈钢在空气中自钝化形成的氧化膜的耐蚀性不佳,因此后续钝化处理是提高不锈钢表面耐蚀性的重要方法.本文综述了提高不锈钢表面耐蚀方法的研究进展.介绍不锈钢的钝化机理、硝酸钝化方法与柠檬酸钝化方法的最佳工艺.总结动电位极化曲线、电化学阻抗谱、Mott-Schottky曲线、循环伏安法和磨损-电化学腐蚀共五种不锈钢钝化膜耐蚀性测试方法.梳理塑性变形对不锈钢耐蚀性的影响,强调适度的塑性变形能够提高不锈钢耐蚀性.展望不锈钢钝化处理及塑性变形增强不锈钢钝化效应的研究趋势.