Ⅱ型糖尿病患者红细胞膜葡萄糖运输特性研究

红细胞膜葡萄糖运输的温度依赖性研究结果表明,Ⅱ型糖尿病患者的葡萄糖输入的活化能比正常增大约30%,这和患者葡萄糖输入速率减小的结果相一致.但葡萄糖跨膜输出的活化能没有显著变化.对在红细胞葡萄糖转运蛋白(GLUT1)内侧特异结合的细胞松弛素B(CB)的抑制效应研究结果表明,糖尿病人的CB抑制常数无明显变化.结合以前我们用根皮素抑制剂的实验,表明Ⅱ型糖尿病患者红细胞膜上GLUT1很可能发生了结构的变化,发生变异的位点在在此膜蛋白的膜外侧区域.     

Ⅱ型糖尿病患者红细胞膜葡萄糖运输体异常的研究

用葡萄糖跨膜运输蛋白的抑制剂－根皮素,观察到它对Ⅱ型糖尿病患者红细胞膜葡萄糖输入的抑制常数显著增大,提示了患者葡萄糖运输体外侧和底物分子结合位点发生了结构改变。进一步,测量了和膜上葡萄糖运输体能特异结合的葡萄糖、细胞松弛素Ｂ、根皮素等对血影膜上色氨酸残基荧光的淬灭效应。由淬灭效应前后血影膜荧光强度的相对变化,证实患者红细胞膜对葡萄糖转运功能的异常和运输蛋白中某些色氨酸残基（特别是膜外侧区段）周围结构的改变有关。     

红细胞膜对葡萄糖运输的快速测定

介绍了一种快速测定红细胞膜对葡萄糖运输特性的方法.实验表明,介质中红细胞的体积变化可用660nm波长处光密度值的变化来表证,由此得出葡萄糖跨膜通透过程中细胞内葡萄糖量的表达式.根据这种变化率即可计算出葡萄糖的通透特性参数K_m及I_(mdx)~(?)为提高测定精度,改装了仪器并联微机进行实时处理.     

Ⅱ型糖尿病的红细胞膜GPA基因表达

为了研究Ⅱ型糖尿病（ＮＩＤＤＭ）患者红细胞膜血型糖蛋白Ａ（ＧＰＡ）的基因表达,采用不连续聚蔗糖（Ｐｅｒｃｏｌ）密度梯度法分离１５名正常人和２５例ＮＩＤＤＭ患者外周血的网织红细胞,提取其总ＲＮＡ,继以Ｎｏｒｔｈｅｒｎ斑点杂交观测此两组的红细胞膜ＧＰＡ基因的表达水平．采用碱性磷酸酶酶联免疫检测完成红细胞膜ＧＰ的Ｗｅｓｔｅｒｎ印迹．结果表明,ＮＩＤＤＭ患者组红细胞膜ＧＰＡ的ｍＲＮＡ含量较正常人组显著增加（分别为１１．９２±１０．５和１０．１８±１．０８积分光密度,Ｐ＜０．０１）．免疫印迹图谱显示,有６例ＮＩＤＤＭ患者的区带３ａ、３ｂ界限模糊,３例的区带３ａ、３ｂ和４明显浅染．推测ＮＩＤＤＭ患者红细胞膜ＧＰＡ减少可能引起其基因表达呈代偿性增强,而障碍或许出现在翻译环节上,这些与ＮＩＤＤＭ患者红细胞变形能力（ＲＣＤ）的明显降低甚为相符．     

辛伐他汀对Ⅱ型糖尿病合并肾病葡萄糖代谢的研究

目的:探讨辛伐他汀治疗对Ⅱ型糖尿病(T2DM)合并肾病患者糖代谢水平的影响.方法:选取新乡医学院第一附属医院60名T2DM合并肾病患者行辛伐他汀治疗3个月.比较治疗前后空腹血糖(FBG)、游离脂肪酸(FFA)、脂联素(ANP)、C肽、HOMA-IR、胰岛素/葡萄糖比率(IGR)、胰岛素敏感指数(ISI)、空腹胰岛素水平(FINS)、C反应蛋白(CRP)、糖基化血红蛋白(HbA1c)水平等变化,以评价辛伐他汀对T2DM病合并肾病患者的治疗效果.结果:在辛伐他汀治疗3个月后的葡萄糖耐量试验(OGTT)中,对比治疗前,各时点血糖水平均显著下降(P＜0.05),而C肽与胰岛素在0 min和30 min时显著下降(P＜0.05).在辛伐他汀治疗后,HO-MA-IR、游离脂肪酸(FFA)、ISI、FINS、胰岛素AUC、血糖曲线下面积(AUC)、CRP、HbA1c、FBG与治疗前相比均显著下降(P＜0.05),尿白蛋白排泄率(UAER)也明显下降(P＜0.01),但是APN(P＜0.01)以及C肽AUC(P ＜0.05)均显著上升,而校正胰岛素反应(CIR)及IGR无显著变化(P＞0.05).结论:辛伐他汀治疗可以改善胰岛素抵抗,提高患者对胰岛素的敏感性,并显著降低血糖,从而改善T2DM合并肾病患者的糖代谢.     

型糖尿病患者红细胞膜中性糖、氨基糖及唾液酸含量的改变

 为阐明Ⅱ型糖尿病（ Ｎ Ｉ Ｄ Ｄ Ｍ ）患者红细胞膜的化学组成在非酶糖基化（ Ｎ Ｅ Ｇ）影响下发生的变化,采用毛细管气相色谱法和分光光度法测定了 ２０ 名正常人和 １９ 例Ⅱ型糖尿病患者红细胞膜的 ４ 种结合中性糖与 ２ 种氨基糖和唾液酸含量以及 ４ 种寡糖链上的末端中性糖和唾液酸含量．结果表明, Ｎ Ｉ Ｄ Ｄ Ｍ 患者红细胞膜几种结合单糖（ Ｇｌｃ, Ｆｕｃ, Ｇｌｃ Ａ, Ｇａｌ Ａ）与游离单糖（ Ｇｌｃ, Ｇａｌ, Ｍａｎ, Ｆｕｃ）含量以及唾液酸含量均较正常对照组明显降低（ Ｐ＜ ００１ 或 ００５）．据此推测,由于患者红细胞膜蛋白的重度糖基化导致某些膜结构蛋白的氧化损伤,细胞膜糖类含量的减少,可能是重度糖基化的继发后果．     

复方金线莲胶囊治疗Ⅱ型糖尿病初步研究

经药效学、急性毒性及临床初步观察表明,复方金线莲胶囊对Ⅱ型糖尿病有明显的疗效。     

Ⅱ型糖尿病动物模型的构建

动物模型在Ⅱ型糖尿病研究中发挥重要作用,对于深入研究糖尿病及其并发症的发病、预防、诊断和治疗有重要意义。本文就Ⅱ型糖尿病动物模型的构建进行了概述,对发展新型构建糖尿病模型的方法具有重要的参考价值。     

蝮蛇抗栓酶治疗Ⅱ型糖尿病256例分析

蝮蛇抗栓酶治疗Ⅱ型糖尿病２５６例分析刘淑珍李知森（山东省即墨市人民医院即墨２６６２００）（青岛市崂山区海军４０９医院青岛２６６１００）自１９８６年１月至１９９７年１月,两家医院共收治Ⅱ型糖尿病病人４８８例,其中２５６例应用蝮蛇抗栓酶治疗,效果良好,现...     

前列腺增生伴Ⅱ型糖尿病患者的尿流动力学分析

目的:探讨前列腺增生伴Ⅱ型糖尿病患者的尿流动力学改变,并对该类患者提出合理的治疗和处理。方法:选取从2010年9月~2013年9月在本院泌尿外科一病房行经尿道前列腺电切,术后病理诊断为前列腺增生术前行尿流动力学检查的患者349例,分为单纯前列腺增生组158例(对照组)及前列腺增生合并Ⅱ型糖尿病组191例(研究组),前列腺增生合并Ⅱ型糖尿病组又分为两个亚组,即空腹血糖≤6.1 mmol/L组(亚1组)96例及空腹血糖6.1 mmol/L组95例(亚2组)。比较各组患者尿流动力学各项检查结果。结果:1)、比较亚2组和对照组患者残余尿量、最大尿流率、最大尿流率时逼尿肌压、最大逼尿肌压及顺应性,P值均0.05。2)、亚1组和对照组患者残余尿量、最大尿流率、最大尿流率时逼尿肌压、最大逼尿肌压及顺应性,除亚1组病程5年的残余尿量、顺应性P值0.05外,其他均0.05。3)、亚1组和亚2组患者残余尿量、最大尿流率、最大尿流率时逼尿肌压、最大逼尿肌压及顺应性,P值均0.05。4)、亚1组和亚2组不稳定膀胱率明显高于对照组。结论:Ⅱ型糖尿病能加重前列腺增生患者膀胱功能障碍,及早控制血糖能减轻、延缓膀胱功能障碍。     

REGULATION OF A GLUCOSE TRANSPORT SYSTEM IN STICHOCOCCUS BACILLARIS1

Glucose and related non-metabolizable analogs were transported into cells of Stichococcus bacillaris Naeg. By a specific and active transport system. Glucose transport capacity was stimulated eight-fold by incubation in medium of low osmotic potential (0.09 osM). Stimulation occurred over 24 h in the dark and over 72 h in low osmotic medium. Inhibition of protein synthesis prevented any transport, stimulation from occurring. Kinetic studies revealed that the stimulation caused an increase in Ike maximal velocity of transport and did not affect the half-saturation constant for transport. It was concluded that incubation of cells in the dark or in low osmolar medium induces a synthesis of the transport system. The glucose analog 2-deoxy-D-glucose was only phosphorylated to a limited extent upon entry into the cells, and the free sugar accumulated linearly in dark pre-incubated tells for a period of at least six minutes to reach an intracellular/extracellular concentration ratio of almost 300. Glucose, in contrast, was rapid h converted to sucrose and other cell constituents. Cells incubated 24 h with, glucose or 6-deoxy-D-glucose did not exhibit any altered transport system activity. Cells incubated 24 h with 7 mM dibutyryl cAMP exhibited a 2.5-fold stimulation of transport activity. No stimulation was observed in cells treated only 30 min with dibutyryl cAMP.     

AXONAL TRANSPORT OF [3H]GLUCOSE RADIOACTIVITY IN THE OPTIC SYSTEM OF SCARDINIUS ERYTHROPHTHALMUS1

Abstract— The optic system of Scardinius erythrophthalmus has been used to study the axonal translocation of radioactivity from [³H]glucose. Intraocularly injected precursors were transported intra-axonally along the optic nerve towards the contralateral optic tectum. In comparison with the well known properties of axonal protein transport there were remarkable differences in the proximo-distal translocation of [³H]glucose. These were: (1) a delay in the labelling of the structures investigated, after tracer application; (2) only a rapid phase of transport; and (3) no accumulation of radioactivity in the region of nerve terminals in the optic tectum connected with the injected eye. The transported material was almost exclusively in the form of TCA-soluble compounds and was mainly glucose itself or its low molecular derivatives, but not glycogen. The rate of transport was decreased by lowered temperatures and was not immediately dependent on retinal protein synthesis. Colchicine blocked the axonal transport of glucose by up to 60–70 per cent.     

THE GLUCOSE TRANSPORT SYSTEM OF AMPHORA COFFEAEFORMIS (BACILLARIOPHYCEAE)1

Amphora coffeaeformis (Ag.) Kütz. var. perpusilla (Grun.) Cleve took up glucose by an inducible transport system. The system was induced by d -fructose, d -mannose, as well as glucose. Some d -pentoses also induced a glucose uptake system but it may not be the same one as that induced by hexose. d -fructose, d -mannose and 2-deoxy-d -glucose inhibited 2 mM glucose uptake at equimolar concentration, but d -pentoses did not. The uptake system decayed in ca. 5 h in the absence of glucose. The half-saturation constant for uptake, K₈ was ca. 0.1 mM glucose with a maximum uptake rate, V_max= 0.4 nmol/10⁶ cells-min^?1.     

REABSORPTION OF GLUCOSE IN THE RENAL SYSTEM OF VIVIPARUS

Glucose is reabsorbed from the pericardial fluid in Viviparusjaponicus, and not from the kidney or the ureter. The cpicardialcells of the ventricle are probably responsible (Received 30 October 1978;     

TRANSPORT OF VIRAL RNA IN KB CELLS INFECTED WITH ADENOVIRUS TYPE 2

Messenger RNA transport was studied in KB cells infected with the nuclear DNA virus adenovirus type 2. Addition of 0.04 µg/ml of actinomycin completes the inhibition of ribosome synthesis normally observed late after infection and apparently does not alter the pattern of viral RNA synthesis: Hybridization-inhibition experiments indicate that similar viral RNA sequences are transcribed in cells treated or untreated with actinomycin. The polysomal RNA synthesized during a 2 hr labeling period in the presence of actinomycin is at least 60% viral specific. Viral messenger RNA transport can occur in the absence of ribosome synthesis. When uridine-³H is added to a late-infected culture pretreated with actinomycin, viral RNA appears in the cytoplasm at 10 min, but the polysomes do not receive viral RNA-³H until 30 min have elapsed. Only 25% of the cytoplasmic viral RNA is in polyribosomes even when infected cells have been labeled for 150 min. The nonpolysomal viral RNA in cytoplasmic extracts sediments as a broad distribution from 10S to 80S and does not include a peak cosedimenting with 45S ribosome subunits. The newly formed messenger RNA that is ribosome associated is not equally distributed among the ribosomes; by comparison to polyribosomes, 74S ribosomes are deficient at least fivefold in receipt of new messenger RNA molecules.     

AXONAL TRANSPORT OF PROTEINS IN THE HYPOTHALAMO-NEUROHYPOPHYSIAL SYSTEM OF THE RAT

—Axonal transport of proteins in the hypothalamo-neurohypophysial system of the rat was studied after a local injection of [³⁵S]cysteine in the region of the supraoptic nucleus. The migration of labelled proteins was followed by measuring the specific radioactivity of the proteins in various parts of the hypothalamo-neurohypophysial tract. Between 2 and 4 h after the isotope injection there was a sharp increase in the protein-bound specific radioactivity of the posterior pituitary lobe, demonstrating that a transport of ³⁵S-labelled proteins had occurred from the supraoptic nucleus to the neurohypophysis. The rate of the transport was 2-3 mm/h. During the first 24 h after the injection a continuous accumulation of labelled material occurred in the neural lobe. Considerable radioactivity could still be recovered 6 days after the isotope injection. Fractionation of the neurohypophysial proteins by polyacrylamide gel electrophoresis revealed that approximately 90 per cent of the radioactivity of the soluble proteins was recovered in a single protein fraction. Labelling of this fraction was not observed until 2 h after isotope injection. The radioactivity increased markedly up to 4 h. It is suggested that this protein component is involved in the neurohypophysial response to osmotic stress since the protein disappeared from the posterior lobe upon dehydration of the rat.