血糖波动与认知功能障碍关系研究进展

糖尿病是一组以高血糖为特征的慢性代谢性疾病，研究发现，糖尿病诱发认知障碍的发生、发展不仅与整体血糖水平升高有关，而且与患者的血糖波动密切相关。血糖波动影响认知功能，认知功能主要与NMDA受体的表达密切相关，故本文综述了血糖波动的原因、危害，并且从氧化应激、细胞凋亡、脑血管病变、胰岛素和胰岛素抵抗及突触可塑性的改变等方面阐述血糖波动对认知功能障碍影响的可能作用机制。     

眼底动脉硬化与血压、血糖、血脂的多元分析与评估

目的探讨眼底动脉硬化与血压、血脂、血糖的相关性，评估中风危险度。方法对2004年5月至2008年10月就诊的患者335例，作为观察组，并与无症状的健康体检者180例作对照，动态检测眼底动脉硬化、血压、血糖、血脂的异常变化，并做综合量化评估。结果脑血管疾病与眼底动脉硬化、血压、血糖、血脂等因素密切相关。结论眼底动脉硬化、血糖、血脂、血压异常的量化评分，能够预估中风，以便采取预防性治疗。     

二甲双胍治疗2型糖尿病患者78例血糖、血脂、体重的观察

2型糖尿病并发症的发生、发展与空腹血糖、餐后血糖和血脂等代谢紊乱相关，了解它们之间的关系及用药后的变化，可以有效地防治2型糖尿病及其并发症。     

国外糖尿病教育模式例析

临床研究提示，糖尿病患者血糖控制与生活质量的好转，除了接受科学的治疗外，饮食控制、血糖监测、适量运动、合理用药等糖尿病教育与管理发挥着非常关键的作用。糖尿病教育与管理已经引起国内外专家的高度重视。     

68例严重颅脑损伤患者血糖水平与颅内压和预后的临床分析

目的：探讨严重颅脑损伤患者血糖水平与病情严重程度及颅内压和预后的关系。方法：分析68例严重颅脑损伤患者，血糖变化与颅内压及治疗效果的关系。结果：68例严重颅脑损伤患者，根据格拉斯哥昏迷量表计分分组，在入院时34分组的血糖水平高于7分组，根据治疗结果分组，术后的血糖水平比较，效果差组明显高于效果良好组。颅内压与入院时血糖水平无明显的相关，然而在术后24h内最大颅内压值和术后血糖水平相关，术后血糖值越高其颅内压也越高。结论：血糖水平与脑损伤的严重程度、颅内压及治疗效果相关，血糖越高病情越严重；术后血糖越高，颅内压越高，治疗效果越差，预后不良。血糖水平是判断严重颅脑损伤预后的重要指标之一。     

动态血糖监测仪

为了方便糖尿病患血糖的监测，新研制的动态血糖检测仪，具有检测功能强、体积小、使用方便、痛苦小等特点。它是由探测头和血糖记录器组成的，使用时，把图钉大小、内有血糖感觉芯片的探测头植入患腹部皮下，体外呼机般大小的记录器就可每10秒钟从测试头接受一次电信号，动态血糖监测仪可连贯地记录患血糖变化，包括夜间的系列血糖数据。医生根据患血糖变化制定出准确的治疗方案。     

2型糖尿病患者血清瘦素水平与血糖、胰岛素、C肽含量的关系

目的:探讨2型糖尿病患血清瘦素水平与血糖、胰岛素、C肽含量的变化。方法：应用放免法测定瘦素、胰岛素和C肽含量，生化法测定血糖。结果：2型糖尿病患女性瘦素水平高于男性，老年人瘦素水平高于中青年人，肥胖组高于非肥胖组，与血糖、C肽浓度呈正相关，与胰岛素浓度呈负相关。结论：血清瘦素水平存在有性别、年龄及体型等方面差异，其变化是否与性激素的调控和瘦素基因表达的下游环节障碍有关尚待研究。     

糖尿病病人血糖连续监测的临床意义

对糖尿病病人血糖进行连续监测，是了解患者的血糖控制情况、判断降糖治疗效果、调整治疗方案、指导临床用药的前提和基础。以往血糖监测要抽患者静脉血，给病人带来一定的痛苦和不便，一般病人不愿意合作，客观上给连续检测血糖带来一定的困难，现丰我们采用手掌式血糖仪对病人外周微量末梢血进行血糖监测，具有微量、方便、微创等特点，其方式已为越来越多的糖尿病病人所了解和接受，开展以来，取得了比较满意的效果，现介绍如下：     

肾综合征出血热痊愈1年后胰岛功能的观察

目的 研究肾综合征出血热合并高血糖病人在肾综合征出血热痊愈1年后的血糖变化情况和胰岛功能状况。方法 对48例肾综合征出血热合并高血糖病人痊愈1年后随访，测定空腹血糖、胰岛素，计算胰岛素敏感指数、胰岛细胞分泌指数，对血糖仍高组与血糖恢复组及正常对照组进行比较。结果 血糖仍高组HOMA—IR高于正常对照组和血糖恢复正常组、血糖仍高组HOMA—IR低于正常对照组和血糖恢复正常组，差异有显著意义。结论 肾综合征出血热合并高血糖病人，57．14％的高血糖为一过性，与应激及治疗有关。42．86％的高血糖为持续性，其原因与胰岛素抵抗和胰岛细胞分泌功能下降均有关，与胰岛素抵抗的关系更明显。     

肢端水肿患者不同采血部位快速血糖值的对比分析

近年来，糖尿病发病率呈逐年上升趋势。在多数危重情况下，机体会出现应激性血糖升高，为准确观察病情，及时发现患者的低血糖、高血糖症状，外周毛细血管的快速血糖监测成为重要的检查项目，检测结果对指导临床抢救意义重大。快速血糖监测部位通常是手指无名指末端指尖侧面，但临床上由于病情复杂或药物作用等因素，许多急危重症患者多伴有肢端水肿。这种情况下末梢血液被挤出的组织液稀释，会导致末梢血糖水平低于同时的静脉血糖水平，不能准确反映患者的真实血糖水平。为探讨不同采血部位对肢端水肿患者快速血糖值的影响，本研究对30例肢端水肿患者进行静脉快速血糖、静脉生化血糖、耳垂快速血糖的检测，并与无肢端水肿患者进行对比研究，以证实肢端水肿患者水肿处血糖值异常，采取耳垂部位快速血糖监测简便快捷、准确可靠，能够替代肢端血糖值。     

Effect of calcium dobesilate on the inhibition of collagen fibrillogenesis by glucose in vitro

Glucose inhibits collagen fibril formation as shown in an in vitro system using thermal fibrillogenesis of collagen type I and type II solutions containing different concentrations of glucose. Studies of the time course and extent of fibril formation indicate that glucose values similar to subjects with normal glucose metabolism effect no significant difference to the control without glucose, whereas high glucose levels mimicking glucose concentrations of diabetics with poor glucose control, significantly delay collagen fibrillogenesis. By defined concentrations of calcium dobesilate (Doxium) the effect of a pathologically high glucose content of collagen fibril formation can be inversed to parameters similar as observed with glucose concentrations of a subject with normal glucose metabolism.     

Reduction of hepatic glucose production as a therapeutic target in the treatment of diabetes

There has been an alarming increase in the population diagnosed with diabetes worldwide. Although there is an ongoing debate as to the role of liver in the pathogenesis of diabetes, reduction of hepatic glucose production has been targeted as a strategy for diabetes treatment. Indeed, reduction of hepatic glucose production can be achieved through modulation of both hepatic and extra-hepatic targets. This review describes the role of the liver in the control of glucose homeostasis. Gluconeogenesis and glycogenolysis are pathways for glucose production, whereas glycolysis and glycogenesis are pathways for glucose utilization/storage. At the biochemical and molecular level, the metabolic and regulatory enzymes integrate hormonal and nutritional signals and regulate glucose flux in the liver. Modulating either activities of or gene expression of these metabolic enzymes can control hepatic glucose production. Dysfunction of one or several enzyme(s) due to insulin deficiency or resistance results in increases in fluxes of glycogenolysis and gluconeogenesis and/or decreases in fluxes of glycolysis and glycogenesis, which thereby lead to glucose generation exceeding glucose consumption/disposal, as well as dysregulation of lipid metabolism. Activation of enzymes that promote glucose utilization/storage and/or inhibition of enzymes that reduce glucose generation achieve reduction of hepatic glucose production, and hence lower levels of plasma glucose in diabetes. This is also beneficial for the correction of dyslipidemia. Therefore, many enzymes are viable therapeutic targets for diabetes.     

DEMONSTRATION OF DEFECTIVE GLUCOSE UPTAKE AND STORAGE IN ERYTHROCYTES FROM NON-INSULIN DEPENDENT DIABETIC PATIENTS AND EFFECTS OF METFORMIN

1. Red blood cells can store glucose and may thus participate in blood glucose homeostasis. We investigated if a defect in this process exists in non-insulin dependent diabetes (NIDD). 2. Blood was obtained in fasting conditions from 10 normal and 10 newly diagnosed NIDD patients (before and after 4 weeks Metformin therapy). Washed erythrocytes were resuspended in media containing various glucose concentrations (4.4, 6.6, 8.8 and 13.2 mmol/L). Total glucose uptake was calculated as the sum of the measurements of lactate as well as free glucose, the latter being determined before and after addition of amyloglucosidase to the pellet. 3. Cells from diabetics showed a pronounced reduction in glucose uptake, particularly in their capacity to store glucose as glycogen (reactive to amyloglucosidase). Metformin treatment almost normalized glycogen levels, whereas lactate declined concomitantly in the pellet. 4. Our data demonstrate that a defect in glucose uptake exists in erythrocytes from NIDD patients, affecting both free and stored glucose, and that this defect is reversed by Metformin treatment, indicating that this drug can increase glycogen levels even in insulin-insensitive cells. 5. Thus, in view of their total mass, erythrocytes may be important in the impaired glucose homeostasis in NIDD, in particular in marked hyperglycaemia such as after a meal.     

应用无水葡萄糖制备注射剂的工艺

目的：对无水葡萄糖制备注射剂工艺进行探讨,方法：以无水葡萄糖为原料,经采用改革后的工艺制备葡萄糖注射液达150批次30万瓶。结果：可提高葡萄糖注射液的质量,减少生产工序,节省时间,降低生产成本,降低生产成本,结论：应用无 表了国际输液生产原料的流行趋势,其改革后的工艺值得推广应用。     

POCT血糖仪与生化分析仪血糖检测结果的比对试验及分析

目的对比床旁检测（POCT）血糖仪与生化分析仪对血糖测定的结果 ,对POCT血糖仪的精密度与准确度进行探讨。方法选用4台POCT血糖仪对同一标本进行测定,并比较贝克曼CX-9生化分析仪与POCT血糖仪的测定结果。结果贝克曼CX-9生化分析仪与POCT血糖仪的测定结果高度相关（P〉0.05）,差异不具有统计学意义。结论 POCT血糖仪与生化分析仪对血糖的测定结果具有一致性,且方便快捷,可作为急诊的检测方法,值得在临床过程中推广、应用。     

肌酸激酶同工酶试剂对血糖测定的干扰及排除

目的：观察肌酸激酶同工酶试剂（CK-MB）对血糖测定的干扰及排除。方法：将新鲜混合血清作为样品,进行以下试验,①单独测定血糖60次,测定结果作为对照组;②CK-MB与血糖同时测定60次,血糖结果作为测定组1;③CK-MB与血糖两个项目之间加入项目TP、ALB、TG、TC、BUN、CRE测定60次,血糖结果作为测定组2;④测定CK-MB后,加入试剂针（R1）特殊冲洗功能,测定血糖60次,血糖结果值作为测定组3。3个测定组结果分别与对照组结果进行比较。结果：对照组与3个测定组的血糖分别是（5.75±0.03）mmol/L、（8.01±0.15）mmol/L、（5.77±0.06）mmol/L、（5.78±0.07）mmol/L,测定组1与对照组结果比较,测定组1血糖结果明显高于对照组,差异有高度统计学意义（P〈0.01）;测定组2和测定组3分别与对照组结果比较,差异均无统计学意义（P〉0.05）。将CK-MB试剂R1、R2作为标本测定血糖20次,R1血糖为（28.67±0.09）mmol/L,R2血糖为（0.03±0.005）mmol/L。结论：CK-MB试剂R1对血糖测定有干扰,通过试剂针特殊冲洗功能和项目间隔可予以排除。     

洛伐他汀发酵培养基配方优化及15L罐放大

利用响应面方法对土曲霉生产洛伐他汀的培养基进行了优化，使用两水平因子实验对培养基中的碳、氮源组分：葡萄糖、豆粕、蛋白胨、麦精和硝酸钠对洛伐他汀效价的影响进行分析，发现主要的影响因素为葡萄糖和豆粕。通过进一步中心组合实验，考察葡萄糖和豆粕浓度对菌浓、效价、残糖浓度、单位菌体产量（Yp/x）和得率（Yp/s）的作用。并通过引进残糖浓度为参考，得到最优的葡萄糖和豆粕配比分别为22％和5％，结果比对照提高了17％。同时在15L发酵罐上放大，确定最适初始葡萄糖浓度为21％，效价为7．34g／L。     

Effects of mercuric chloride on glucose transport in 3T3-L1 adipocytes.

Mercury, as well as the other Group IIB metals, stimulates glucose transport in adipocytes. Here we characterize the action of mercury on adipocyte glucose transport and examine several potential mechanisms of action. Mercury exposure causes a modest (compared to insulin) 1.8-fold increase in glucose transport. This glucose transport corresponds with an increase in GLUT 1, but not GLUT 4 glucose transporters. Phosphorylation of p38 kinase and c-Jun N-terminal kinase (JNK) were examined as possible mediators of mercury induced GLUT 1 levels. Phosphorylation of p38 kinase, but not JNK, increased with mercury exposure. Activation of p38 and an increase in glucose transport corresponding to an increase in GLUT 1 are indicative the induction of a stress response, which can contribute to the induction of insulin resistance in adipocytes. However, inhibition of p38 by the p38 inhibitor SB203580 did not prevent mercury-mediated glucose uptake. While the magnitude of the action of mercury is modest, its effects were sustained over many days of exposure and impacted subsequent insulin-mediated glucose transport. Pre-treatment with HgCl2 decreased insulin-mediated glucose transport 1.3-fold suggesting that exposure to mercury may contribute to pathologies associated with glucose homeostasis.     

Interference of maltose, icodextrin, galactose, or xylose with some blood glucose monitoring systems

Maltose, a disaccharide composed of two glucose molecules, is used in a number of biological preparations as a stabilizing agent or osmolality regulator. Icodextrin, which is converted to maltose, is present in a peritoneal dialysis solution. Galactose and xylose are found in some foods, herbs, and dietary supplements; they are also used in diagnostic tests. When some blood glucose monitoring systems are used--specifically, those that use test strips containing the enzymes glucose dehydrogenase-pyrroloquinolinequinone or glucose dye oxidoreductase--in patients receiving maltose, icodextrin, galactose, or xylose, interference of blood glucose levels can occur. Maltose, icodextrin, galactose, and xylose are misinterpreted as glucose, which can result in erroneously elevated serum glucose levels. This interference can result in the administration of insulin, which may lead to hypoglycemia. In severe cases of hypoglycemia, deaths have occurred. If patients are receiving maltose, icodextrin, galactose, or xylose, clinicians must review the package inserts of all test strips to determine the type of glucose monitoring system being used and to use only those systems whose tests strips contain glucose oxidase, glucose dehydrogenase-nicotinamide adenine dinucleotide, or glucose dehydrogenase-flavin adenine dinucleotide.     

Glucose phosphorylation as a barrier to muscle glucose uptake

1. Glucose phosphorylation is the first irreversible step of the muscle glucose uptake pathway and is catalysed by a hexokinase isozyme. 2. While glucose transport is the primary barrier to muscle glucose uptake during basal conditions, glucose phosphorylation becomes an important barrier to muscle glucose uptake during stimulated conditions such as hyperinsulinaemia or exercise. 3. High fat feeding markedly impairs insulin- and exercise-stimulated muscle glucose uptake. As hexokinase II overexpression corrects this dietary-induced deficit during exercise, glucose phosphorylation is a site of impairment following high fat feeding. 4. Exercise is an important tool for diagnosing deficits in glucose phosphorylation.