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首页 > 医学词汇大全 > Hypoglycemia
Hypoglycemia

内分泌

关键词内分泌 临床研究术语 糖尿病

词汇介绍

拓展阅读

解析

Hypoglycemia   美 /,haɪpoglaɪ'simɪə/

       n. 低血糖症;血糖过低

       In the intensive insulin group, 17 percent had severe hypoglycemia compared to just 4 percent of those on standard insulin therapy. 在强化胰岛素治疗组,17%的患者出现了严重低血糖症而标准胰岛素治疗组仅4%出现。

概述

低血糖症是由体内主要能量来源的血糖(葡萄糖)水平极低引起的。低血糖通常与糖尿病的治疗有关。当血糖水平为70毫克/分升(mg/dL)或3.9毫摩尔/升(mmol/L)或更低时,必须立即治疗低血糖症。治疗包括快速使用高糖食物或饮料或药物将血糖水平恢复到正常范围。长期治疗需要识别和治疗低血糖的根本原因。临床表现如果血糖水平过低,症状和体征可能包括:心律不齐、疲劳、肤色苍白、颤抖、焦虑、出汗、饥饿、易怒、口腔周围有刺痛感、在睡觉时哭泣。随着低血糖症的恶化,症状和体征可能包括异常行为、视觉障碍、癫痫发

Hypoglycemia causes dysregulation of Neuregulin 1, ErbB receptors, Ki67 in cerebellum and brainstem during diabetes: Implications in motor function复制标题

低血糖导致糖尿病期间小脑和脑干中神经调节蛋白1、ErbB受体、Ki67的失调: 运动功能的意义

发表时间:2019-10-17

影响因子:2.8

作者: Madhavi Joshi

期刊:Behav Brain Res

Adult neurogenesis has added newer dimension to brain plasticity. Previously, regeneration in adult mammalian brain was considered rather unsuccessful due to several intrinsic and extrinsic factors. Neuregulin 1 (NRG1), the major signaling protein of neuregulin family, is implicated in migration, proliferation and differentiation of both neuronal and glial cells by binding to ErbB receptors including ErbB2, ErbB3 and ErbB4 via endocrine or juxtacrine signaling. Brain injury evokes NRG1-ErbB signals to trigger regeneration and replacement of the affected cells during adulthood and developmental stages. It is responsible for survival of newly formed neural cells in adult injured tissues by reducing oxidative stress and accelerating glucose transport via translocation of GLUT to meet the energy demand during cellular restoration. ErbB2 shows reduced rate of ligand dissociation and high activation of MAP-kinase; this significantly increases its receptor strength. Since it lacks a ligand binding domain, it requires hetero-dimerization with ErbB3 or ErbB4 for signal transduction. ErbB3, in turn, is a functional receptor possessing weak kinase activity. Re-expression of ErbB2 in adult brain is necessary for radial glia formation and loss of its activity disturbs neuronal migration. While ErbB3 is associated with proliferating cells, ErbB4 expression has been correlated with the appearance of a differentiated phenotype. Discrepancies in glucose metabolism and elevated oxidative stress are the major culprits of brain damage during diabetes. Excess extracellular glucose leads to activation of the polyol pathway, the hexosamine pathway and accumulation of advanced glycated end products which ultimately generates free radicals. Persistent oxidative stress disrupts cellular homeostasis and microenvironment needed for regeneration in brain. Furthermore, tight glycemic regulation by insulin treatment often leads to iatrotrogenic hypoglycemia in diabetic patients as a result of therapeutic insulin excess and compromised glucose counter-regulation. Such recurrent incidents amplify reactive oxygen species (ROS) generation, lipid peroxidation and cellular inflammation in already vulnerable brain cells leading to irreversible damage despite glucose normalization later.

译文

成人神经发生为大脑可塑性增加了新的维度。以前,由于几种内在和外在因素,成人哺乳动物大脑的再生被认为是相当不成功的。神经调节蛋白1(NRG1)是神经调节蛋白家族的主要信号蛋白,通过内分泌或邻分泌信号通过与ErbB受体(包括ErbB2,ErbB3和ErbB4)结合,参与神经元和神经胶质细胞的迁移,增殖和分化。脑损伤引起NRG1-ErbB信号,以在成年期和发育期触发受影响细胞的再生和替代。它通过减少氧化应激和通过GLUT易位加速葡萄糖转运来满足成体损伤组织中新形成的神经细胞的存活,以满足细胞恢复期间的能量需求。 ErbB2显示配体解离率降低和MAP激酶的高活化;这显着增加了它的受体强度。由于它缺乏配体结合结构域,因此需要与ErbB3或ErbB4进行异二聚化以进行信号转导。反过来,ErbB3是具有弱激酶活性的功能性受体。成年大脑中ErbB2的重新表达是放射状胶质细胞形成所必需的,其活性的丧失会干扰神经元的迁移。虽然ErbB3与增殖细胞相关,但ErbB4表达与分化表型的出现相关。葡萄糖代谢的差异和氧化应激的升高是糖尿病期间脑损伤的主要原因。过量的细胞外葡萄糖导致多元醇途径的活化,己糖胺途径和最终产生自由基的晚期糖化终产物的积累。持续的氧化应激破坏了脑内再生所需的细胞稳态和微环境。此外,由于治疗性胰岛素过量和葡萄糖反调节受损,胰岛素治疗的严格血糖调节经常导致糖尿病患者的致痉挛性低血糖症。这种复发事件放大了已经脆弱的脑细胞中的活性氧(ROS)产生,脂质过氧化和细胞炎症,导致不可逆的损害,尽管后来葡萄糖正常化。