内分泌
词汇介绍
拓展阅读
解析
Hypoglycemia 美 /,haɪpoglaɪ'simɪə/
释 义 n. 低血糖症;血糖过低
例 句 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
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、癫痫发作、意识丧失。
预防
如果患有糖尿病,请仔细遵循医生制定的糖尿病管理计划。如果正在服用新药,改变的饮食或用药时间表或添加新的运动,告诉医生,这些变化可能会影响糖尿病管理和低血糖风险。
连续血糖监测仪(CGM)特别是那些没有意识到低血糖症的人。这些设备在皮肤下面插入一根细线,可以将血糖读数发送到接收器。
要随身携带速效碳水化合物,如果汁或葡萄糖片,这样你就可以在降低血糖之前治疗血糖下降。
如果没有糖尿病但反复发作低血糖症,那么每天经常吃少量食物是一种权宜之计,有助于防止血糖水平过低。但是,这种方法不是一个明智的长期策略。最好与医生一起确定和治疗低血糖的根本原因。
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
影响指数: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.
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