标题:Beta2-Adrenergic Receptor and Astrocyte Glucose Metabolism
作者:Dong, Jun-hong; Chen, Xin; Cui, Min; Yu, Xiao; Pang, Qi; Sun, Jin-peng
通讯作者:Sun, JP
作者机构:[Dong, Jun-hong; Sun, Jin-peng] Shandong Univ, Sch Med, Dept Biochem & Mol Biol, Key Lab Expt Teratol,Minist Educ, Jinan 250012, Shandong, Peoples R C 更多
会议名称:16th International Symposium on Chromaffin Cell Biology (ISCCB)
会议日期:JUL 11-15, 2011
来源:JOURNAL OF MOLECULAR NEUROSCIENCE
出版年:2012
卷:48
期:2
页码:456-463
DOI:10.1007/s12031-012-9742-4
关键词:Beta2-adrenergic receptor; Astrocytes; Glucose metabolism; G; protein-coupled receptors
摘要:Astrocyte glucose metabolism functions to maintain brain activity in both normal and stress conditions. Dysregulation of astrocyte glucose metabolism relates to development of neuronal disease, such as multiple sclerosis and Alzheimer's disease. In response to acute stress, beta2-adrenergic receptor is activated and initiates multiple signaling events mediated by Gs, Gi, arrestin, or other effectors depending on specific cellular contexts. In astrocytes, beta2-adrenergic receptor promotes glucose uptake through GLUT1 and accelerates glycogen degradation via coupling to Gs and second messenger cAMP-dependent pathway. Beta2-adrenergic receptor may regulate other steps in astrocyte glucose metabolism, such as lactate production or transduction. Inappropriate regulation of beta2-adrenergic receptor activity can disrupt normal glucose metabolism, and leads to accelerate neuronal disease development. It was demonstrated that the absence of beta2-adrenergic receptor in astrocytes occurred in multiple sclerosis patients, and the increased beta2-adrenergic receptor activity relates to Alzheimer's disease. A clear view of beta2-adrenergic receptor-mediated signaling pathways in regulating astrocyte glucose metabolism could help us to develop neuronal diseases treatment by targeting to the beta2-adrenergic receptor.
收录类别:CPCI-S;SCOPUS;SCIE
WOS核心被引频次:22
Scopus被引频次:23
资源类型:会议论文;期刊论文
原文链接:https://www.scopus.com/inward/record.uri?eid=2-s2.0-84868212231&doi=10.1007%2fs12031-012-9742-4&partnerID=40&md5=74544349aa65d13a8868a468333f12f3
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