Fluctuations in glucose levels induce glial toxicity with glutamatergic, oxidative and inflammatory implications

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• 作者：André ; Quincozes-Santos ; ¹ ; ^{andrequincozes@ufrgs.br} ; Larissa Daniele Bobermin¹ ; Adriano M. de Assis ; Carlos-Alberto Gonç ; alves ; Diogo Onofre Souza
• 关键词：CNS ; central nervous system ; DM ; diabetes mellitus ; EAAC1 ; excitatory amino acid carrier 1 ; GLUT ; glucose transporters ; GS ; glutamine synthetase ; GSH ; glutathione ; IL-1β ; interleukin 1β ; IL-6 ; interleukin 6 ; IL-10 ; interleukin 10 ; NADPH ; nicotinamide adenine dinucleotide phosphate reduced ; NFκB ; nuclear factor κB ; NO ; nitric oxide ; NOX ; NADPH oxidase ; p38 MAPK ; p38 mitogen-activated protein kinase ; ROS/RNS ; reactive oxygen/nitrogen species ; TNF-α ; tumor necrosis factor α ; ΔΨm ; mitochondrial memb
• 刊名：Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
• 出版年：2017
• 出版时间：January 2017
• 年：2017
• 卷：1863
• 期：1
• 页码：1-14
• 全文大小：1534 K
• 卷排序：1863

文摘

Glial cells are responsible for uptake and metabolism of glucose in the brain. Diabetes impairs glial function. Fluctuations in glucose levels induce changes in glial metabolism. Changes in glucose levels induce oxidative/nitrosative stress and inflammation. NFκB and p38 are underlying mechanisms of the glucose-induced glial toxicity.