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Permanent link (DOI): https://doi.org/10.7939/R3T12D

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The effects of glucose-induced metabolic injury on microglia activity and survival Open Access

Descriptions

Other title
Subject/Keyword
Diabetes
Glucose
Microglia
Type of item
Thesis
Degree grantor
University of Alberta
Author or creator
Kenawy, Sara M
Supervisor and department
Kathryn G Todd (Centre for Neurosciences)
Examining committee member and department
Kerr Bradely (Pharmacology)
Ian winship (Centre for Neurosciences)
Glenn Baker (Centre for Neurosciences)
Kathryn G Todd (Centre for Neurosciences)
Department
Centre for Neuroscience
Specialization

Date accepted
2013-01-08T09:08:41Z
Graduation date
2013-06
Degree
Master of Science
Degree level
Master's
Abstract
Glucose is the sole fuel for the brain in normal physiological conditions. Absence of glucose or its presence in high concentrations has been shown to be harmful to neurons. Microglia, the innate immune cells of the brain, are the first line of defense against changes in the CNS environment and their activity influences neuronal survival to a great extent. The effects of glucose-induced metabolic injury on microglia are unclear. Thus, the aim of this study was to investigate how hyperglycemia and hypoglycemia affect microglial phagocytotic activity, survival and secretory profile. Results showed that glucose concentration significantly affected microglia release of pro-inflammatory cytokines and growth factors. Microglia phagocytic activity was decreased at high and low glucose concentrations as compared to normal. Interestingly, microglia deprived of glucose showed better survival, exhibited increased ramification and a more quiescent phenotype where microglia released significantly less pro-inflammatory cytokines and growth factors as compared to controls
Language
English
DOI
doi:10.7939/R3T12D
Rights
Permission is hereby granted to the University of Alberta Libraries to reproduce single copies of this thesis and to lend or sell such copies for private, scholarly or scientific research purposes only. Where the thesis is converted to, or otherwise made available in digital form, the University of Alberta will advise potential users of the thesis of these terms. The author reserves all other publication and other rights in association with the copyright in the thesis and, except as herein before provided, neither the thesis nor any substantial portion thereof may be printed or otherwise reproduced in any material form whatsoever without the author's prior written permission.
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