Please use this identifier to cite or link to this item: https://biore.bio.bg.ac.rs/handle/123456789/140
Title: Molecular basis of hippocampal energy metabolism in diabetic rats: The effects of SOD mimic
Authors: Stančić, Ana
Otašević, Vesna
Janković, Aleksandra
Vučetić, Milica
Ivanović-Burmazović, Ivana
Filipović, Miloš R.
Korać, Aleksandra 
Markelić, Milica 
Veličković, Ksenija 
Golić, Igor 
Buzadžić, Biljana
Korać, Bato 
Keywords: Diabetes;Glycolysis;hippocampus;Oxidative phosphorylation;SOD mimic
Issue Date: 1-Oct-2013
Rank: M22
Project: White or/and brown: importance of adipose tissue in overall redox dependent metabolic control in physiological adaptations and metabolic disorders 
Journal: Brain Research Bulletin
Abstract: 
Hippocampal structural changes associated with diabetes-related cognitive impairments are well described, but their molecular background remained vague. We examined whether/how diabetes alters molecular basis of energy metabolism in hippocampus readily after diabetes onset, with special emphasis on its redox-sensitivity.To induce diabetes, adult Mill Hill hybrid hooded rats received a single alloxan dose (120mg/kg). Both non-diabetic and diabetic groups were further divided in two subgroups receiving (i) or not (ii) superoxide dismutase (SOD) mimic, [Mn(II)(pyane)Cl2] for 7 days, i.p. Treatment of the diabetic animals started after blood glucose level ≥12mM.Diabetes decreased protein levels of oxidative phosphorylation components: complex III and ATP synthase. In contrast, protein amounts of glyceraldehyde-3-phosphate dehydrogenase, pyruvate dehydrogenase, and hypoxia-inducible factor-1α - the key regulator of energy metabolism in stress conditions, were higher in diabetic animals. Treatment with SOD mimic restored/increased the levels of oxidative phosphorylation components and returned hypoxia-inducible factor-1α to control level, while diabetes-induced up-regulation of glycolytic enzyme, glyceraldehyde-3-phosphate dehydrogenase, was additionally stimulated.To conclude, our results provide insight into the earliest molecular changes of energy-producing pathways in diabetes that may account for structural/functional disturbance of hippocampus, seen during disease progression. Also, data suggest [Mn(II)(pyane)Cl2] as potential therapeutic agent in cutting-edge approaches to threat this widespread metabolic disorder. © 2013 Elsevier Inc.
URI: https://biore.bio.bg.ac.rs/handle/123456789/140
ISSN: 0361-9230
DOI: 10.1016/j.brainresbull.2013.09.009
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