Altered Glycogen Metabolism in Cultured Astrocytes from Mice with Chronic Glutathione Deficit; Relevance for Neuroenergetics in Schizophrenia 英文参考文献.docVIP
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Altered Glycogen Metabolism in Cultured Astrocytes from Mice with Chronic Glutathione Deficit; Relevance for Neuroenergetics in Schizophrenia 英文参考文献
AlteredGlycogenMetabolisminCulturedAstrocytes
fromMicewithChronicGlutathioneDeficit;Relevance
forNeuroenergeticsinSchizophrenia
SuzieLavoie1*,IgorAllaman2,Jean-MariePetit2,KimQ.Do1,PierreJ.Magistretti1,2
1Department of Psychiatry, Centre for Psychiatric Neuroscience, University Hospital Centre and University of Lausanne, Lausanne, Switzerland, 2Laboratory of
NeuroenergeticsandCellularDynamics,BrainMindInstitute,EcolePolytechniqueFe′de′rale deLausanne(EPFL),Lausanne,Switzerland
Abstract
NeurodegenerativeandpsychiatricdisordersincludingAlzheimer’s,Parkinson’sorHuntington’sdiseasesandschizophrenia
havebeenassociatedwithadeficitinglutathione(GSH).Inparticular,apolymorphisminthegeneofglutamatecysteine
ligasemodulatorysubunit(GCLM)isassociatedwithschizophrenia.GSHisthemostimportantintracellularantioxidantand
isnecessaryfortheremovalofreactiveby-productsgeneratedbytheutilizationofglucoseforenergysupply.Furthermore,
glucosemetabolismthroughthepentosephosphatepathwayisamajorsourceofNADPH,thecofactornecessaryforthe
regenerationofreducedglutathione.ThisstudyaimsatinvestigatingglucosemetabolisminculturedastrocytesfromGCLM
knockoutmice,whichshowdecreasedGSHlevels.Nodifferenceinthebasalmetabolismofglucosewasobservedbetween
wild-typeandknockoutcells.Incontrast,glycogenlevelswereloweranditsturnoverwashigherinknockoutastrocytes.
Thesechangeswereaccompaniedbyadecreaseintheexpressionofthegenesinvolvedinitssynthesisanddegradation,
includingtheproteintargetingtoglycogen.Duringanoxidativechallengeinducedbytert-Butylhydroperoxide,wild-type
cells increased their glycogen mobilization and glucose uptake. However, knockout astrocytes were unable to mobilize
glycogenfollowingthesamestressandtheycouldincreasetheirglucoseutilizationonlyfollowingamajoroxidativeinsult.
Altogether,theseresultsshowthatglucosemetabolismandglycogenutilizationaredysregulatedinastrocytesshowinga
chronicdeficitinGSH,suggestingthatalterationsofafundamentalaspectofbrainenergymetabolismiscausedbyGSH
deficitandmaythe
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