Metabolic, enzymatic and gene involvement in cerebral glucose dysmetabolism after traumatic brain injury
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- 作者：Angela Maria Amorinia ; angela.amorini@rm.unicatt.it" class="auth_mail" title="E-mail the corresponding author ; Giacomo Lazzarinoa ; g.lazzarino@libero.it" class="auth_mail" title="E-mail the corresponding author ; Valentina Di Pietrob ; v.dipietro@bham.ac.uk" class="auth_mail" title="E-mail the corresponding author ; Stefano Signorettic ; stefano.signoretti@tiscali.it" class="auth_mail" title="E-mail the corresponding author ; Giuseppe Lazzarinod ; lazzarig@unict.it" class="auth_mail" title="E-mail the corresponding author ; Antonio Bellib ; e ; a.belli@bham.ac.uk" class="auth_mail" title="E-mail the corresponding author ; Barbara Tavazzia ; btavazzi@rm.unicatt.it" class="auth_mail" title="E-mail the corresponding author
- 关键词：Traumatic brain injury ; Glucose dysmetabolism ; Glycolysis ; Pentose phosphate pathway ; Energy metabolism ; Mitochondrial dysfunction
- 刊名：Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
- 出版年：2016
- 出版时间：April 2016
- 年：2016
- 卷：1862
- 期：4
- 页码：679-687
- 全文大小：1293 K
文摘
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Metabolic, enzymatic and gene changes are involved in glucose dysmetabolism after TBI.
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Activation of glycolysis in mild TBI occurs on recovery of mitochondrial functions.
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Activation of glycolysis in severe TBI occurs during mitochondrial malfunctioning.
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Pentosephosphate pathway changes in severe TBI are limited to NADPH supply.
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Metabolic and gene mechanisms of glucose dysregulation depend on TBI severity.