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Decreased Carbon Shunting From Glucose Towards Oxidative Metabolism In Diet-Induced Ketotic Rat Brain.
MedLine Citation:
PMID:  25314677     Owner:  NLM     Status:  Publisher    
The mechanistic link of ketosis to neuroprotection under certain pathological conditions continues to be explored. We investigated whether chronic ketosis induced by ketogenic diet results in the partitioning of ketone bodies towards oxidative metabolism in brain. We hypothesized that diet-induced ketosis results in increased shunting of ketone bodies towards citric acid cycle (CAC) and amino acids with decreased carbon shunting from glucose. Rats were fed standard (STD) or ketogenic (KG) diets for 3.5 weeks and then infused with [U-(13) C]glucose or [U-(13) C]acetoacetate tracers. Concentrations and (13) C-labeling pattern of CAC intermediates and amino acids were analyzed from brain homogenates using stable isotopomer mass spectrometry analysis. The contribution of [U-(13) C]glucose to acetyl-CoA and amino acids decreased by ~30% in the KG group vs STD, whereas [U-(13) C]acetoacetate contributions were more than 2-fold higher. The concentration of GABA remained constant across all groups; however, the (13) C-labeling of GABA was markedly increased in the KG group infused with [U-(13) C]acetoacetate compared to STD. This study reveals that there is a significant contribution of ketone bodies to oxidative metabolism and GABA in diet-induced ketosis. We propose that this represents a fundamental mechanism of neuroprotection under pathological conditions. This article is protected by copyright. All rights reserved.
Yifan Zhang; Shenghui Zhang; Isaac Marin-Valencia; Michelle A Puchowicz
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-10-14
Journal Detail:
Title:  Journal of neurochemistry     Volume:  -     ISSN:  1471-4159     ISO Abbreviation:  J. Neurochem.     Publication Date:  2014 Oct 
Date Detail:
Created Date:  2014-10-14     Completed Date:  -     Revised Date:  2014-10-15    
Medline Journal Info:
Nlm Unique ID:  2985190R     Medline TA:  J Neurochem     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
This article is protected by copyright. All rights reserved.
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