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BioMed Research International
Volume 2014, Article ID 472459, 22 pages
http://dx.doi.org/10.1155/2014/472459
Review Article

Fatty Acids in Energy Metabolism of the Central Nervous System

1Institute of Molecular Biology and Biophysics, Siberian Division of the Russian Academy of Medical Sciences (SB RAMS), 2 Timakova st., Novosibirsk 630117, Russia
2Department of Surgery, Drexel University College of Medicine, Philadelphia, PA, USA

Received 2 February 2014; Revised 29 March 2014; Accepted 29 March 2014; Published 4 May 2014

Academic Editor: Ancha Baranova

Copyright © 2014 Alexander Panov et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

In this review, we analyze the current hypotheses regarding energy metabolism in the neurons and astroglia. Recently, it was shown that up to 20% of the total brain’s energy is provided by mitochondrial oxidation of fatty acids. However, the existing hypotheses consider glucose, or its derivative lactate, as the only main energy substrate for the brain. Astroglia metabolically supports the neurons by providing lactate as a substrate for neuronal mitochondria. In addition, a significant amount of neuromediators, glutamate and GABA, is transported into neurons and also serves as substrates for mitochondria. Thus, neuronal mitochondria may simultaneously oxidize several substrates. Astrocytes have to replenish the pool of neuromediators by synthesis de novo, which requires large amounts of energy. In this review, we made an attempt to reconcile -oxidation of fatty acids by astrocytic mitochondria with the existing hypothesis on regulation of aerobic glycolysis. We suggest that, under condition of neuronal excitation, both metabolic pathways may exist simultaneously. We provide experimental evidence that isolated neuronal mitochondria may oxidize palmitoyl carnitine in the presence of other mitochondrial substrates. We also suggest that variations in the brain mitochondrial metabolic phenotype may be associated with different mtDNA haplogroups.