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This Article Full Text Full Text (PDF) All Versions of this Article: 583/2/469    most recent jphysiol.2007.138594v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Pierre, K. Articles by Pellerin, L. Search for Related Content PubMed PubMed Citation Articles by Pierre, K. Articles by Pellerin, L. Related Collections Neuroscience

¹ Departement de Physiologie, Universite de Lausanne, Lausanne, Switzerland
² Centre Botnar de Recherche Clinique, Departement de medecine interne, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland ³Department of Biochemistry, School of Medical Sciences, University of Bristol, Bristol BS8 1TD, UK

Monocarboxylate transporters (MCTs) are membrane carriers for lactate and ketone bodies. Three isoforms, MCT1, MCT2 and MCT4, have been described in the central nervous system but little information is available about the regulation of their expression in relation to altered metabolic and/or nutritional conditions. We show here that brains of mice fed on a high fat diet (HFD) up to 12 weeks as well as brains of genetically obese (ob/ob) or diabetic (db/db) mice exhibit an increase of MCT1, MCT2 and MCT4 expression as compared to brains of control mice fed a standard diet. Enhanced expression of each transporter was visible throughout the brain but most prominently in the cortex and in the hippocampus. Using immunohistochemistry, we observed that neurons (expressing mainly MCT2 but also sometimes low levels of MCT1 under normal conditions) were immunolabelled for all three transporters in HFD mice as well as in ob/ob and db/db mice. At the subcellular level, changes were most remarkable in neuronal cell bodies. Western blotting performed on brain structure extracts allowed us to confirm quantitatively the enhancement of MCT1 and MCT2 expression. Our data demonstrate that the expression of cerebral MCT isoforms can be modulated by alterations of peripheral metabolism, suggesting that the adult brain is sensitive and adapts to new metabolic states. This observation could be relevant in the context of obesity development and its consequences for brain function.

(Received 13 June 2007; accepted after revision 21 June 2007; first published online 28 June 2007)
Corresponding author L. Pellerin: Departement de Physiologie, Rue du Bugnon 7 CH-1005 Lausanne, Switzerland. Email: luc.pellerin{at}unil.ch

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