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Enhanced expression of three monocarboxylate transporter isoforms in the brain of obese mice
Author(s) -
Pierre Karin,
Parent Annabelle,
Jayet PierreYves,
Halestrap Andrew P.,
Scherrer Urs,
Pellerin Luc
Publication year - 2007
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2007.138594
Subject(s) - gene isoform , monocarboxylate transporter , endocrinology , medicine , transporter , context (archaeology) , hippocampus , ketone bodies , immunohistochemistry , blot , biology , central nervous system , glucose transporter , chemistry , metabolism , microbiology and biotechnology , insulin , biochemistry , gene , paleontology
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.