| Literature DB >> 25564238 |
Matthias K Auer1, Markus Sack2, Jenny N Lenz1, Mira Jakovcevski3, Sarah V Biedermann4, Claudia Falfán-Melgoza2, Jan Deussing3, Jörg Steinle5, Maximilian Bielohuby6, Martin Bidlingmaier6, Frederik Pfister7, Günter K Stalla8, Gabriele Ende4, Wolfgang Weber-Fahr2, Johannes Fuss5, Peter Gass5.
Abstract
Excessive intake of high-caloric diets as well as subsequent development of obesity and diabetes mellitus may exert a wide range of unfavorable effects on the central nervous system (CNS). It has been suggested that one mechanism in this context is the promotion of neuroinflammation. The potentially harmful effects of such diets were suggested to be mitigated by physical exercise. Here, we conducted a study investigating the effects of physical exercise in a cafeteria-diet mouse model on CNS metabolites by means of in vivo proton magnetic resonance spectroscopy ((1)HMRS). In addition postmortem histologic and real-time (RT)-PCR analyses for inflammatory markers were performed. Cafeteria diet induced obesity and hyperglycemia, which was only partially moderated by exercise. It also induced several changes in CNS metabolites such as reduced hippocampal glutamate (Glu), choline-containing compounds (tCho) and N-acetylaspartate (NAA)+N-acetyl-aspartyl-glutamic acid (NAAG) (tNAA) levels, whereas opposite effects were seen for running. No association of these effects with markers of central inflammation could be observed. These findings suggest that while voluntary wheel running alone is insufficient to prevent the unfavorable peripheral sequelae of the diet, it counteracted many changes in brain metabolites. The observed effects seem to be independent of neuroinflammation.Entities:
Mesh:
Substances:
Year: 2015 PMID: 25564238 PMCID: PMC4420876 DOI: 10.1038/jcbfm.2014.231
Source DB: PubMed Journal: J Cereb Blood Flow Metab ISSN: 0271-678X Impact factor: 6.200