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Free keywords:
diabetes; exercise; 1HMRS; inflammation; obesity; spectroscopy
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
((HMRS)-H-1). 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.
