Auer Matthias K, Sack Markus, Lenz Jenny N, Jakovcevski Mira, Biedermann Sarah V, Falfán-Melgoza Claudia, Deussing Jan, Steinle Jörg, Bielohuby Maximilian, Bidlingmaier Martin, Pfister Frederik, Stalla Günter K, Ende Gabriele, Weber-Fahr Wolfgang, Fuss Johannes, Gass Peter
1] RG Neuroendocrinology, Max Planck Institute of Psychiatry, Munich, Germany [2] RG Animal Models in Psychiatry, Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim, University of Heidelberg, Heidelberg, Germany.
1] RG Translational Imaging, Central Institute of Mental Health, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany [2] Department of Neuroimaging, Central Institute of Mental Health Mannheim, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany.
J Cereb Blood Flow Metab. 2015 Mar 31;35(4):554-64. doi: 10.1038/jcbfm.2014.231.
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.
高热量饮食的过量摄入以及随后肥胖症和糖尿病的发展可能会对中枢神经系统(CNS)产生广泛的不利影响。有人提出,在这种情况下的一种机制是促进神经炎症。有人认为,体育锻炼可以减轻此类饮食的潜在有害影响。在此,我们进行了一项研究,通过体内质子磁共振波谱((1)HMRS)研究体育锻炼对自助餐饮食小鼠模型中枢神经系统代谢物的影响。此外,还进行了死后组织学分析和炎症标志物的实时(RT)-PCR分析。自助餐饮食导致肥胖和高血糖,运动仅部分缓解了这种情况。它还引起了中枢神经系统代谢物的几种变化,例如海马谷氨酸(Glu)、含胆碱化合物(tCho)和N-乙酰天门冬氨酸(NAA)+N-乙酰天门冬氨酰谷氨酸(NAAG)(tNAA)水平降低,而跑步则产生相反的效果。未观察到这些影响与中枢炎症标志物之间的关联。这些发现表明,虽然单独的自愿轮转跑步不足以预防饮食带来的不利外周后遗症,但它抵消了大脑代谢物的许多变化。观察到的效果似乎与神经炎症无关。