背景:2型糖尿病(T2DM)是一种代谢紊乱,在大脑中具有广泛的并发症,取决于发病前的条件,如肥胖和代谢综合征。已经提出,神经递质和代谢扰动甚至可能在T2DM的早期阶段之前出现,并且高热量摄入可能在这种状态下不利地影响大脑。尽管如此,在这些情况下神经化学和结构改变的证据仍然很少和有争议。
目的:评估高脂饮食对啮齿动物大脑神经化学特征和结构完整性的影响。
方法:前瞻性。
方法:Wistar大鼠(n=12/组)。
■A新闻,ISIS,稀有,和EPI序列在9.4T进行。
结果:通过磁共振波谱评估神经化学和结构参数,基于体素的形态计量学,容积,和扩散张量成像。
方法:通过Student和Mann-Whitney测试比较测量值。Pearson相关性用于评估参数之间的关系。
结果:接受高热量摄入的动物体重增加(P=0.003),出现葡萄糖耐受不良(P<0.001),但未出现高血糖症。在海马中,由谷氨酰胺(P=0.016)和谷氨酸能(Glx)水平升高(P=0.036)反映的饮食诱导的谷氨酸能代谢产物的扰动,与葡萄糖不耐受呈负相关(谷氨酰胺,r=-0.804,P=0.029),提示与神经代谢失调有关.在尾状壳核,高脂饮食导致N-乙酰天门冬氨酸(P=0.028)。葡萄糖耐受不良与该区域谷氨酸能代谢物水平之间的负相关再次表明了与代谢变化的关系(谷氨酸,r=-0.845,P=0.014;Glx,r=-0.834,P=0.020)。两个区域均未观察到磷酸盐化合物的变化或主要结构改变。
结论:我们发现证据表明,高脂饮食诱导的肥胖在存在早期糖耐量异常的情况下导致明显的早期和区域特异性代谢/神经化学失衡,即使结构改变或T2DM不存在。
方法:1技术功效:第三阶段J.Magn。雷森。成像2018。
BACKGROUND: Type-2 diabetes mellitus (T2DM) is a metabolic disorder with a broad range of complications in the brain that depend on the conditions that precede its onset, such as obesity and metabolic syndromes. It has been suggested that neurotransmitter and metabolic perturbations may emerge even before the early stages of T2DM and that high-caloric intake could adversely influence the brain in such states. Notwithstanding, evidence for neurochemical and structural alterations in these conditions are still sparse and controversial.
OBJECTIVE: To evaluate the influence of high-fat diet in the neurochemical profile and structural integrity of the rodent brain.
METHODS: Prospective.
METHODS: Wistar rats (n = 12/group).
UNASSIGNED: A PRESS, ISIS, RARE, and EPI sequences were performed at 9.4T.
RESULTS: Neurochemical and structural parameters were assessed by magnetic resonance spectroscopy, voxel-based morphometry, volumetry, and diffusion tensor imaging.
METHODS: Measurements were compared through Student and Mann-Whitney tests. Pearson correlation was used to assess relationships between parameters.
RESULTS: Animals submitted to high-caloric intake gained weight (P = 0.003) and developed glucose intolerance (P < 0.001) but not hyperglycemia. In the hippocampus, the diet induced perturbations in glutamatergic metabolites reflected by increased levels of glutamine (P = 0.016) and glutamatergic pool (Glx) (P = 0.036), which were negatively correlated with glucose intolerance (glutamine, r = -0.804, P = 0.029), suggesting a link with neurometabolic dysregulation. At caudate-putamen, high-fat diet led to a surprising increase in the pool of N-acetylaspartate (P = 0.028). A relation with metabolic changes was again suggested by the negative correlation between glucose intolerance and levels of glutamatergic metabolites in this region (glutamate, r = -0.845, P = 0.014; Glx, r = -0.834, P = 0.020). Neither changes in phosphate compounds nor major structural alterations were observed for both regions.
CONCLUSIONS: We found evidence that high-fat diet-induced obesity leads to distinct early and region-specific metabolic/neurochemical imbalances in the presence of early glucose intolerance even when structural alterations or T2DM are absent.
METHODS: 1 Technical Efficacy: Stage 3 J. Magn. Reson. Imaging 2018.