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食用西式饮食后大鼠的大脑和行为扰动。

Brain and behavioral perturbations in rats following Western diet access.

作者信息

Hargrave Sara L, Davidson Terry L, Lee Tien-Jui, Kinzig Kimberly P

机构信息

Ingestive Behavior Research Center, Department of Psychological Sciences, Purdue University, 703 Third Street, West Lafayette, IN 47907, USA; Center for Behavioral Neuroscience, American University, Asbury Hall, 4400 Massachusetts Ave., NW., Washington, DC 20016, USA.

Center for Behavioral Neuroscience, American University, Asbury Hall, 4400 Massachusetts Ave., NW., Washington, DC 20016, USA.

出版信息

Appetite. 2015 Oct;93:35-43. doi: 10.1016/j.appet.2015.03.037. Epub 2015 Apr 8.

DOI:10.1016/j.appet.2015.03.037
PMID:25862980
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4546854/
Abstract

Energy dense "Western" diets (WD) are known to cause obesity as well as learning and memory impairments, blood-brain barrier damage, and psychological disturbances. Impaired glucose (GLUT1) and monocarboxylate (MCT1) transport may play a role in diet-induced dementia development. In contrast, ketogenic diets (KD) have been shown to be neuroprotective. We assessed the effect of 10, 40 and 90 days WD, KD and Chow maintenance on spontaneous alternation (SA) and vicarious trial and error (VTE) behaviors in male rats, then analyzed blood glucose, insulin, and ketone levels; and hippocampal GLUT1 and MCT1 mRNA. Compared to Chow and KD, rats fed WD had increased 90 day insulin levels. SA was decreased in WD rats at 10, but not 40 or 90 days. VTE was perturbed in WD-fed rats, particularly at 10 and 90 days, indicating hippocampal deficits. WD rats had lower hippocampal GLUT1 and MCT1 expression compared to Chow and KD, and KD rats had increased 90 day MCT1 expression compared to Chow and WD. These data suggest that WD reduces glucose and monocarboxylate transport at the hippocampus, which may result in learning and memory deficits. Further, KD consumption may be useful for MCT1 transporter recovery, which may benefit cognition.

摘要

众所周知,能量密集型的“西方”饮食(WD)会导致肥胖以及学习和记忆障碍、血脑屏障损伤和心理障碍。葡萄糖(GLUT1)和单羧酸(MCT1)转运受损可能在饮食诱导的痴呆症发展中起作用。相比之下,生酮饮食(KD)已被证明具有神经保护作用。我们评估了10天、40天和90天的WD、KD以及正常饮食对雄性大鼠自发交替(SA)和替代性试错(VTE)行为的影响,然后分析了血糖、胰岛素和酮水平;以及海马体GLUT1和MCT1 mRNA。与正常饮食和KD相比,喂食WD的大鼠90天胰岛素水平升高。WD大鼠在10天时SA降低,但在40天和90天时没有降低。WD喂养的大鼠VTE受到干扰,尤其是在10天和90天时,表明海马体存在缺陷。与正常饮食和KD相比,WD大鼠海马体GLUT1和MCT1表达较低,与正常饮食和WD相比,KD大鼠90天MCT1表达增加。这些数据表明,WD会降低海马体中的葡萄糖和单羧酸转运,这可能导致学习和记忆缺陷。此外,食用KD可能有助于MCT1转运蛋白的恢复,这可能有益于认知。

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