Sims-Robinson Catrina, Bakeman Anna, Bruno Elizabeth, Jackson Samuel, Glasser Rebecca, Murphy Geoffrey G, Feldman Eva L
Department of Neurology, Medical University of South Carolina, Charleston, South Carolina, 29425, United States of America.
Department of Neurology, University of Michigan, Ann Arbor, Michigan, 48109, United States of America.
PLoS One. 2016 Sep 27;11(9):e0163883. doi: 10.1371/journal.pone.0163883. eCollection 2016.
A high-fat diet (HFD), one of the major factors contributing to metabolic syndrome, which is associated with an increased risk of neurodegenerative diseases, leads to insulin resistance and cognitive impairment. It is not known whether these alterations are improved with dietary intervention. To investigate the long-term impact of a HFD on hippocampal insulin signaling and memory, C57BL6 mice were placed into one of three groups based on the diet: a standard diet (control), a HFD, or a HFD for 16 weeks and then the standard diet for 8 weeks (HF16). HFD-induced impairments in glucose tolerance and hippocampal insulin signaling occurred concurrently with deficits in both short- and long-term memory. Furthermore, these conditions were improved with dietary intervention; however, the HFD-induced decrease in insulin receptor expression in the hippocampus was not altered with dietary intervention. Our results demonstrate that memory deficits due to the consumption of a HFD at an early age are reversible.
高脂饮食(HFD)是导致代谢综合征的主要因素之一,与神经退行性疾病风险增加相关,会导致胰岛素抵抗和认知障碍。目前尚不清楚这些改变是否能通过饮食干预得到改善。为了研究高脂饮食对海马体胰岛素信号传导和记忆的长期影响,将C57BL6小鼠根据饮食分为三组:标准饮食(对照组)、高脂饮食组,或先进行16周高脂饮食,然后进行8周标准饮食的组(HF16)。高脂饮食诱导的葡萄糖耐量和海马体胰岛素信号传导损伤与短期和长期记忆缺陷同时出现。此外,这些情况通过饮食干预得到了改善;然而,高脂饮食诱导的海马体胰岛素受体表达下降并未因饮食干预而改变。我们的结果表明,早年食用高脂饮食导致的记忆缺陷是可逆 的。