Miles Keila N, Skelton Matthew R
Department of Pediatrics, University of Cincinnati College of Medicine and Division of Neurology, Cincinnati Children's Research Foundation. Cincinnati, OH 45229, United States.
Department of Pediatrics, University of Cincinnati College of Medicine and Division of Neurology, Cincinnati Children's Research Foundation. Cincinnati, OH 45229, United States.
Brain Res. 2020 May 1;1734:146697. doi: 10.1016/j.brainres.2020.146697. Epub 2020 Jan 31.
The ketogenic diet (KD) is a non-pharmacological treatment for specific types of epilepsy. In addition, it has been shown to be effective in mitigating other neurologic disorders. The KD is also effective in reducing body mass, leading to an increase in use by the general population for weight loss. As the popularity of the clinical and general use of the KD has increased, it is important to develop adequate mouse models to better understand the effects of the KD in both normal and diseased states. Many times, the best outcome for disorders treatable with the KD would be achieved by commencing treatment in early life. Few studies have evaluated the cognitive effect of starting the KD in early life. To better understand these effects, male C57BL6/J mice were placed on a KD from postnatal day (P) 21 through young adulthood (~P90). KD-fed mice had increased blood ketone levels, reduced blood glucose, and reduced weight gain versus mice fed a control diet (CD). The weight loss in the KD-fed mice was not accompanied by a change in body fat percentage, suggesting that there was a loss of lean mass. Behavioral testing began on P60 while the mice were still on the diet. KD-fed mice were hypoactive with CD-fed mice. In the Morris water maze, KD-fed mice showed decreased path efficiency, suggesting a spatial learning deficits. No differences were observed in spatial memory or in novel object recognition memory. In a contextual and conditioned fear paradigm, the KD-fed mice had an increase in freezing behavior. These data suggest that early-life exposure to a KD leads to impaired body composition and long-term cognitive changes.
生酮饮食(KD)是针对特定类型癫痫的一种非药物治疗方法。此外,已证明它在减轻其他神经系统疾病方面有效。KD在减轻体重方面也很有效,这导致普通人群为减肥而增加对其的使用。随着KD在临床和一般应用中的普及,开发合适的小鼠模型以更好地了解KD在正常和患病状态下的作用变得很重要。很多时候,对于可用KD治疗的疾病,最好的结果是在生命早期开始治疗。很少有研究评估在生命早期开始使用KD的认知效果。为了更好地理解这些影响,将雄性C57BL6/J小鼠从出生后第21天(P21)开始直至成年早期(约P90)置于生酮饮食中。与喂食对照饮食(CD)的小鼠相比,喂食KD的小鼠血酮水平升高、血糖降低且体重增加减少。喂食KD的小鼠体重减轻并未伴随着体脂百分比的变化,这表明瘦体重有所减少。行为测试在P60小鼠仍在饮食期间开始。喂食KD的小鼠与喂食CD的小鼠相比活动减少。在莫里斯水迷宫实验中,喂食KD的小鼠路径效率降低,表明存在空间学习缺陷。在空间记忆或新物体识别记忆方面未观察到差异。在情境性和条件性恐惧范式中,喂食KD的小鼠僵住行为增加。这些数据表明,生命早期接触KD会导致身体组成受损和长期认知变化。