Biological Clock Research Group, Biomedical Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba, Ibaraki, Japan; Department of Applied Biological Science, Graduate School of Science and Technology, Tokyo University of Science, Noda, Chiba, Japan.
Biological Clock Research Group, Biomedical Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba, Ibaraki, Japan.
Biochem Biophys Res Commun. 2020 Mar 26;524(1):129-134. doi: 10.1016/j.bbrc.2020.01.077. Epub 2020 Jan 21.
Acute or chronic effects of consuming or skipping breakfast on cognitive performance in humans are controversial. To evaluate the effects of chronically skipping breakfast (SB) on hippocampus-dependent long-term memory formation, we examined hippocampal gene expression and applied the novel object recognition test (NORT) after two weeks of repeated fasting for six hours from lights off to mimic SB in mice. We also examined the effects of SB on circadian rhythms of locomotor activity, food intake, core body temperature (CBT) and sleep-wake cycles. Skipping breakfast slightly but significantly decreased total daily food intake without affecting body weight gain. Locomotor activity and CBT significantly decreased during the fasting period under SB. The degree of fasting-dependent CBT reduction gradually increased and then became stabilized after four days of SB. Electroencephalographic data revealed that repeated SB significantly decreased the duration of wakefulness and increased that of rapid eye movement (REM) and of non-REM (NREM) sleep during the period of SB. Furthermore, total daily amounts of wakefulness and NREM sleep were significantly decreased and increased, respectively, under SB, suggesting that SB disrupts sleep homeostasis. Skipping breakfast significantly suppressed mRNA expression of the memory-related genes, Camk2a, Fkbp5, Gadd45b, Gria1, Sirt1 and Tet1 in the hippocampus. Recognition memory assessed by NORT was impaired by SB in accordance with the gene expression profiles. These findings suggested that chronic SB causes dysregulated CBT, sleep-wake cycles and hippocampal gene expression, which results in impaired long-term memory formation.
在人类中，进食或不吃早餐对认知表现的急性或慢性影响是有争议的。为了评估长期不吃早餐（SB）对海马依赖的长期记忆形成的影响，我们检查了海马体的基因表达，并在两周内对小鼠进行了六小时的反复禁食，以模拟 SB，随后进行了新物体识别测试（NORT）。我们还检查了 SB 对运动活动、食物摄入、核心体温（CBT）和睡眠-觉醒周期的昼夜节律的影响。不吃早餐会轻微但显著地减少每日总食物摄入量，而不会影响体重增加。在 SB 期间，运动活动和 CBT 在禁食期间显著下降。在 SB 四天后，禁食依赖的 CBT 减少程度逐渐增加并趋于稳定。脑电图数据显示，反复 SB 显著缩短了 SB 期间的清醒时间，增加了快速眼动（REM）和非快速眼动（NREM）睡眠的时间。此外，SB 下总清醒时间和 NREM 睡眠时间分别显著减少和增加，表明 SB 破坏了睡眠稳态。SB 显著抑制了海马体中与记忆相关的基因 Camk2a、Fkbp5、Gadd45b、Gria1、Sirt1 和 Tet1 的 mRNA 表达。NORT 评估的识别记忆受到 SB 的损害，与基因表达谱一致。这些发现表明，慢性 SB 导致 CBT、睡眠-觉醒周期和海马体基因表达失调，从而导致长期记忆形成受损。
