Intermittent metabolic switching, neuroplasticity and brain health.

Intermittent metabolic switching, neuroplasticity and brain health.
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DOI:
10.1038/nrn.2017.156
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发表时间:
2018-03
期刊:
Nature reviews. Neuroscience
影响因子:
--
通讯作者:
Cheng A
Cheng A
中科院分区:
其他
文献类型:
--
作者:
Mattson MP;Moehl K;Ghena N;Schmaedick M;Cheng A

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在进化过程中,大脑和身体在禁食状态下运作良好的个体能够成功地获得食物,使他们能够生存和繁殖。随着禁食和长时间运动,肝糖原储备被耗尽,脂肪细胞衍生的脂肪酸产生酮。细胞燃料源的这种代谢转换伴随着大脑中神经网络的细胞和分子适应,增强了它们的功能并增强了它们对压力,损伤和疾病的抵抗力。在这里,我们考虑间歇性代谢转换,重复周期的代谢挑战,诱导酮症(禁食和/或运动),然后是恢复期(进食,休息和睡眠),可以优化整个生命周期的大脑功能和恢复力,重点是参与认知和情绪的神经元回路。这种代谢转换影响多种信号通路,促进神经可塑性和大脑对损伤和疾病的抵抗力。
During evolution, individuals whose brains and bodies functioned well in a fasted state were successful in acquiring food, enabling their survival and reproduction. With fasting and extended exercise, liver glycogen stores are depleted and ketones are produced from adipose-cell-derived fatty acids. This metabolic switch in cellular fuel source is accompanied by cellular and molecular adaptations of neural networks in the brain that enhance their functionality and bolster their resistance to stress, injury and disease. Here, we consider how intermittent metabolic switching, repeating cycles of a metabolic challenge that induces ketosis (fasting and/or exercise) followed by a recovery period (eating, resting and sleeping), may optimize brain function and resilience throughout the lifespan, with a focus on the neuronal circuits involved in cognition and mood. Such metabolic switching impacts multiple signalling pathways that promote neuroplasticity and resistance of the brain to injury and disease.
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