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3
SIRT3 mediates hippocampal synaptic adaptations to intermittent fasting and ameliorates deficits in APP mutant mice.SIRT3 介导了间歇性禁食引起的海马突触适应性变化,并改善了 APP 突变小鼠的缺陷。
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4
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PLoS One. 2019 Apr 16;14(4):e0215471. doi: 10.1371/journal.pone.0215471. eCollection 2019.
5
Intermittent Fasting in Cardiovascular Disorders-An Overview.间歇性禁食与心血管疾病。概述。
Nutrients. 2019 Mar 20;11(3):673. doi: 10.3390/nu11030673.
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Genome-wide methylation is modified by caloric restriction in Daphnia magna.热量限制可改变大型溞基因组的甲基化状态。
BMC Genomics. 2019 Mar 8;20(1):197. doi: 10.1186/s12864-019-5578-4.
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Loss of Hepatic Oscillatory Fed microRNAs Abrogates Refed Transition and Causes Liver Dysfunctions.肝振荡喂养 microRNAs 的缺失阻止了再喂养转换并导致肝功能障碍。
Cell Rep. 2019 Feb 19;26(8):2212-2226.e7. doi: 10.1016/j.celrep.2019.01.087.
8
Intermittent administration of a fasting-mimicking diet intervenes in diabetes progression, restores β cells and reconstructs gut microbiota in mice.间歇性给予模拟禁食饮食可干预小鼠糖尿病进展、恢复β细胞并重建肠道微生物群。
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Histone H3 threonine 11 phosphorylation by Sch9 and CK2 regulates chronological lifespan by controlling the nutritional stress response.组蛋白 H3 苏氨酸 11 的磷酸化由 Sch9 和 CK2 调控,通过控制营养应激反应来调节时序寿命。
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10
Global remodeling of the mouse DNA methylome during aging and in response to calorie restriction.小鼠 DNA 甲基化组在衰老过程中的全局重编程及其对热量限制的响应。
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饮食限制的表观遗传调控:第二部分。

Epigenetic Regulation by Dietary Restriction: Part II.

作者信息

Yong-Quan Ng Gavin, Fann David Yang-Wei, Jo Dong-Gyu, Sobey Christopher G, Arumugam Thiruma V

机构信息

Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.

School of Pharmacy, Sungkyunkwan University, Suwon, Republic of Korea.

出版信息

Cond Med. 2019 Dec;2(6):300-310.

PMID:32039346
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7007178/
Abstract

In the first part of our review, we extensively discuss the different variants of dietary restriction (DR) regimens, as well as its corresponding mechanism(s) and subsequent effects. We also provide a detailed analysis of the different epigenetic mechanisms based on current knowledge. We postulate that DR may represent an environmental intervention that can modulate the epigenomic profile of an individual. It is highly plausible that epigenetic regulation by DR may help explain the asymmetric manifestation of DR effects in different individuals. Additionally, epigenetic modifications via DR may lead to epigenetic programming, providing protection against age-associated diseases, which in turn could lead to reduced morbidity and increased lifespan. In the second part of the review, we summarize recent findings that highlight the epigenomic axis of DR, which provides a better understanding of the mechanisms by which its numerous health benefits are achieved.

摘要

在我们综述的第一部分,我们广泛讨论了饮食限制(DR)方案的不同变体,以及其相应的机制和后续影响。我们还根据现有知识对不同的表观遗传机制进行了详细分析。我们推测,饮食限制可能代表一种环境干预,能够调节个体的表观基因组特征。饮食限制的表观遗传调控很可能有助于解释其在不同个体中效应的不对称表现。此外,通过饮食限制进行的表观遗传修饰可能导致表观遗传编程,提供针对与年龄相关疾病的保护,这反过来可能导致发病率降低和寿命延长。在综述的第二部分,我们总结了近期的研究发现,这些发现突出了饮食限制的表观基因组轴,从而能更好地理解实现其众多健康益处的机制。