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营养基因组学与氧化还原调控:与营养基因组学特刊相关的概念。

Nutrigenomics and redox regulation: Concepts relating to the Special Issue on nutrigenomics.

机构信息

Institute of Nutritional Sciences, Nutrigenomics Section, Friedrich Schiller University Jena, Jena, Germany.

Institute of Animal Reproduction and Food Research, Polish Academy of Sciences, PL-10-748, Olsztyn, Poland; School of Medicine, Institute of Biomedicine, University of Eastern Finland, FI-70211, Kuopio, Finland.

出版信息

Redox Biol. 2023 Dec;68:102920. doi: 10.1016/j.redox.2023.102920. Epub 2023 Oct 4.

DOI:10.1016/j.redox.2023.102920
PMID:37839954
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10624588/
Abstract

During our whole lifespan, from conception to death, the epigenomes of all tissues and cell types of our body integrate signals from the environment. This includes signals derived from our diet and the uptake of macro- and micronutrients. In most cases, this leads only to transient changes, but some effects of this epigenome programming process are persistent and can even be transferred to the next generation. Both epigenetic programming and redox processes are affected by the individual choice of diet and other lifestyle decisions like physical activity. The nutrient-gene communication pathways have adapted during human evolution and are essential for maintaining health. However, when they are maladaptive, such as in long-term obesity, they significantly contribute to diseases like type 2 diabetes and cancer. The field of nutrigenomics investigates nutrition-related signal transduction pathways and their effect on gene expression involving interactions both with the genome and the epigenomes. Several of these diet-(epi)genome interactions and the involved signal transduction cascades are redox-regulated. Examples include the effects of the NAD/NADH ratio, vitamin C levels and secondary metabolites of dietary molecules from plants on the acetylation and methylation state of the epigenome as well as on gene expression through redox-sensitive pathways via the transcription factors NFE2L2 and FOXO. In this review, we summarize and extend on these topics as well as those discussed in the articles of this Special Issue and take them into the context of redox biology.

摘要

在我们的整个生命周期中,从受孕到死亡,我们身体的所有组织和细胞类型的表观基因组整合来自环境的信号。这包括来自我们的饮食和宏量营养素和微量营养素吸收的信号。在大多数情况下,这只会导致短暂的变化,但这种表观基因组编程过程的一些影响是持久的,甚至可以传递给下一代。表观基因组编程和氧化还原过程都受到个体饮食选择和其他生活方式决策(如体育活动)的影响。营养基因通讯途径在人类进化过程中已经适应,对于维持健康至关重要。然而,当它们不适应时,例如长期肥胖,它们会显著导致 2 型糖尿病和癌症等疾病。营养基因组学研究涉及与基因组和表观基因组相互作用的与营养相关的信号转导途径及其对基因表达的影响。这些饮食(表观基因组)相互作用和涉及的信号转导级联中的一些是氧化还原调节的。例如,NAD/NADH 比、维生素 C 水平以及植物膳食分子的次生代谢物对表观基因组的乙酰化和甲基化状态以及通过转录因子 NFE2L2 和 FOXO 通过氧化还原敏感途径对基因表达的影响。在这篇综述中,我们总结并扩展了这些主题以及本期特刊中讨论的主题,并将它们纳入氧化还原生物学的背景中。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac1a/10624588/8df6c5f5479b/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac1a/10624588/1d895c547e99/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac1a/10624588/90653e2ac79a/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac1a/10624588/bd74f29f41a5/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac1a/10624588/8df6c5f5479b/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac1a/10624588/1d895c547e99/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac1a/10624588/90653e2ac79a/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac1a/10624588/bd74f29f41a5/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac1a/10624588/8df6c5f5479b/gr4.jpg

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