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营养因素、DNA 甲基化与 2 型糖尿病和肥胖风险:观点与挑战。

Nutritional Factors, DNA Methylation, and Risk of Type 2 Diabetes and Obesity: Perspectives and Challenges.

机构信息

Department of Translation Medicine, Federico II University of Naples, 80131 Naples, Italy.

URT Genomic of Diabetes, Institute of Experimental Endocrinology and Oncology, National Research Council, 80131 Naples, Italy.

出版信息

Int J Mol Sci. 2019 Jun 19;20(12):2983. doi: 10.3390/ijms20122983.

DOI:10.3390/ijms20122983
PMID:31248068
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6627657/
Abstract

A healthy diet improves life expectancy and helps to prevent common chronic diseases such as type 2 diabetes (T2D) and obesity. The mechanisms driving these effects are not fully understood, but are likely to involve epigenetics. Epigenetic mechanisms control gene expression, maintaining the DNA sequence, and therefore the full genomic information inherited from our parents, unchanged. An interesting feature of epigenetic changes lies in their dynamic nature and reversibility. Accordingly, they are susceptible to correction through targeted interventions. Here we will review the evidence supporting a role for nutritional factors in mediating metabolic disease risk through DNA methylation changes. Special emphasis will be placed on the potential of using DNA methylation traits as biomarkers to predict risk of obesity and T2D as well as on their response to dietary and pharmacological (epi-drug) interventions.

摘要

健康饮食可延长预期寿命,并有助于预防 2 型糖尿病(T2D)和肥胖等常见慢性疾病。虽然这些影响的机制尚未完全阐明,但可能涉及表观遗传学。表观遗传机制控制基因表达,维持 DNA 序列,因此保持从父母那里遗传的完整基因组信息不变。表观遗传变化的一个有趣特征在于其动态性和可逆性。因此,它们容易受到靶向干预的纠正。在这里,我们将回顾支持营养因素通过 DNA 甲基化变化介导代谢疾病风险的证据。特别强调的是,将 DNA 甲基化特征用作预测肥胖和 T2D 风险以及对饮食和药物干预(表观遗传药物)反应的生物标志物的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b8a/6627657/8da412ac5c40/ijms-20-02983-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b8a/6627657/8da412ac5c40/ijms-20-02983-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b8a/6627657/8da412ac5c40/ijms-20-02983-g001.jpg

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