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肥胖的双重调节机制:DNA甲基化与肠道菌群

Dual Regulation Mechanism of Obesity: DNA Methylation and Intestinal Flora.

作者信息

Ren Yi, Huang Peng, Zhang Lu, Tang Yu-Fen, Luo Sen-Lin, She Zhou, Peng Hong, Chen Yu-Qiong, Luo Jin-Wen, Duan Wang-Xin, Liu Ling-Juan, Liu Li-Qun

机构信息

Department of Pediatrics, The Second Xiangya Hospital of Central South University, Changsha 410011, China.

Children's Brain Development and Brain Injury Research Office, The Second Xiangya Hospital of Central South University, Changsha 410011, China.

出版信息

Biomedicines. 2024 Jul 23;12(8):1633. doi: 10.3390/biomedicines12081633.


DOI:10.3390/biomedicines12081633
PMID:39200098
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11351752/
Abstract

Obesity is a multifactorial chronic inflammatory metabolic disorder, with pathogenesis influenced by genetic and non-genetic factors such as environment and diet. Intestinal microbes and their metabolites play significant roles in the occurrence and development of obesity by regulating energy metabolism, inducing chronic inflammation, and impacting intestinal hormone secretion. Epigenetics, which involves the regulation of host gene expression without changing the nucleotide sequence, provides an exact direction for us to understand how the environment, lifestyle factors, and other risk factors contribute to obesity. DNA methylation, as the most common epigenetic modification, is involved in the pathogenesis of various metabolic diseases. The epigenetic modification of the host is induced or regulated by the intestinal microbiota and their metabolites, linking the dynamic interaction between the microbiota and the host genome. In this review, we examined recent advancements in research, focusing on the involvement of intestinal microbiota and DNA methylation in the etiology and progression of obesity, as well as potential interactions between the two factors, providing novel perspectives and avenues for further elucidating the pathogenesis, prevention, and treatment of obesity.

摘要

肥胖是一种多因素慢性炎症性代谢紊乱疾病,其发病机制受遗传和非遗传因素(如环境和饮食)影响。肠道微生物及其代谢产物通过调节能量代谢、诱导慢性炎症和影响肠道激素分泌,在肥胖的发生发展中发挥重要作用。表观遗传学涉及在不改变核苷酸序列的情况下对宿主基因表达进行调控,为我们理解环境、生活方式因素及其他风险因素如何导致肥胖提供了确切方向。DNA甲基化作为最常见的表观遗传修饰,参与了各种代谢疾病的发病机制。宿主的表观遗传修饰由肠道微生物群及其代谢产物诱导或调节,将微生物群与宿主基因组之间的动态相互作用联系起来。在本综述中,我们考察了近期的研究进展,重点关注肠道微生物群和DNA甲基化在肥胖病因及进展中的作用,以及这两个因素之间的潜在相互作用,为进一步阐明肥胖的发病机制、预防和治疗提供新的视角和途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c9/11351752/d8a926a4ea03/biomedicines-12-01633-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c9/11351752/29c626a6a44a/biomedicines-12-01633-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c9/11351752/ffc089f264e1/biomedicines-12-01633-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c9/11351752/d8a926a4ea03/biomedicines-12-01633-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c9/11351752/29c626a6a44a/biomedicines-12-01633-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c9/11351752/ffc089f264e1/biomedicines-12-01633-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60c9/11351752/d8a926a4ea03/biomedicines-12-01633-g002.jpg

相似文献

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[7]
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引用本文的文献

[1]
DNA methylation in adaptation to high-altitude environments and pathogenesis of related diseases.

Hum Genomics. 2025-8-30

[2]
Molecular Mechanisms Against Successful Weight Loss and Promising Treatment Options in Obesity.

Biomedicines. 2025-8-15

[3]
Pulp Residues Polysaccharide Alleviates High-Fat Diet-Induced Obesity by Modulating Intestinal Mucus Secretion and Glycosylation.

Foods. 2025-8-1

本文引用的文献

[1]
Alterations of DNA methylation profile in peripheral blood of children with simple obesity.

Health Inf Sci Syst. 2024-3-18

[2]
Probiotic Clostridium butyricum ameliorates cognitive impairment in obesity via the microbiota-gut-brain axis.

Brain Behav Immun. 2024-1

[3]
Integrated genetic and epigenetic analyses uncovered GLP1R association with metabolically healthy obesity.

Int J Obes (Lond). 2024-3

[4]
Gut microbiota-bile acid-vitamin D axis plays an important role in determining oocyte quality and embryonic development.

Clin Transl Med. 2023-10

[5]
Early-set POMC methylation variability is accompanied by increased risk for obesity and is addressable by MC4R agonist treatment.

Sci Transl Med. 2023-7-19

[6]
Epigenetic Regulation of Hepatic Lipid Metabolism by DNA Methylation.

Adv Sci (Weinh). 2023-7

[7]
Post-stroke depression: epigenetic and epitranscriptomic modifications and their interplay with gut microbiota.

Mol Psychiatry. 2023-10

[8]
The gut microbiota-bile acid axis mediates the beneficial associations between plasma vitamin D and metabolic syndrome in Chinese adults: A prospective study.

Clin Nutr. 2023-6

[9]
Microbiota-gut-brain axis: relationships among the vagus nerve, gut microbiota, obesity, and diabetes.

Acta Diabetol. 2023-8

[10]
The Association of the Hypothalamic-Pituitary-Adrenal Axis with Appetite Regulation in Children with Fetal Alcohol Spectrum Disorders (FASDs).

Nutrients. 2023-3-11

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