Nutritional Sciences and Toxicology Department, University of California Berkeley, Berkeley, CA 94720, United States of America.
Nutritional Sciences and Toxicology Department, University of California Berkeley, Berkeley, CA 94720, United States of America.
Biochim Biophys Acta Mol Cell Biol Lipids. 2021 Nov;1866(11):159019. doi: 10.1016/j.bbalip.2021.159019. Epub 2021 Jul 29.
Obesity is a strong risk factor for insulin resistance. Chronic low-grade tissue inflammation and systemic inflammation have been proposed as major mechanisms that promote insulin resistance in obesity. Adipose tissue has been recognized as a nexus between inflammation and metabolism, but how exactly inflammatory gene expression is orchestrated during the development of obesity is not well understood. Epigenetic modifications are defined as heritable changes in gene expression and cellular function without changes to the original DNA sequence. The major epigenetic mechanisms include DNA methylation, histone modification, noncoding RNAs, nucleopositioning/remodeling and chromatin reorganization. Epigenetic mechanisms provide a critical layer of gene regulation in response to environmental changes. Accumulating evidence supports that epigenetics plays a large role in the regulation of inflammatory genes in adipocytes and adipose-resident immune cell types. This review focuses on the association between adipose tissue inflammation in obesity and major epigenetic modifications.
肥胖是胰岛素抵抗的一个强危险因素。慢性低度组织炎症和全身炎症被认为是促进肥胖中胰岛素抵抗的主要机制。脂肪组织已被认为是炎症和代谢之间的纽带,但在肥胖的发展过程中,炎症基因表达是如何精确调控的尚不清楚。表观遗传修饰被定义为基因表达和细胞功能的可遗传变化,而不改变原始 DNA 序列。主要的表观遗传机制包括 DNA 甲基化、组蛋白修饰、非编码 RNA、核定位/重塑和染色质重排。表观遗传机制为基因调控提供了一个关键的层面,以响应环境变化。越来越多的证据支持表观遗传学在调节脂肪细胞和脂肪组织驻留免疫细胞类型中的炎症基因方面起着重要作用。这篇综述重点介绍了肥胖症中脂肪组织炎症与主要表观遗传修饰之间的关联。