先前的研究发现，酮体的主要成分β-羟基丁酸（BHB）作为饥饿期间的备用能量来源具有重要的生理意义，或者在胰岛素缺乏时诱发糖尿病酮症酸中毒。生酮饮食（KD）作为代谢疗法已有一百多年的历史，众所周知，酮体和 BHB 不仅可以作为葡萄糖的辅助燃料替代品，还可以通过诱导抗氧化、抗炎和心脏保护功能。与多种靶蛋白结合，包括组蛋白脱乙酰酶 (HDAC) 或 G 蛋白偶联受体 (GPCR)。表观遗传学的最新进展，特别是新型组蛋白翻译后修饰（HPTMs），不断更新了我们对BHB的认识，BHB也作为信号转导分子和修饰底物，调控组蛋白乙酰化、组蛋白β等一系列表观遗传现象。 -羟基丁酰化、组蛋白甲基化、DNA 甲基化和 microRNA。这些表观遗传事件在不改变DNA结构的情况下改变基因的活性，并进一步参与相关疾病的发病机制。本综述重点介绍了BHB的代谢过程以及BHB介导的表观遗传学在心血管疾病、糖尿病及糖尿病并发症、神经精神疾病、癌症、骨质疏松、肝肾损伤、胚胎和胎儿发育以及肠道稳态等方面的代谢过程，并讨论了潜在的分子机制。 、药物靶点和应用前景。© 2023 作者。由爱思唯尔有限公司出版

Previous studies have found that β-Hydroxybutyrate (BHB), the main component of ketone bodies, is of physiological importance as a backup energy source during starvation or induces diabetic ketoacidosis when insulin deficiency occurs. Ketogenic diets (KD) have been used as metabolic therapy for over a hundred years, it is well known that ketone bodies and BHB not only serve as ancillary fuel substituting for glucose but also induce anti-oxidative, anti-inflammatory, and cardioprotective features via binding to several target proteins, including histone deacetylase (HDAC), or G protein-coupled receptors (GPCRs). Recent advances in epigenetics, especially novel histone post-translational modifications (HPTMs), have continuously updated our understanding of BHB, which also acts as a signal transduction molecule and modification substrate to regulate a series of epigenetic phenomena, such as histone acetylation, histone β-hydroxybutyrylation, histone methylation, DNA methylation, and microRNAs. These epigenetic events alter the activity of genes without changing the DNA structure and further participate in the pathogenesis of related diseases. This review focuses on the metabolic process of BHB and BHB-mediated epigenetics in cardiovascular diseases, diabetes and complications of diabetes, neuropsychiatric diseases, cancers, osteoporosis, liver and kidney injury, embryonic and fetal development, and intestinal homeostasis, and discusses potential molecular mechanisms, drug targets, and application prospects.© 2023 The Authors. Published by Elsevier Ltd.