Hepatosteatosis, which is frequently associated with development of metabolic syndrome and insulin resistance, manifests when triglyceride (TG) input in the liver is greater than TG output, resulting in the excess accumulation of TG. Dysregulation of lipogenesis therefore has the potential to increase lipid accumulation in the liver, leading to insulin resistance and type 2 diabetes. Recently, efforts have been made to examine the epigenetic regulation of metabolism by histone-modifying enzymes that alter chromatin accessibility for activation or repression of transcription. For regulation of lipogenic gene transcription, various known lipogenic transcription factors, such as USF1, ChREBP, and LXR, interact with and recruit specific histone modifiers, directing specificity toward lipogenesis. Alteration or impairment of the functions of these histone modifiers can lead to dysregulation of lipogenesis and thus hepatosteatosis leading to insulin resistance and type 2 diabetes.

中文翻译：

---

肝脂肪生成的表观遗传调控：在肝脂肪变性和糖尿病中的作用

肝脂肪变性常与代谢综合征和胰岛素抵抗的发展有关，当肝脏中的甘油三酯（TG）输入大于TG输出时，会导致TG过度积累。因此，脂肪生成的失调有可能增加肝脏中的脂质积累，导致胰岛素抵抗和 2 型糖尿病。最近，已经努力通过组蛋白修饰酶来检查代谢的表观遗传调节，这些酶改变染色质的可及性以激活或抑制转录。对于脂肪生成基因转录的调节，各种已知的脂肪生成转录因子，如 USF1、ChREBP 和 LXR，与特定的组蛋白修饰剂相互作用并招募特定的组蛋白修饰剂，将特异性导向脂肪生成。