College of Animal Science and Veterinary Medicine, Shandong Agricultural University, 61 Daizong Street, Tai'an City, Shandong Province, 271018, China; Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, Shandong Agricultural University, 61 Daizong Street, Tai'an City, Shandong Province, 271018, China; Shandong Provincial Engineering Technology Research Center of Animal Disease Control and Prevention, Shandong Agricultural University, 61 Daizong Street, Tai'an City, Shandong Province, 271018, China.
Tai'an City Central Hospital, 29 Longtan Road, Tai'an City, Shandong Province, 271000, China.
Chem Biol Interact. 2020 Oct 1;330:109199. doi: 10.1016/j.cbi.2020.109199. Epub 2020 Aug 15.
Obesity is characterized by the deposition of excessive body fat, and is caused by energy imbalance, especially when consuming fat-rich diets. High fat diet (HFD)-associated obesity is greatly common in patients with non-alcoholic fatty liver disease (NAFLD) that is emerging as one of the most universal causes of liver disease worldwide, especially in Western countries. In spite of its high prevalence, only a small proportion of affected individuals will become inflamed, followed by fibrosis and chronic liver diseases, and most patients only show simple steatosis. In this case, the full comprehension of the mechanisms underlying the progression of NAFLD is of extreme significance; in spite of progress in this field, awareness on the development of NAFLD is still incomplete. Traditionally, liver steatosis is commonly connected with HFD, obesity, and insulin resistance (IR). Recently, various possible mechanisms have been put forward for liver damage, including endoplasmic reticulum stress, perturbation of autophagy, mitochondrial dysfunction, hepatocellular apoptosis, gut microbiota imbalance, dysregulation of microRNAs, and genetic/epigenetic risk factors, as well as an increase in inflammatory responses, among many others. Collectively, these proposed mechanisms allow for a variety of hits acting together on subjects to mediated NAFLD and will offer a more accurate explanation for progression of NAFLD. Therefore, this review summarizes the present information concerning NAFLD after HFD exposure, as well as discusses possible mechanisms through which it may arise.
肥胖的特征是体脂肪过度沉积，是由能量失衡引起的，尤其是在摄入高脂肪饮食时。高脂肪饮食（HFD）相关的肥胖在非酒精性脂肪性肝病（NAFLD）患者中非常常见，NAFLD 正在成为全球最普遍的肝病病因之一，尤其在西方国家。尽管其患病率很高，但只有一小部分受影响的个体会出现炎症，随后是纤维化和慢性肝病，而大多数患者仅表现为单纯性脂肪变性。在这种情况下，深入了解 NAFLD 进展的机制具有极其重要的意义；尽管在这一领域取得了进展，但对 NAFLD 发展的认识仍不完整。传统上，肝脂肪变性通常与 HFD、肥胖和胰岛素抵抗（IR）有关。最近，已经提出了各种可能导致肝损伤的机制，包括内质网应激、自噬失调、线粒体功能障碍、肝细胞凋亡、肠道微生物群失衡、microRNAs 失调以及遗传/表观遗传风险因素，以及炎症反应增加等。总的来说，这些提出的机制允许各种因素共同作用于个体，介导 NAFLD 的发生，并为 NAFLD 的进展提供更准确的解释。因此，本文综述了 HFD 暴露后 NAFLD 的现有信息，并讨论了其可能发生的机制。
