Guangdong Provincial Key Laboratory of Microbial Culture Collection and Application, State Key Laboratory of Applied Microbiology Southern China, Institute of Microbiology, Guangdong Academy of Sciences, Guangzhou 510070, China.
State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan 430072, China.
Int J Mol Sci. 2023 Jan 17;24(3):1850. doi: 10.3390/ijms24031850.
Human obesity has become a global epidemic that can lead to many metabolic diseases, including insulin resistance, type 2 diabetes, dyslipidemia, hypertension and nonalcoholic fatty liver. The development of obesity is closely associated with excess food intake and energy imbalance, family history, lifestyle, psychology and other factors, but molecular mechanisms underlying the induction and development of obesity remain to be intensively studied under a variety of internal and external pathogenesis conditions. In this study, we generated two obesity models of zebrafish that were treated with a high-fat diet (HFD) or an overfeeding diet (DIO). Both HFD and DIO zebrafish exhibited higher levels of lipid accumulation, fat distribution, microvascular steatosis and ectopic accumulation of lipid droplets in liver and muscle than normal diet (NOD) fish. The comparison of transcriptome sequencing data for the livers of HFD, DIO and NOD groups identified common and specific genes and signaling pathways that are potentially associated with zebrafish obesity induced by HFD and/or DIO. These findings provide clues for further understanding the mechanisms of obesity development and preventing nutritionally induced obesity through targeting the common signaling pathways and biological processes.
人类肥胖已成为一种全球性流行病,可导致许多代谢疾病,包括胰岛素抵抗、2 型糖尿病、血脂异常、高血压和非酒精性脂肪肝。肥胖的发展与过量的食物摄入和能量失衡、家族史、生活方式、心理等因素密切相关,但在各种内在和外在发病机制条件下,肥胖的诱导和发展的分子机制仍需深入研究。在这项研究中,我们生成了两种高脂肪饮食(HFD)或过食饮食(DIO)处理的斑马鱼肥胖模型。与正常饮食(NOD)鱼相比,HFD 和 DIO 斑马鱼的脂质积累、脂肪分布、微血管脂肪变性以及肝脏和肌肉中脂质滴的异位积累水平更高。HFD、DIO 和 NOD 组肝脏转录组测序数据的比较鉴定了与 HFD 和/或 DIO 诱导的斑马鱼肥胖相关的共同和特定基因及信号通路。这些发现为进一步了解肥胖发展的机制以及通过靶向共同信号通路和生物学过程预防营养诱导的肥胖提供了线索。