脂代谢是机体重要代谢之一,肝脏作为脂质合成、储存以及代谢的中心器官,二者相互影响。肿瘤细胞所处的局部环境称为肿瘤微环境,为适应肿瘤微环境而发生的代谢改变称为代谢重编。目前脂代谢与肝癌之间的相关性尚不完全清楚,肝癌脂代谢重编的具体过程亦尚未完全揭示。本文介绍了肝癌发生、发展各阶段脂代谢特点,总结了肝癌脂代谢重编过程的最新发现,旨在探究脂代谢在肝癌发生、发展以及预后中的作用,为肝癌防治提供新的思路与依据。Lipid metabolism is one of the important metabolic processes in the body, and the liver is the central organ for lipid synthesis, storage, and metabolism, with a mutual influence between them. The local environment in which the tumour cells are located is called the tumor microenvironment, and the metabolic changes that occur to adapt to the tumor microenvironment are called metabolic reprogramming. At present, the relationship between lipid metabolism and liver cancer is not completely clear, and the specific process of lipid metabolic reprogramming in liver cancer has not yet been fully elucidated. This review introduces the lipid metabolic characteristics of liver cancer at each stage of its occurrence and development, summarizes the latest findings on the lipid metabolic reprogramming process in liver cancer, and aims to explore the role of lipid metabolism in the occurrence, development, and prognosis of liver cancer, providing new ideas and evidence for the prevention and treatment of liver cancer.
在过去的四十年中,非酒精性脂肪性肝病(non-alcoholic fatty liver disease, NAFLD)已成为最常见的慢性肝病,全球患病率约为成年人群的25%,其发病率持续上升,是全球的重大公共卫生问题。近年来,多项研究表明肠道菌群与NAFLD之间关系密切,NAFLD、慢性肝炎、肝硬化及肝癌等肝病患者均存在不同程度的肠道菌群失调,临床前研究证实了肠道菌群在NAFLD中的潜在因果作用。肠道菌群的组成、结构失衡会影响肠黏膜屏障及肠道代谢物,引起肠道通透性增加,产生肠源性内毒素血症,进而促进肝脏炎症反应,而肝损伤会进一步加重肠道通透性及全身炎症反应,由此形成恶性循环促进NAFLD的发生、发展。因而干预肠道菌群,可能是治疗及预防NAFLD的新策略。因此本文主要从肠道菌群的角度对NAFLD的发病机制及治疗作一综述。Over the past four decades, non-alcoholic fatty liver disease (NAFLD) has become the most common chronic liver disease, with a global prevalence of approximately 25% of the adult population, and its incidence continues to rise, making it a major public health NAFLD has become the most common chronic liver disease. In recent years, several studies have demonstrated the close relationship between intestinal flora and NAFLD. Patients with NAFLD, chronic hepatitis, cirrhosis and hepatocellular carcinoma, and other liver diseases have varying degrees of intestinal dysbiosis, and preclinical studies have confirmed the potential causal role of intestinal flora in NAFLD. Imbalance in the composition and structure of intestinal flora affects the intestinal mucosal barrier and intestinal metabolites, causing an increase in intestinal permeability, generating intestinal endotoxemia, which in turn promotes hepatic inflammatory response, and hepatic injury further exacerbates intestinal permeability and systemic inflammatory response, resulting in the formation of a vicious circle that promotes the onset and development of NAFLD. Thus, intervention of intestinal flora may be a new strategy for the treatment and prevention of NAFLD. Therefore, this article mainly reviews the pathogenesis and treatment of NAFLD from the perspective of intestinal flora.
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