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丙型肝炎病毒核心蛋白 1

反式脂肪酸 1

肝细胞癌 1

脂肪变性 1

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饱和脂肪酸 1

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Role of Akkermansia muciniphila in the development of nonalcoholic fatty liver disease: current knowledge and perspectives

《医学前沿（英文）》 2022年第16卷第5期页码 667-685 doi: 10.1007/s11684-022-0960-z

摘要： Nonalcoholic fatty liver disease (NAFLD) is a hepatic manifestation of metabolic syndrome and a common cause of liver cirrhosis and cancer. Akkermansia muciniphila (A. muciniphila) is a next-generation probiotic that has been reported to improve metabolic disorders. Emerging evidence indicates the therapeutic potential of A. muciniphila for NAFLD, especially in the inflammatory stage, nonalcoholic steatohepatitis. Here, the current knowledge on the role of A. muciniphila in the progression of NAFLD was summarized. A. muciniphila abundancy is decreased in animals and humans with NAFLD. The recovery of A. muciniphila presented benefits in preventing hepatic fat accumulation and inflammation in NAFLD. The details of how microbes regulate hepatic immunity and lipid accumulation in NAFLD were further discussed. The modulation mechanisms by which A. muciniphila acts to improve hepatic inflammation are mainly attributed to the alleviation of inflammatory cytokines and LPS signals and the downregulation of microbiota-related innate immune cells (such as macrophages). This review provides insights into the roles of A. muciniphila in NAFLD, thereby providing a blueprint to facilitate clinical therapeutic applications.

关键词： Akkermansia muciniphila NAFLD NASH steatosis inflammation

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Metformin and metabolic diseases: a focus on hepatic aspects

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《医学前沿（英文）》 2015年第9卷第2期页码 173-186 doi: 10.1007/s11684-015-0384-0

摘要：

Metformin has been widely used as a first-line anti-diabetic medicine for the treatment of type 2 diabetes (T2D). As a drug that primarily targets the liver, metformin suppresses hepatic glucose production (HGP), serving as the main mechanism by which metformin improves hyperglycemia of T2D. Biochemically, metformin suppresses gluconeogenesis and stimulates glycolysis. Metformin also inhibits glycogenolysis, which is a pathway that critically contributes to elevated HGP. While generating beneficial effects on hyperglycemia, metformin also improves insulin resistance and corrects dyslipidemia in patients with T2D. These beneficial effects of metformin implicate a role for metformin in managing non-alcoholic fatty liver disease. As supported by the results from both human and animal studies, metformin improves hepatic steatosis and suppresses liver inflammation. Mechanistically, the beneficial effects of metformin on hepatic aspects are mediated through both adenosine monophosphate-activated protein kinase (AMPK)-dependent and AMPK-independent pathways. In addition, metformin is generally safe and may also benefit patients with other chronic liver diseases.

关键词： metformin diabetes hepatic steatosis inflammatory response insulin resistance

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脂肪变性诱发肝癌发生机制——HCV核心基因转基因小鼠的经验教训 Review

Pan Diao, Fangping Jia, Xiaojing Wang, Xiao Hu, Takefumi Kimura, Takero Nakajima, Toshifumi Aoyama, Kyoji Moriya, Kazuhiko Koike, Naoki Tanaka

《工程（英文）》 2021年第7卷第12期页码 1797-1805 doi: 10.1016/j.eng.2021.08.019

摘要：

丙型肝炎病毒（HCV）感染是全球慢性肝炎、肝硬化和肝细胞癌（HCC）的主要病因。在HCV的结构蛋白中，HCV核心蛋白具有调控基因转录、脂质代谢、细胞增殖、细胞凋亡和自噬的能力，所有这些都与HCC的发展密切相关。携带HCV核心基因的转基因小鼠表现出与慢性丙型肝炎患者的临床特征相似的年龄依赖性胰岛素抵抗、肝脂肪变性和HCC。一些饮食习惯的调整，包括限制热量和富含饱和脂肪酸（SFA）、反式脂肪酸（TFA）或胆固醇的饮食，被证明会影响HCV核心基因转基因小鼠的肝脏脂肪生成和肿瘤形成。这些饮食的改变除了调节肝纤维化过程和微环境外，还调节了肝细胞的应激和增殖，从而证实了饮
食习惯与脂肪变性相关的肝癌发生之间的密切联系。本文综述了HCV基因组转基因小鼠模型的研究结果，重点介绍了HCV核心基因转基因小鼠的研究结果，并讨论了HCV核心蛋白诱导脂肪变性和肝癌发生的机制，以及饮食习惯对脂肪变性所致肝癌的影响。

关键词：脂肪变性肝细胞癌反式脂肪酸饱和脂肪酸饮食限制丙型肝炎病毒核心蛋白