AMP依赖的蛋白激酶在非酒精性脂肪肝中的作用
AMP-Activated Protein Kinase in Nonalcoholic Fatty Liver Diseases
DOI: 10.12677/PI.2023.123028, PDF,  被引量    国家自然科学基金支持
作者: 刘尚奇, 胡艳波, 张慧明, 高 倩, 王敏杰*：内蒙古医科大学基础医学院，内蒙古 呼和浩特；高 峰, 杨 艳：内蒙古医科大学药学院，内蒙古 呼和浩特
关键词: 非酒精性脂肪性肝病；非酒精性脂肪性肝炎；AMP依赖的蛋白激酶；脂肪变性；Nonalcoholic Fatty Liver Disease； Nonalcoholic Steatohepatitis； AMP-Activated Protein Kinase； Steatosis Inflammation
摘要: 非酒精性脂肪性肝病(NAFLD)，尤其是非酒精性脂肪性肝炎(NASH)已成为肝移植和肝相关性死亡的主要原因。然而，NASH的发病机制仍不清楚。目前，还没有FDA批准的药物来治疗这种疾病。AMP依赖的蛋白激酶(AMPK)可以感知能量状态并调节代谢过程以维持体内平衡。AMPK的活性受到碳水化合物、脂肪和氨基酸等营养物质的调节。AMPK活性因营养缺乏而增加，但在肥胖期间因营养过剩、炎症和某些合成代谢激素(如胰岛素)的过度分泌而受到抑制。抑制肝脏AMPK活性可以使其从单纯性脂肪变性转变为肝细胞死亡，因此激活AMPK可能改善NASH的相关症状。
Abstract: Nonalcoholic fatty liver diseases (NAFLD), especially nonalcoholic steatohepatitis (NASH), have become a major cause of liver transplant and liver-associated death. However, the pathogenesis of NASH is still unclear. Currently, there is no FDA-approved medication to treat this devastating disease. AMP-activated protein kinase (AMPK) senses energy status and regulates metabolic processes to maintain homeostasis. The activity of AMPK is regulated by the availability of nutrients, such as carbohydrates, lipids and amino acids. AMPK activity is increased by nutrient deprivation, and inhibited by overnutrition, inflammation and hypersecretion of certain anabolic hormones, such as insulin, during obesity. The repression of hepatic AMPK activity permits the transition from simple steatosis to hepatocellular death, and thus activation might ameliorate multiple aspects of NASH. Here, we review the pathogenesis of NAFLD and the impact of AMPK activity state on hepatic steatosis, inflammation, liver injury and fibrosis during the transition of NAFL to NASH and liver failure.
文章引用：刘尚奇, 高峰, 杨艳, 胡艳波, 张慧明, 高倩, 王敏杰. AMP依赖的蛋白激酶在非酒精性脂肪肝中的作用[J]. 药物资讯, 2023, 12(3): 224-232. https://doi.org/10.12677/PI.2023.123028

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