2022 年第 1 期 第 17 卷

腺苷酸活化蛋白激酶调控相关通路与糖脂代谢异常相关疾病的发病机制研究进展

Research progress on adenosine monophosphate-activated protein kinase regulation related pathways and the pathogenesis of diseases with glucose and lipid pathobolism

作者：侯铖宇1宋炜熙1陈丽2周忠志3刘泽2梁生姣2周欣蓉2叶永鑫2高文娟2周佳俞4张欢欢2奉水华5

英文作者：Hou Chengyu1 Song Weixi1 Chen Li2 Zhou Zhongzhi3 Liu Ze2 Liang Shengjiao2 Zhou Xinrong2 Ye Yongxin2 Gao Wenjuan2 Zhou Jiayu4 Zhang Huanhuan2 Feng Shuihua5

单位：1湖南中医药大学中西医结合学院，长沙410208；2湖南中医药大学医学院，长沙410208；3湖南中医药大学第一附属医院烧伤疮疡整形科，长沙410007；4湖南中医药大学中医学院，长沙410208；5湖南中医药大学第一附属医院护理部，长沙410007

英文单位：1College of Integrated Traditional Chinese and Western Medicine Hunan University of Chinese Medicine Changsha 410208 China; 2Medical College Hunan University of Chinese Medicine Changsha 410208 China; 3Department of Burn Sore and Plastics the First Affiliated Hospital of Hunan University of Chinese Medicine Changsha 410007 China; 4College of Chinese Medicine Hunan University of Chinese Medicine Changsha 410208 China; 5Department of Nursing the First Affiliated Hospital of Hunan University of Chinese Medicine Changshu 410007 China

关键词：糖脂代谢异常；腺苷酸活化蛋白激酶；能量代谢；信号通路 

英文关键词：Glucoseandlipidpathobolism;Adenosinemonophosphate-activatedproteinkinase;Energymetabolism;Signalingpathway 

• 摘要：

• 糖脂代谢异常会造成线粒体功能紊乱，从而导致相关疾病的发生发展。研究表明，腺苷酸活化蛋白激酶（AMPK）是体内重要的能量代谢感受器，激活后的AMPK通过调控多条相关通路参与机体糖脂代谢和能量调节活动，以减轻糖脂代谢紊乱对机体的损害或促进机体相关正常功能的恢复。本文对AMPK调控相关通路在糖脂代谢异常相关疾病中的研究进展进行综述。

• Glucose and lipid pathobolism may cause mitochondrial dysfunction, which leads to the occurrence and development of related diseases. Studies have found that adenosine monophosphate-activated protein kinase (AMPK) is an important energy metabolism receptor in the body. Activated AMPK participates in glucose-lipid metabolism and energy regulation by regulating multiple related pathways, so as to alleviate the damage of glucose-lipid pathobolism to the body or promote the recovery of related normal functions. This article reviews the progress of AMPK regulation related pathways in diseases with glucose and lipid pathobolism.