AMPK激活剂在腺病毒36诱导肥胖研究中的进展  

Research Progress of AMPK Activator and Adenovirus 36 Induced Obesity

作　　者：张哲铭 董剑 洪俊 高亮 高挚逸 艾孜哈尔·艾海提 张弘睿 张晓峥 Zhang Zheming;Dong Jian;Hong Jun(Department of Biochemistry and Molecular Biology,Xinjiang Medical University,Urumqi,Xinjiang,830017,China)

机构地区：[1]新疆医科大学基础医学院生物化学与分子生物学教研室·省部共建中亚高发病成因与防治国家重点实验室·新疆地方病分子生物学重点实验室,新疆乌鲁木齐830017

出　　处：《黑龙江医学》2024年第23期2930-2932,共3页Heilongjiang Medical Journal

基　　金：新疆维吾尔自治区2022年国家级大学生创新创业训练计划项目(202210760020);新疆维吾尔自治区自然科学基金项目(2022D01C207)。

摘　　要：肥胖是影响人类生活的许多疾病之一,其发生机制与炎症因子、激素作用、酶调节等多种作用有关,人类腺病毒36(Ad36)后会出现胰岛素敏感性,但血清脂质水平正常,这与肥胖似乎是矛盾的。5-氨基咪唑-4-甲酰胺核苷酸(AICAR)作为AMP-激活的蛋白激酶(AMPK)的激活剂,可进一步探究AMPK在Ad36引起的肥胖中发挥调节糖脂代谢的作用。Obesity(fat)is one of many diseases affecting human life,and its pathogenesis is related to inflammatory factors,hormone action,enzyme regulation and other functions.After human adenovirus 36 infection,people will have insulin sensitivity and normal serum lipid level,which is a contradictory type of obesity.AMPK plays a key role in the regulation of glucose metabolism and fat metabolism.There is crossover between the action pathway of AMPK and the mechanism of Ad36 affecting mammalian obesity.

关 键 词：肥胖 AMP-激活的蛋白激酶 腺病毒36 5-氨基味唑-4-甲酰胺核苷酸 信号转导通路 

分 类 号：R589.2[医药卫生—内分泌]