Comments on 'Downregulation of hepatic ceruloplasmin ameliorates NAFLD via SCO1-AMPK-LKB1 complex'.

Comments on 'Downregulation of hepatic ceruloplasmin ameliorates NAFLD via SCO1-AMPK-LKB1 complex'.
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DOI:
10.1093/jmcb/mjad026
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发表时间:
2023-08-03
影响因子:
5.5
通讯作者:
--
中科院分区:
生物学1区
文献类型:
--
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人类健康需要大量营养素,如氨基酸、葡萄糖和脂质,以及微量营养素,包括铜和铁。铜是组装各种酶所必需的,例如铜/锌超氧化物歧化酶和细胞色素c氧化酶(Kim等人,2008年)。已有大量文献证明,腺苷一磷酸活化蛋白激酶(AMPK)可检测细胞内葡萄糖浓度(Li等人,2019年),mTOR负责监测细胞内氨基酸水平(Liu和Sabatini,2020),而CD36可作为细胞内脂类含量的传感器(Hao等人,2020)。然而,目前尚不清楚细胞内铜的动态变化是如何被感知的,以及铜是否在调控大量营养素的代谢中扮演着重要的信使角色。肝脏是负责铜储存和体内平衡的主要器官,因此必须严格控制肝脏铜的水平,并将其维持在一个狭窄的范围内。非酒精性脂肪性肝病(NAFLD)与肝脏铜缺乏有关(Engström等人,2003年;Aigner等人,2008年)。相比之下,膳食铜摄入量-
Human health requires macronutrients, such as amino acids, glucose, and lipids, as well as micronutrients, including copper and iron. Copper is required for the assembly of various enzymes, such as copper/zinc superoxide dismutase and cytochrome c oxidase (Kim et al., 2008). It has been well documented that adenosine monophosphate-activated protein kinase (AMPK) senses intracellular glucose concentrations (Li et al., 2019), mTOR is responsible for monitoring in-tracellular amino acid levels ( Liu and Sabatini, 2020), and CD36 functions as a sensor for intracellular lipid amounts (Hao et al., 2020). However, it is still unclear how intracellular copper dynamic changes are sensed and whether copper plays a crucial messenger role in the regulation of metabolism of macronutrients. The liver is the primary organ responsible for copper storage and homeostasis, and thus the level of hepatic copper must be tightly regulated and maintained within a narrow range. Non-alcoholic fatty liver disease (NAFLD) is associated with the deficiency in hepatic copper (Engström et al., 2003; Aigner et al., 2008). By contrast, dietary copper sup-
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