小檗碱
安普克
胰岛素抵抗
过剩4
蛋白激酶A
葡萄糖摄取
AMP活化蛋白激酶
内科学
化学
腺苷
内分泌学
胰岛素
医学
药理学
生物
激酶
生物化学
作者
Juanjuan Cheng,Xingdong Ma,Gaoliang Yan,Qiuxia Yu,Zhen Huang,Guoshu Lin,Mengyao Li,Fengkun Guan,Ziren Su,Fang Yan,Yuhong Liu,Qingfeng Xie
标识
DOI:10.1016/j.fct.2023.113731
摘要
AMP-activated protein kinase (AMPK) is a master regulator of energy homeostasis that is activated in response to an elevated intracellular AMP/ATP ratio. Although many studies have shown berberine is an AMPK activator widely used in metabolic syndrome, how to properly control AMPK activity remains obscure. Our present study aimed to examine the protective effect of berberine against fructose-induced insulin resistance in rats and L6 cells, as well as its potential activation mechanism on AMPK. The results showed that berberine effectively reversed body weight gain, Lee's index, dyslipidemia and insulin intolerance. Moreover, berberine alleviated inflammatory response, antioxidant capacity and promoted glucose uptake in vivo and in vitro. The beneficial effect was associated with upregulation of both Nrf2 and AKT/GLUT4 pathways, which were regulated by AMPK. Notably, berberine could increase the level of AMP and the ratio of AMP/ATP, then further activate AMPK. Mechanistic experiments revealed that berberine suppressed the expression of adenosine monophosphate deaminase 1 (AMPD1) and promoted the expression of adenylosuccinate synthetase (ADSL). Taken together, berberine exerted excellent therapeutic effect on insulin resistance. And its mode of action may be related to the AMP‐AMPK pathway by regulating AMPD1 and ADSL.
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