Sulforaphane alleviates high fat diet-induced insulin resistance via AMPK/Nrf2/GPx4 axis

莱菔硫烷 胰岛素抵抗 安普克 氧化应激 化学 内分泌学 内科学 胰岛素 抗氧化剂 高脂血症 GPX4 谷胱甘肽 糖尿病 药理学 谷胱甘肽过氧化物酶 生物化学 医学 超氧化物歧化酶 蛋白激酶A
作者
Ya Zhang,Qifang Wu,Jian Liu,Zhongshan Zhang,Xiaojing Ma,Yaoyue Zhang,Jiawen Zhu,Ronald W. Thring,Mingjiang Wu,Yitian Gao,Haibin Tong
出处
期刊:Biomedicine & Pharmacotherapy [Elsevier]
卷期号:152: 113273-113273 被引量:41
标识
DOI:10.1016/j.biopha.2022.113273
摘要

Insulin resistance is a characteristic feature of type 2 diabetes. Sulforaphane (SFN) is a natural antioxidant extracted from the cruciferous vegetables. Recent study reported that SFN exhibits excellent anti-diabetic effects, however, the underlying mechanism is still unclear. This study aimed to investigate the therapeutic effects of SFN on a high-fat diet (HFD)-induced insulin resistance and potential mechanism. SFN was found to effectively reduce body weight, fasting blood glucose and hyperlipidemia, and improve liver function in HFD-fed mice. Furthermore, SFN effectively increased glucose uptake and improved insulin signaling in palmitic acid (PA)-induced HepG2 cells. SFN also led to increased expression of antioxidant genes downstream of Nrf2 and decreased accumulation of lipid peroxides MDA and 4-HNE, both in vivo and in vitro. Further studies revealed that SFN significantly reduced glutathione peroxidase 4 (GPx4) inactivation-mediated oxidative stress by activating the AMPK and Nrf2 signaling pathways. In PA-induced HepG2 cells and flies, the alleviation of insulin resistance by SFN was diminished by GPx4 inhibitor. Taken together, SFN ameliorated HFD-induced insulin resistance by activating the AMPK-Nrf2-GPx4 pathway, providing new insights into SFN as a therapeutic compound for the alleviation of insulin resistance.
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