化学
生物化学
棕榈酸
转录因子
β氧化
脂肪性肝炎
脂肪酸
脂肪变性
多不饱和脂肪酸
基因沉默
染色体易位
饱和脂肪酸
脂肪肝
过氧化物酶体
脂质代谢
脂肪生成
新陈代谢
脂肪酸代谢
TFEB
细胞
体内
KEAP1型
代谢途径
活性氧
细胞生物学
氧化磷酸化
脂质氧化
作者
Cong Zhang,Yingxi Luo,Yangkun Xiong,Liang Chen,Haixia Zhao,Zhenpeng Qiu,Yuan Yang
标识
DOI:10.1021/acs.jafc.5c09366
摘要
, has been demonstrated to have hepatoprotective potential, but its effect in the treatment of metabolic dysfunction-associated steatohepatitis (MASH) remains unclear. Here, we found that gigantol treatment greatly corrected dyslipidemia, hepatic dysfunction, and hepatic histological changes that arrested MASH occurrence in high-fat and high-fructose-diet (HFFD)-fed mice. Mechanistically, gigantol promoted the nuclear translocation of the transcription factor EB (TFEB) to regulate the key factors of lipophagy and fatty acid oxidation to maintain hepatic lipid metabolism homeostasis. Consistent results were observed in palmitic acid-induced cell models. Notably, silencing TFEB reversed the effect of gigantol in enhancing lipophagy and fatty acid oxidation in vivo and in vitro. In summary, this study provides strong evidence to demonstrate that gigantol attenuates HFFD-induced MASH by promoting TFEB-dependent lipophagy and fatty acid oxidation, suggesting that gigantol, an edible plant-derived compound, is promising to be developed as a therapeutic drug for MASH in the future.
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