Acerola polysaccharides ameliorate high-fat diet-induced non-alcoholic fatty liver disease through reduction of lipogenesis and improvement of mitochondrial functions in mice

脂肪生成 脂肪肝 内分泌学 内科学 氧化应激 非酒精性脂肪肝 TFAM公司 生物 线粒体 抗氧化剂 脂肪变性 肝功能 脂质代谢 化学 生物化学 医学 线粒体生物发生 疾病
作者
Yuanyuan Hu,Fawen Yin,Zhongyuan Liu,Hongkai Xie,Yunsheng Xu,Dayong Zhou,Beiwei Zhu
出处
期刊:Food & Function [Royal Society of Chemistry]
卷期号:11 (1): 1037-1048 被引量:54
标识
DOI:10.1039/c9fo01611b
摘要

Acerola polysaccharides (ACPs) were purified from acerola (Malpighia emarginata DC.), a tropical fruit with strong antioxidant and anti-inflammatory activities. However, the biological activities of ACPs have barely been investigated. The present study was designed to investigate the efficacy of ACPs in the treatment of high-fat diet (HFD)-induced nonalcoholic fatty liver disease (NAFLD) in C57BL/6 mice. Male C57BL/6 mice were fed with a high-fat diet and treated with different doses of ACPs for 9 continuous weeks. NAFLD was examined in terms of body weight, lipid profiles, liver function markers, and histology. Gene expression was determined by using both qRT-PCR and western blot. Our results showed that administration of ACPs significantly reduced HFD-induced hyperlipidemia and hepatic lipid deposition by inhibiting the SREBP1c pathway in mice. ACP treatment normalized oxidative stress by activating nuclear factor (erythroid-derived-2)-like 2 (Nrf2) and reduced the expressions of pro-inflammatory cytokines in HFD fed mice. Furthermore, ACPs reduced uncoupling protein 2 (UCP2) expression, restored mitochondrial ATP content, increased mitochondrial complex I, IV, and V activity, and increased mitochondrial beta-oxidation by stimulating peroxisomal proliferator-activated receptor-gamma coactivator-1α (PGC-1α) in the liver of HFD-fed mice. Our study indicated that ACPs may be an effective dietary supplement for preventing HFD-induced NAFLD by regulating lipogenesis, reducing inflammation and oxidative stress, and promoting the mitochondrial function.
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