101. Acerola polysaccharides ameliorate high-fat diet-induced non-alcoholic fatty liver disease through reduction of lipogenesis and improvement of mitochondrial functions in mice
- Author
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Yunsheng Xu, Hong-Kai Xie, Beiwei Zhu, Da-Yong Zhou, Fa-Wen Yin, Zhong-Yuan Liu, and Yuanyuan Hu
- Subjects
0301 basic medicine ,Male ,medicine.medical_specialty ,Antioxidant ,medicine.medical_treatment ,medicine.disease_cause ,Diet, High-Fat ,Antioxidants ,03 medical and health sciences ,Mice ,0302 clinical medicine ,Non-alcoholic Fatty Liver Disease ,Polysaccharides ,Internal medicine ,Hyperlipidemia ,Nonalcoholic fatty liver disease ,medicine ,Animals ,Chemistry ,Lipogenesis ,Fatty liver ,General Medicine ,Peroxisome ,medicine.disease ,Mitochondria ,Mice, Inbred C57BL ,Oxidative Stress ,030104 developmental biology ,Endocrinology ,030220 oncology & carcinogenesis ,lipids (amino acids, peptides, and proteins) ,Liver function ,Sterol Regulatory Element Binding Protein 1 ,Oxidation-Reduction ,Oxidative stress ,Food Science ,Malpighiaceae - Abstract
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.
- Published
- 2019