Key Laboratory of Ministry of Education for Medicinal Resource and Natural Pharmaceutical Chemistry, College of Life Sciences, Shaanxi Normal University, Xi'an 710062, China.
Key Laboratory of Ministry of Education for Medicinal Resource and Natural Pharmaceutical Chemistry, College of Life Sciences, Shaanxi Normal University, Xi'an 710062, China.
Food Res Int. 2020 Apr;130:108929. doi: 10.1016/j.foodres.2019.108929. Epub 2019 Dec 23.
This study aimed to explore a novel strategy for dietary okra fruit powder (OFP) consumption on attenuation of non-alcohol fatty liver damage, lipid metabolic disorder and gut microbiota dysbiosis and associated mechanisms in high-fat diet (HFD)-induced obese mice. C57BL/6J mice were fed a normal diet and HFD feeds supplemented with or without OFP (2.5%, 5% and 10%, n = 10) for 12 weeks. The results showed that supplementation of OFP caused strong inhibition on HFD-caused high blood glucose, body weight gain and liver fat accumulation, as well as dyslipidemia involved in a dose-dependent modulation of hepatic FAS and CD36 expressions of obese mice. The hepatic LXR-α energy metabolism and PPAR-α pathway were also doubly activated by OFP to alleviate lipogenesis, obesity and metabolic syndrome. Malonaldehyde production was effectively antagonized, and glutathione peroxidase and superoxide dismutase activities were elevated by OFP supplementation in HFD-fed mice. OFP also significantly improved colonic SCFAs (acetic acid, propionic acid and butyrate acid) formation, especially for butyrate production via increasing the proportion of selected butyrate-producing bacteria. OFP also dramatically modified the gut microbial species at the family level with suppressing an increase in Proteobacteria, Actinobacteria and F/B ratio, and the decrease in Bacteroidetes caused by HFD. These findings support that dietary OFP consumption is a novel strategy to prevent obesity, metabolic syndrome and gut microbiota imbalance.
本研究旨在探索食用秋葵果粉（OFP）的新策略，以减轻高脂肪饮食（HFD）诱导肥胖小鼠的非酒精性脂肪肝损伤、脂质代谢紊乱和肠道菌群失调及其相关机制。C57BL/6J 小鼠分别喂食正常饮食和 HFD 饲料，并补充或不补充 OFP（2.5%、5%和 10%，n=10）12 周。结果表明，OFP 的补充强烈抑制了 HFD 引起的高血糖、体重增加和肝脂肪堆积，以及涉及肥胖小鼠肝 FAS 和 CD36 表达的血脂异常的剂量依赖性调节。OFP 还通过双重激活肝 LXR-α 能量代谢和 PPAR-α 通路，减轻脂肪生成、肥胖和代谢综合征。OFP 补充还能有效拮抗丙二醛的产生，提高谷胱甘肽过氧化物酶和超氧化物歧化酶的活性。OFP 还显著改善了 HFD 喂养小鼠结肠中 SCFAs（乙酸、丙酸和丁酸）的形成，特别是通过增加特定的丁酸产生菌的比例来增加丁酸的产生。OFP 还显著改变了肠道微生物种类在科水平上，抑制了厚壁菌门、放线菌门和 F/B 比值的增加，以及 HFD 引起的拟杆菌门的减少。这些发现支持食用 OFP 是预防肥胖、代谢综合征和肠道菌群失衡的一种新策略。
