| Abstract: | 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. |
