4.7 Article

Red cabbage microgreen modulation of gut microbiota is associated with attenuation of diet-induced obesity risk factors in a mouse model

Journal

FOOD & FUNCTION
Volume 14, Issue 14, Pages 6654-6664

Publisher

ROYAL SOC CHEMISTRY
DOI: 10.1039/d3fo01249b

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Cruciferous vegetable microgreens, such as red cabbage microgreens, have been found to have more health benefits compared to their mature counterparts. However, little is known about the biological effects of microgreens. This study examined the impact of consuming red cabbage microgreens on the gut microbiota using a rodent diet-induced obesity model and found significant changes in microbial composition.
Cruciferous vegetable microgreens, such as red cabbage microgreens (RCMG), are of special interest due to their well-documented health-promoting effects compared to their mature counterparts. However, little is known of the biological effects of microgreens. The present study used a rodent diet-induced obesity model to investigate the effect of consuming RCMG on the gut microbiota. We found that the consumption of RCMG exerted profound impacts on the microbial composition in mice. Specifically, the species diversity of mice on both low fat (LF) and high fat (HF) diets was significantly increased by the consumption of RCMG. In comparison with the LF control group, the intake of RCMG increased the gut Firmicutes/Bacteroidetes (F/B) ratio. Furthermore, an unidentified species of the Clostridiales order, increased by RCMG, was found to be negatively correlated with the hepatic cholesterol ester level in mice (r = -0.43, p < 0.05). In addition, RCMG significantly inhibited HF diet-induced elevation of the genus AF12, of which the abundance was positively correlated with the body weight gain (r = 0.52, p < 0.01) and fecal bile acid in mice (r = 0.59, p < 0.01). Overall, our results demonstrated that the consumption of RCMG in the diet can alter the gut microbiota, and attenuation of HF diet-induced body weight gain and altered cholesterol metabolism may be mediated through regulation of the gut microbiota.

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