Foxtail millet proteins and their hydrolysates have the potential to prevent atherosclerosis (AS). In our present study, a novel Bowman-Birk type major trypsin inhibitor from foxtail millet bran (FMB-BBTI) with an anti-AS effect was obtained by in vitro gastrointestinal bionic digestion. Further, the anti-AS activity of FMB-BBTI was verified by the classic apoE−/− mice model, characterized by the decreases of the inflammatory cytokines (TNF-α and IL-1β) and atherosclerotic plaque. Importantly, FMB-BBTI remodeled the structure of gut microbiota in apoE−/− mice, including the increase of Firmicutes at the phylum level, and the abundance alteration of five genera at the genus level, especially significant enrichment of Lactobacillus. Collectively, FMB-BBTI markedly restrains the AS progress, suggesting that the remodeling of gut microbiota induced by FMB-BBTI may be the critical factor for its anti-AS activity. This study indicates that FMB-BBTI may serve as a vital functional component contributing to the anti-AS potential of foxtail millet bran.

The potentially beneficial effects of probiotics in the treatment of obesity have been generally demonstrated. In the present study, a new strain of Lactobacillus reuteri SY523 (L. reuteri SY523) with an anti-obesity effect was isolated from the fecal microbiota of diet-induced obese mice. Untargeted metabolomics analysis of mice serum showed that the significantly differential metabolite indole-3-carboxaldehyde (3-IAId) was markedly elevated in the L. reuteri SY523-treated group, and interestingly, the abundance of 3-IAId was significantly negatively associated with obesity-related indicators. As expected, in the HepG2 cell induced by free fatty acids, the potential activity of 3-IAId in restraining lipid deposition was verified. Further, we found that 3-IAId was involved in the anti-obesity effect of L. reuteri SY523 mainly via regulating the cGMP/cAMP signaling pathway. The highlight of this study lies in clarifying the pivotal role of metabolite 3-IAId in the anti-obesity effect induced by L. reuteri SY523, which is conducive to the development of probiotics for anti-obesity agents.

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Non-alcoholic fatty liver disease (NAFLD) is a serious health problem worldwide. Impeding fatty acid uptake may be an attractive therapeutic strategy for NAFLD. In the current study, we found that millet bran protein hydrolysate (MBPH) prepared by in vitro gastrointestinal bionic digestion exhibits the potential of anti-NAFLD in vitro and in vivo, characterized by the alleviation of hepatic steatosis and the reduction of lipid accumulation. Further, MBPH significantly decreased the expression levels of fatty acid uptake related genes (FABP1, FABP2, FABP4, CD36, and CPT-1α) of liver tissue in a NAFLD mice model through activating peroxisome proliferator-activated receptor γ (PPARγ) and efficiently restrained the fatty acid uptake of liver tissue, thus exerting anti-NAFLD activity. As expected, the anti-NAFLD effect induced by MBPH, characterized by the alleviation of hepatic vacuolar degeneration, hepatic steatosis, and fibrosis, was effectively abrogated with PPARγ inhibitor (GW9662) treatment. These results indicate that the retardant of fatty acid uptake induced by PPARγ activation may be the critical factor for the anti-NAFLD effect of MBPH. Collectively, MBPH has the potential as a next-generation dietary supplementation for the prevention and treatment of NAFLD.