Obesity has become a major social problem related to health and quality of life. Our previous work demonstrated that Lactobacillus plantarum FRT10 alleviated obesity in high-fat diet (HFD)-fed mice by alleviating gut dysbiosis. However, the underlying functions of FRT10 in regulating liver and cecum contents metabolism remain unknown. Liver and cecum contents metabonomics combined with pathway analysis based on ultraperformance liquid chromatography-quadrupole-time-of-flight mass spectrometry (UHPLC-Q-TOF/MS) were performed to evaluate the alterations of metabolic profiles between obese control mice and obese mice in FRT10-treated groups. The orthogonal partial least squares discriminant analysis (OPLS-DA) score plots showed that there were significant differences in cecum contents and liver markers between experimental groups. In total, 26 potential biomarkers were identified in the liver and 15 in cecum contents that could explain the effect of FRT10 addition in HFD-fed mice. In addition, gut–liver axis analysis indicated that there was a strong correlation between cecum contents metabolites and hepatic metabolites. The mechanism of FRT10 against obesity might be related to the alterations in glycerophospholipid metabolism, primary bile acid biosynthesis, amino metabolism, and purine and pyrimidine metabolism. Studies on these metabolites could help us better understand the role of FRT10 in obesity induced by HFD.

Bacillus licheniformis is considered a potential alternative to antibiotic growth promoters of animal growth and health. However, the effects of Bacillus licheniformis on the foregut and hindgut microbiota, and their relationships with nutrient digestion and health, in broiler chickens remain unclear. In this study, we aimed to identify the effects of Bacillus licheniformis BCG on intestinal digestion and absorption, tight junctions, inflammation, and the fore- and hind-gut microbiota. We randomly assigned 240 1-day-old male AA broilers into three treatment groups: CT (basal diet), BCG1 (basal diet + 1.0 × 108 CFU/kg B. licheniformis BCG), and BCG2 (basal diet + 1.0 × 109 CFU/kg B. licheniformis BCG). On day 42, the jejunal and ileal chyme and mucosa were subjected to analysis of digestive enzyme activity, nutrient transporters, tight junctions, and signaling molecules associated with inflammation. The ileal and cecal chyme were subjected to microbiota analysis. Compared with the CT group, the B. licheniformis BCG group showed significantly greater jejunal and ileal α-amylase, maltase, and sucrase activity; moreover, the α-amylase activity in the BCG2 group was higher than that in the BCG1 group (P < 0.05). The transcript abundance of FABP-1 and FATP-1 in the BCG2 group was significantly greater than that in the CT and BCG1 groups, and the GLUT-2 and LAT-1 relative mRNA levels were greater in the BCG2 group than the CT group (P < 0.05). Dietary B. licheniformis BCG resulted in significantly higher ileal occludin, and lower IL-8 and TLR-4 mRNA levels than observed in the CT group (P < 0.05). B. licheniformis BCG supplementation significantly decreased bacterial community richness and diversity in the ileum (P < 0.05). Dietary B. licheniformis BCG shaped the ileac microbiota by increasing the prevalence of f_Sphingomonadaceae, Sphingomonas, and Limosilactobacillus, and contributed to nutrient digestion and absorption; moreover, it enhanced the intestinal barrier by increasing the prevalence of f_Lactobacillaceae, Lactobacillus, and Limosilactobacillus. Dietary B. licheniformis BCG decreased microbial community diversity by diminishing Desulfovibrio, Alistipes, Campylobacter, Vibrio, Streptococcus, and Escherichia coli-Shigella levels, and down-regulating inflammatory associated molecule expression. Therefore, dietary B. licheniformis BCG contributed to digestion and absorption of nutrients, enhanced the intestinal physical barrier, and decreased intestinal inflammation in broilers by decreasing microbial diversity and optimizing the microbiota structure.