Probiotics, known for regulating gut microbiota, may aid those with overweight or obesity, but their mechanisms require more research. This study involved 75 overweight or obese young adults, randomly assigned to either a Bifidobacterium breve BBr60 (BBr60) group or a placebo group. Both groups received diet guidance and took either BBr60 (1 × 10¹⁰ CFU/day) or a placebo for 12 weeks. Researchers analyzed body composition, serum glucose, lipids, liver and kidney function, comprehensive metabolome, and intestinal homeostasis before and after the intervention. After 12 weeks, BBr60 significantly reduced weight and BMI compared to pretreatment levels and outperformed the placebo. The BBr60 group also showed improved blood biochemistry, with notably lower fasting blood glucose (FBG) levels than the placebo group (p < 0.05). Additionally, BBr60 influenced vital serum and fecal metabolites related to three amino acid metabolic pathways and regulated the bacteria Dialister, Klebsiella, and Bacteroides, which correlated strongly with serum metabolites. These findings indicate that BBr60 can safely and effectively regulate BMI, body weight, serum glucose, lipids, and liver function markers, which may involve BBr60’s impact on key gut bacteria, which influence metabolites related to the valine, leucine, and isoleucine biosynthesis; glycine, serine, and threonine metabolism; and alanine, aspartate, and glutamate metabolism.

Objectives: Constipation is one of the most prevalent gastrointestinal disorders worldwide. Recent studies have demonstrated that probiotics may alleviate constipation by restoring gut microbiota balance. Methods: This study investigated the effects of Weizmannia coagulans BC99 (formerly Bacillus coagulans BC99) on gut microbiota and intestinal function in a loperamide-induced mouse model of functional constipation. BALB/c mice were randomly divided into six groups: control, model, phenolphthalein, BC99-L (2 × 10⁷ CFU/day), BC99-M (2 × 10⁸ CFU/day), and BC99-H (2 × 10⁹ CFU/day). After 14 days of supplementation, constipation was induced in mice via loperamide administration. Results: BC99 significantly increased fecal water content, gastrointestinal transit rate, microbial metabolic activity, and butyric acid production, while decreasing the abundance of inflammation-related metabolic pathways. Moreover, BC99 improved levels of gastrointestinal regulatory peptides, including motilin and somatostatin. The Firmicutes-to-Bacteroidetes ratio was elevated in the BC99-M and the BC99-H group compared to the model group, indicating that BC99 effectively modulated gut microbiota composition and host biosynthetic pathways. Conclusions: Weizmannia coagulans BC99 alleviated and prevented loperamide-induced functional constipation in mice by enhancing intestinal peristalsis and restoring gut microbial homeostasis.

Background/Objectives: With the improvement of living standards, alcoholic liver disease caused by long-term drinking has been a common multiple disease. Probiotic interventions may help mitigate liver damage caused by alcohol intake, but the mechanisms need more investigation. Methods: This study involved 70 long-term alcohol drinkers (18–65 years old, alcohol consumption ≥20 g/day, lasting for more than one year) who were randomly assigned to either the BC99 group or the placebo group. Two groups were given BC99 (3 g/day, 1 × 10¹⁰ CFU) or placebo (3 g/day) for 60 days, respectively. Before and after the intervention, blood routine indicators, liver function, renal function, inflammatory factors and intestinal flora were evaluated. Results: The results showed that intervention with Weizmannia coagulans BC99 reduced the levels of alanine aminotransferase, aspartate aminotransferase, glutamyl transpeptidase, serum total bilirubin, blood urea nitrogen, uric acid and ‘blood urea nitrogen/creatinine’. Weizmannia coagulans BC99 also reduced the levels of pro-inflammatory factors TNF-α and IL-6 and increased the levels of anti-inflammatory factor IL-10. The results of intestinal flora analysis showed that Weizmannia coagulans BC99 regulated the imbalance of intestinal flora, increased the beneficial bacteria abundance (Prevotella, Faecalibacterium and Roseburia) and reduced the conditionally pathogenic bacteria abundance (Escherichia-Shigella and Klebsiella). Both LEfSe analysis and random forest analysis indicated that the increase in the abundance of Muribaculaceae induced by BC99 was a key factor in alleviating alcohol-induced liver damage. Conclusions: These findings demonstrate that Weizmannia coagulans BC99 has the potential to alleviate alcoholic liver injury and provide an effective strategy for liver protection in long-term drinkers.

Obesity, a prevalent metabolic disorder in youth, leads to complications and economic strain. Gut dysbiosis significantly contributes to obesity and metabolic issues. Bifidobacterium breve, a probiotic strain, may help regulate gut dysbiosis and benefit obese individuals. However, more research is needed on its effect on serum metabolism. A total of 75 overweight or obese young adults (aged 19–45) participated in the current study, and were randomly divided into probiotic and placebo groups using a random number table. Both groups received dietary guidance and underwent twelve weeks of intervention with either oral Bifidobacterium breve BBr60 (BBr60) or a placebo. After the intervention, collection and analysis of fasting serum samples were conducted using mass spectrometry coupled with liquid chromatography. Analyses of associations were conducted in order to determine the correlations between key serum metabolites and clinical obesity indicators, aiming to understand the influence of BBr60. Due to 10 participants dropping out for personal reasons, the study included 32 and 33 participants in the placebo and the BBr60 groups, respectively. The BBr60 intervention significantly regulated 134 serum metabolites and influenced crucial metabolic pathways in obesity management (p < 0.05), including ascorbate and aldarate metabolism for oxidative stress reduction, cholesterol metabolism for lipid regulation, parathyroid hormone synthesis, secretion and action for the endocrine system, oxidative phosphorylation for enhanced energy efficiency, and glycolysis/gluconeogenesis for glucose metabolism. Analysis showed a positive relationship between fasting blood glucose (FBG), aspartate aminotransferase (AST), total protein (TP), and the content of 5-Methyl DL-glutamate (p < 0.05). Similarly, body mass index (BMI), weight, and body fat percentage (BFP) were positively linked to serum metabolites (1-Hydroxycyclohexyl) acetic acid, and 5-Oxooctanoic acid (p < 0.05). Significant associations of AST levels with key serum metabolites in cholesterol metabolism pathways further suggest BBr60’s potential to improve liver function and overall metabolic health in overweight or obese individuals. These findings support BBr60’s effectiveness in modulating serum metabolic profiles and suggest it may improve liver function and BMI in overweight or obese individuals by regulating key serum metabolites.

Acute alcoholic liver injury (AALI) remains a significant global health concern, primarily driven by oxidative stress. This study investigated the protective mechanisms of Weizmannia coagulans BC99 against alcohol-induced oxidative stress using a dual model in rats and Caenorhabditis elegans. In rats, excessive alcohol was predominantly metabolized via the CYP2E1 pathway, leading to severe oxidative stress. However, intervention with BC99 suppressed CYP2E1 expression and enhanced antioxidant enzyme activities through the Nrf2/SKN-1 pathway, thereby alleviating oxidative stress. Additionally, BC99 treatment elevated glutamate and aspartate levels while reducing glycerate and glucose, which collectively increased glutathione levels and mitigated oxidative stress triggered by glucose metabolism disorders. In C. elegans, BC99 reduced excessive ROS by upregulating Nrf2/skn-1, daf-16, and their downstream antioxidant genes, consequently alleviating the biotoxicity associated with alcohol-induced oxidative damage. The protective effects of BC99 were markedly diminished in the skn-1 mutant (GR2245) and daf-16 mutant (CF1038), further confirming the pivotal roles of SKN-1 and DAF-16 pathways in BC99-mediated antioxidant protection. Taken together, these findings reveal that BC99 mitigates alcohol-induced oxidative stress by activating the Nrf2/SKN-1 pathway and regulating liver metabolites to eliminate excess ROS, thereby providing a theoretical basis for the application of probiotics in preventing acute alcoholic liver injury.

Adequate protein consumption is essential for optimal physical fitness and enhancing athletic performance. This study explored the impact of Weizmannia coagulans BC99 on protein-supplemented male fatigued mice, examining aspects such as protein digestion, exercise endurance, fatigue-related biochemistry, oxidative stress, and gut microbiota alterations. Results indicate that the synergistic effect of probiotics and protein significantly boosts the activity of protein-digesting enzymes, enhances protein absorption, and reduces serum levels of urea nitrogen, lactate, lactate dehydrogenase, creatine kinase, malondialdehyde, and the inflammatory cytokines interleukin-1β and interleukin-6 in skeletal muscle. Additionally, serum catalase, glutathione, superoxide dismutase levels, interleukin-4 in skeletal muscle, and glycogen stores in muscle and liver were notably increased. The study also found elevated mRNA expression levels of Nrf2 and HO-1 in skeletal muscle. Furthermore, an increase in short-chain fatty acids was observed in the probiotic treatment group, and 16S rDNA sequencing revealed that Weizmannia coagulans BC99 enhanced gut microbiota diversity and augmented beneficial bacterial populations including Roseburia, Mucispirillum, Rikenella, and Kineothrix. Collectively, these findings suggest that combining BC99 with protein supplementation can effectively improve gut flora, thereby enhancing exercise capacity and exerting potent anti-fatigue effects. Our research provides a new possibility for alleviating exercise-induced fatigue.