ATP-binding cassette transporter subfamily G member 2 (ABCG2) is responsible for the excretion of foreign substances, such as uric acid (UA) and indoxyl sulfate (IS), from the body. Given the importance of increased ABCG2 expression in UA excretion, we investigated the enhancement of intestinal ABCG2 expression using Lactiplantibacillus plantarum 06CC2 (LP06CC2). Mice were reared on a potassium oxonate-induced high-purine model at doses of 0.02% or 0.1% LP06CC2 for three weeks. Results showed that LP06CC2 feeding resulted in increased ABCG2 expression in the small intestine. The expression level of large intestinal ABCG2 also showed a tendency to increase, suggesting upregulation of the intestinal excretion transporter ABCG2 by LP06CC2. Overall, LP06CC2 treatment increased fecal UA excretion and showed a trend towards increased fecal excretion of IS, suggesting that LP06CC2 treatment enhanced the expression of intestinal ABCG2, thereby promoting the excretion of UA and other substances from the intestinal tract.

Background/Objectives: The increase in the global prevalence of obesity has created a need for safe and effective preventive strategies. Probiotics have gained attention for their potential to modulate the gut microbiota and improve metabolic health. In this study, we examined the anti-obesity effects of Lactiplantibacillus plantarum strain 06CC2 (LP06CC2) in a mouse model of mild diet-induced obesity that mimics early-stage metabolic imbalance without significant body weight gain. Methods: Mice were fed a high-fat diet for 8 weeks, with or without LP06CC2 supplementation. Biochemical assays were used to determine the metabolic effects of LP06CC2, and 16S rRNA sequencing was performed to analyze the gut microbiota. Results: LP06CC2 attenuated epididymal fat accumulation and adipocyte hypertrophy, improved the gene expression profiles related to lipid metabolism and inflammation in adipose tissue, and reduced early hepatic steatosis. 16S rRNA sequencing revealed that LP06CC2 modulated the diversity and composition of the gut microbiota, notably suppressing HFD-induced increases in Mucispirillum schaedleri and other taxa associated with inflammation. LP06CC2-treated mice exhibited higher alpha diversity and partial restoration of their microbial profiles toward those of the normal diet-fed animals. LP06CC2 also downregulated pro-inflammatory cytokines and genes related to lipid uptake while modulating markers of thermogenesis and lipolysis. Conclusions: These findings indicate that LP06CC2 can prevent fat accumulation and gut dysbiosis in the pre-obese state, supporting its potential as a functional food ingredient for early intervention in obesity. Further human trials and studies using advanced obesity models are warranted to confirm its efficacy and elucidate its underlying mechanisms of action.