Heat-killed Bifidobacterium longum LB-P23 ameliorates metabolic dysfunction in high-fat and high-sucrose diet-fed mice through gut microbiota modulation

The gut microbiota plays a pivotal role in obesity and metabolic disorders. This study evaluated the anti-obesity effects of heat-killed Bifidobacterium longum LB-P23 in a high-fat, high-sucrose diet-induced obese mouse model. Mice received low (1 × 10 8 TCC) or high (1 × 10 9 TCC) doses of B. longum LB-P23 for 8 weeks. High-dose B. longum LB-P23 significantly reduced body weight gain, insulin resistance and hepatic steatosis, while enhancing thermogenesis, and gut barrier integrity by regulating genes related to insulin signaling, β-oxidation, thermogenesis, and tight junctions. It also alleviated diet-induced dysbiosis, reducing Parabacteroides , and Colidextribacter , while enriching Romboustia, whose abundance positively correlated with plasma IL-22, indicating activation of IL-22 signaling. In vitro , B. longum LB-P23 suppressed lipid accumulation in 3T3-L1 adipocytes. Collectively, heat-killed B. longum LB-P23 exerts multi-organ metabolic benefits through modulation of insulin signaling, thermogenesis, and gut–immune interactions, supporting its potential as a safe anti-obesity intervention.