Bifidobacterium animalis subsp. lactis lkm512 attenuates obesity-associated inflammation and insulin resistance through the modification of gut microbiota in high-fat diet-induced obese mice.

Abstract

Scope: The impacts of longevity-promoting probiotic Bifidobacterium animalis subsp. lactis LKM512 (LKM512) on metabolic disease remain unclear. Here, the authors aim to explore the potential of LKM512 on the host physiological function and gut microbiota in high-fat diet-induced obese mice.

Methods and results: LKM512 are orally administrated for 12 weeks, and the effects of LKM 512 on systemic inflammation and insulin resistance, as well as gut microbiota, are investigated in high-fat (HF) diet-induced obese mice. LKM512 supplementation ameliorates hepatic lipid accumulation, attenuates hepatic and adipose tissue inflammation, and improves intestinal barrier function. These results are associated with improved insulin sensitivity and metabolic endotoxemia. Furthermore, the colonization of LKM512 induces an increase in polyamine metabolism and production, together with significant alternations in the composition and function of gut microbiota in obese mice, which are correlated with these improved metabolic phenotypes in the host.

Conclusion: The probiotic strain LKM512 may become a promising strategy to improve obesity and related metabolic disorders.

Keywords: gut barrier; gut microbiota; inflammation; obesity; probiotics.