Abstract: Objective: To study the regulatory effect and underlying mechanism of Pediococcus acidilactici AS185 on metabolic syndrome (MS) in mice. Methods: ICR mice were given a high-fat and high-fructose diet once a day for 6 consecutive weeks to establish an MS model, and AS185 was administered by gavage to the animals once a day from week 7 to 14. The body mass, blood glucose, blood lipid and serum inflammatory factors were determined and Western blot was performed to analyze the expression of relevant proteins. Results: The administration of P. acidilactici AS185 could reduce the serum levels of total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, insulin (INS), fasting blood glucose (FBG), free fatty acid (FFA), C-reactive protein (CRP) and lipopolysaccharide (LPS) in the mouse model. Western blot analysis showed that P. acidilactici AS185 inhibited the activation of nuclear factor (NF)-κB, and the expression of Toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88), suppressed inflammatory signaling pathways and the expression of inflammatory factors in the high-fat and high-fructose diet-fed mice. Moreover, it activated liver kinase B1 (LKB1) and the expression of adenylate activated protein kinase (AMPK), thereby enhancing the expression of phosphorylated AMPK (p-AMPK) and phosphorylated acetyl-CoA carboxylase (p-ACC), down-regulating the expression of sterol regulatory element-binding protein-1c (SREBP-1c) and finally regulating the lipid metabolism pathway. Conclusion: P. acidilactici AS185 can improve high-fat and high-fructose diet-induced metabolic syndrome in mice by activating the TLR4-MyD88-NF-κB pathway to regulate inflammatory factor levels, and activating the LKB1-AMPK signaling pathway to improve blood lipid disorders.

Key words: lactic acid bacteria; Pediococcus acidilactici; metabolic syndrome; insulin resistance; nuclear factor kappa-B; adenylate activated protein kinase