Probiotic Mixture Golden Bifid Attenuates Dyslipidemia in Obesity and Reshapes Gut Microbiota through FABP2 Modulation

Background Our previous study demonstrated that the expression of fatty acid binding protein 2 (FABP2) was significantly upregulated in mice fed a high-fat diet (HFD). In the present study we evaluated the effects of a probiotic mixture Golden Bifid consisting of Bifidobacterium longum subsp. longum , Streptococcus salivarius subsp. thermophilus and Lactobacillus delbrueckii subsp. bulgaricus (BSL) on HFD-induced obesity, gut microbiota composition, and the underlying mechanisms. Methods Male C57BL/6 mice were fed either a normal diet or an HFD. HFD-fed mice were orally administered either saline or BSL by gavage. After 6 weeks of treatment, organ indices, blood lipid profiles, fasting blood glucose, gene expression, and gut microbiota composition were analyzed. Results BSL treatment reduced body weight gain, fasting blood glucose, and epididymal white adipose tissue (eWAT) mass, increased the brown adipose tissue (BAT) index, and improved serum, fecal, and hepatic lipids profiles in HFD-induced obese mice. After BSL intervention also significantly altered the expression of genes involved in lipid metabolism and transport in the jejunum. Specifically, the mRNA expression levels of peroxisome proliferator-activated receptor γ (PPARγ) and fatty acid-binding protein 2 (FABP2), 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA reductase), and peroxisome proliferator-activated receptor α (PPARα) were significantly decreased, whereas liver X receptor α (LXR-α) expression was significantly increased. KEGG pathway analysis further showed that BSL suppressed fatty acid metabolism and the PPAR signaling pathway. In addition, BSL increased the relative abundance of Rikenellaceae, Bifidobacteriaceae, Barnesiella and Paramuribaculum , while decreasing the relative abundance of Allobaculum, Blautia and Kribbibacteriaceae . Conclusion BSL may improve obesity and obesity-associated lipid metabolism disorders by suppressing the FABP2-PPAR axis, downregulating the expression of HMG-CoA reductase and PPARα, and upregulating the expression of LXR-α, and modulating the gut microbiota composition.