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Published on: August 30, 2019
Bifidobacterium breve BBr60 Improves Metabolic Abnormalities by Regulating Gut Microbiota Balance in a High-Fat
Yu Liao1, Xun Yuan2, An-Qi Qin2
1Department of Endocrinology and Metabolism, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Aim:
This study aimed to evaluate the modulatory effects of Bifidobacterium breve BBr60 on gut microbiota dysbiosis and metabolic abnormalities in a high-fat diet (HFD) -induced obese mouse model.
Methods:
Thirty mice aged 6 weeks were divided into a normal diet group (CTL), an HFD group, and a BBr60 intervention group (HFD + BBr60). During 8 weeks, the food intake and body weight of the mice were monitored. Subsequently, an oral glucose tolerance test (OGTT) was conducted, and fasting insulin levels, lipid profiles, and the gut microbiota composition were determined. Liver lesions, inflammation levels, and tight junction protein expression were examined using Oil Red O staining, haematoxylin and eosin staining, and reverse transcription polymerase chain reaction analysis, respectively. 16s rRNA high-throughput sequencing techniques were used to investigate the diversity and richness of the gut microbiota.
Results:
BBr60 not only ameliorated HFD-induced metabolic disorders, including weight gain (body weight, p < 0.001), hyperglycaemia (FBG, p < 0.001), insulin resistance (HOMA-IR, p = 0.002), dyslipidaemia (TC, p < 0.001), and liver steatosis, but also mitigated systemic inflammation and impaired intestinal permeability. Furthermore, BBr60 reversed gut microbiota dysbiosis, as evidenced by a significant reduction in the relative abundance of opportunistic pathogens such as Duncaniella, Allobaculum, and Parasutterella while increasing beneficial bacteria such as Clostridium cluster XIVa, Limosilactobacillus, and Bifidobacterium. Time-dynamic analyses showed that BBr60 regulated the relative abundance of the gut microbiota and improved HFD-induced dysbiosis of the gut microbiota.
Conclusion:
BBr60 significantly ameliorated glucose and lipid metabolic disorders and gut microbiota dysbiosis in an HFD-induced obese mouse model, and these effects were associated with changes in gut microbiota composition, suggesting its potential as a therapeutic intervention for obesity-related metabolic abnormalities.
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