Journal
MOLECULAR NUTRITION & FOOD RESEARCH
Volume 63, Issue 6, Pages -Publisher
WILEY
DOI: 10.1002/mnfr.201800978
Keywords
anxiety; colitis; gut microbiota; Lactobobacillus sakei; obesity
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Funding
- Korea Institute of Planning and Evaluation for Technology in Food, Agriculture and Forestry (IPET) through Technology Commercialization Support Program - Ministry of Agriculture, Food and Rural Affairs (MAFRA) [816003-3]
- Medical Research Program through the National Research Foundation of Korea (NRF) - Ministry of Science and ICT [NRF-2017R1A5A2014768]
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Scope Long-term feeding of a high-fat diet (HFD) causes gastrointestinal inflammation and gut microbiota disturbance, leading to the increased occurrence of obesity and anxiety. In the present study, the effects of heat-labile Lactobacillus sakei OK67, tyndallized OK67 (tOK67), and heat-stable Lactobacillus sakei PK16 on HFD-induced obesity and anxiety in mice are examined. Methods and results Obesity is induced in mice by feeding with HFD. Oral administration of live OK67, tOK67, or PK16 reduces HFD-induced body and liver weights and blood triglyceride, total cholesterol, corticosterone, and lipopolysaccharide levels. These treatments also suppress HFD-induced NF-kappa B activation and increased HFD-suppressed AMP-activated protein kinase (AMPK) activation and SIRT-1 expression in the liver. OK67 or PK16 treatment alleviates HFD-induced anxiety-like behaviors and increases BDNF expression and NF-kappa B activation in the hippocampus. Moreover, OK67 or PK16 treatment suppresses HFD-induced colitis and suppresses the Proteobacteria population and fecal lipopolysaccharide levels in mice. OK67 or PK16 treatment inhibits NF-kappa B activation and induced AMPK activation and SIRT-1 expression in lipopolysaccharide-stimulated Caco-2 cells. Overall, the antiobesity and anxiolytic effects of live OK67 are more potent than those of tOK67. Conclusion Lactobacillus sakei can alleviate HFD-induced obesity, colitis, and anxiety by regulating gut microbiota-mediated AMPK and NF-kappa B activation and SIRT-1 expression.
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