Abstract
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. 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-κB 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-κB 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-κB 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. Lactobacillus sakei can alleviate HFD-induced obesity, colitis, and anxiety by regulating gut microbiota-mediated AMPK and NF-κB activation and SIRT-1 expression.
Published Version
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