Effect of Lactobacillus sakei OK67 in Reducing Body and Visceral Fat in Lifestyle-Modified Overweight Individuals: A 12-Week, Randomized, Double-Blind, Placebo-Controlled Clinical Trial.

Obesity is a global health problem that affects the quality of life. It is a multidimensional chronic risk factor for major medical conditions, such as cardiovascular diseases, diabetes, and cancer. This clinical trial evaluated the efficacy of Lactobacillus sakei OK67 (DW2010), a lactic acid bacterium, in reducing body and visceral fat in overweight individuals (body mass index ≥25 kg/m2 and <30 kg/m2), aged 20-60 years. A total of 100 subjects placed in a lifestyle modification program were randomly assigned to receive either DW2010 (2.0 g/day, 1.0 × 1010 CFU) or a placebo for 12 weeks. The efficacy of DW2010 was evaluated by measuring body fat mass using dual-energy X-ray absorptiometry and visceral fat area using computed tomography. After 12 weeks, the change in body fat in the DW2010 group was not markedly different from that in the placebo group. However, visceral fat area decreased more in the DW2010 group than in the placebo group (p = 0.035). During the clinical trial, no major adverse events were reported. Moreover, no statistical differences were observed in the biochemical parameters of the DW2010 and placebo groups. Overall, we concluded that the intake of DW2010 for 12 weeks is safe and potentially reduces visceral fat in lifestyle-modified overweight subjects.

Lactobacillus sakei Alleviates High-Fat-Diet-Induced Obesity and Anxiety in Mice by Inducing AMPK Activation and SIRT1 Expression and Inhibiting Gut Microbiota-Mediated NF-κB Activation.

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

Inhibition of HCV replicon cell growth by 2-arylbenzofuran derivatives isolated from Mori Cortex Radicis.

Medicinal herbs are increasingly used in the search for safe and efficient drug candidates for hepatitis C virus infection. In this study, we have investigated the anti-HCV effect of compounds from Mori Cortex Radicis. During a screening for extracts with anti-HCV affinity from medicinal plants (173 species), the methanol extract of Mori Cortex Radicis was selected. Fractionation of the extract by monitoring antiviral activity with a replicon cell-based assay resulted in the isolation of five compounds, mulberroside C ( 1), moracin P ( 2), moracin O ( 3), moracin M ( 4) and mulberrofuran K ( 5) from the ethyl acetate-soluble fraction. Compounds 1 approximately 4 showed significant inhibitory activities. Compounds 2 and 3 showed potent inhibitory activity (IC (50) 35.6 microM, 80.8 microM, respectively) in the replicon cell assay, which was confirmed by NS3 helicase inhibitory activity (IC (50) 42.9 microM, 27.0 microM, respectively).