Journal
NUTRITION RESEARCH
Volume 67, Issue -, Pages 78-89Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.nutres.2019.03.008
Keywords
High-fat diet; Liver steatosis; Obesity; Colitis; Lactobobacillus plantarum; Bifidobacterium longum
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Funding
- Ministry of Trade, Industry and Energy (MOTIE)
- Korea Institute for Advancement of Technology(KIAT) [N0002485]
- Korea Evaluation Institute of Industrial Technology (KEIT) [N0002485] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Long-term feeding of a high-fat diet (HFD) induces endotoxemia and gastrointestinal inflammation by disturbing gut microbiota composition and membrane permeability, resulting in the acceleration of obesity. Some probiotics exhibit anti-inflammatory effects in vitro and in vivo. Therefore, we hypothesized that anti-inflammatory probiotics could lead to the simultaneous attenuation of endotoxemia, liver steatosis, obesity, and colitis in mice with HFD-induced obesity. Herein, we examined whether Lactobacillus plantarum LC27 and/or Bifidobacterium longum LC, which significantly suppressed NF-kappa B activation in lipopolysaccharide-or fecal lysate-stimulated Caco-2 cells, could simultaneously alleviate liver steatosis and colitis in mice with HFD-induced obesity. Oral administration of LC27, LC67, or their (3:1) mixture (LM) reduced HFD-induced aspartate transaminase, alanine transaminase, triglyceride, total cholesterol, and lipopolysaccharide levels in the blood and liver. Their treatments also suppressed HFD-induced NF-kappa B activation and increased AMP-activated protein kinase (AMPK) activation and claudin-1 and occludin expression in the liver and colon. Moreover, LC27, LC67, or LM treatment reduced HFD-induced Firmicutes and Proteobacteria populations in gut microbiota and fecal lipopolysaccharide production. The hypothesis was supported by the findings that anti-inflammatory LC27 and/or LC67 simultaneously alleviated liver steatosis, obesity, and colitis by regulating NF-kappa B and AMPK activation through the inhibition of gut microbiota lipopolysaccharide production. (C) 2019 Elsevier Inc. All rights reserved.
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