Lactobacillus sakei OK67 ameliorates high-fat diet-induced blood glucose intolerance and obesity in mice by inhibiting gut microbiota lipopolysaccharide production and inducing colon tight junction protein expression
| Autor: | Myung Joo Han, Jin-Ju Jeong, Su-Min Lim, Kyung Hee Woo, Dong-Hyun Kim |
|---|---|
| Rok vydání: | 2015 |
| Předmět: |
0301 basic medicine
Lipopolysaccharides Male medicine.medical_specialty Lipopolysaccharide Colon Endocrinology Diabetes and Metabolism Adipose tissue Gene Expression Inflammation Biology Gut flora Diet High-Fat Real-Time Polymerase Chain Reaction Proinflammatory cytokine 03 medical and health sciences chemistry.chemical_compound Mice Endocrinology Latilactobacillus sakei Internal medicine Glucose Intolerance medicine Animals Obesity Nutrition and Dietetics Tight Junction Proteins Probiotics digestive oral and skin physiology food and beverages biology.organism_classification Lactobacillus sakei Gastrointestinal Microbiome Mice Inbred C57BL Fatty acid synthase 030104 developmental biology chemistry Immunology biology.protein lipids (amino acids peptides and proteins) Tumor necrosis factor alpha medicine.symptom |
| Zdroj: | Nutrition research (New York, N.Y.). 36(4) |
| ISSN: | 1879-0739 |
| Popis: | A high-fat diet (HFD) induces obesity and the associated increases in blood glucose and inflammation through changes in gut microbiota, endotoxemia, and increased gut permeability. To counteract this, researchers have suggested that the use of probiotics that suppress production of proinflammatory lipopolysaccharide (LPS). Here, we tested whether Lactobacillus sakei OK67, which inhibits gut microbiota LPS production selected from among the lactic acid bacteria isolated from kimchi, exerted antihypoglycemic or anti-inflammatory effects in HFD-fed mice. Mice were randomly divided into 2 groups and fed an HFD or a low-fat diet for 4 weeks. These groups were further subdivided; 1 subgroup was treated with L sakei OK67 and fed the experimental diet for 4.5 weeks, whereas the other subgroup was fed the experimental diet alone. L sakei OK67 treatment lowered HFD-elevated LPS levels in blood and colonic fluid and significantly decreased HFD-elevated fasting blood glucose levels and the area under the curve in an oral glucose tolerance test. L sakei OK67 treatment inhibited HFD-induced body and epididymal fat weight gains, suppressed HFD-induced tumor necrosis factor-α and interleukin-1β expression and nuclear factor-κB activation in the colon, and significantly increased HFD-suppressed interleukin-10 and tight junction protein expression in the colon. Oral administration of L sakei OK67 significantly downregulated HFD-induced expression of peroxisome proliferator-activated receptor γ, fatty acid synthase, and tumor necrosis factor-α in adipose tissue. In addition, L sakei OK67 treatment strongly inhibited nuclear factor-κB activation in LPS-stimulated peritoneal macrophages. We report that L sakei OK67 ameliorates HFD-induced hyperglycemia and obesity by reducing inflammation and increasing the expression of colon tight junction proteins in mice. |
| Databáze: | OpenAIRE |
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