Format

Send to

Choose Destination
Nutr Res. 2016 Apr;36(4):337-348. doi: 10.1016/j.nutres.2015.12.001. Epub 2015 Dec 4.

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.

Author information

1
Department of Life and Nanopharmaceutical Sciences, Kyung Hee University, Seoul 130-701, Korea.
2
Department of Life and Nanopharmaceutical Sciences, Kyung Hee University, Seoul 130-701, Korea; Department of Pharmacy, Kyung Hee University, Seoul 130-701, Korea.
3
Department of Pharmacy, Kyung Hee University, Seoul 130-701, Korea.
4
Department of Food and Nutrition, Kyung Hee University, Seoul, 130-701 Korea.
5
Department of Life and Nanopharmaceutical Sciences, Kyung Hee University, Seoul 130-701, Korea; Department of Pharmacy, Kyung Hee University, Seoul 130-701, Korea. Electronic address: dhkim@khu.ac.kr.

Abstract

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.

KEYWORDS:

Colitis-associated inflammation; Gut microbiota lipopolysaccharide; Hyperglycemia; Lactobacillus sakei; Obesity

PMID:
27001279
DOI:
10.1016/j.nutres.2015.12.001
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center