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, 8 (1), e54617

Anti-obesity Effect of Lactobacillus Gasseri BNR17 in High-Sucrose Diet-Induced Obese Mice

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Anti-obesity Effect of Lactobacillus Gasseri BNR17 in High-Sucrose Diet-Induced Obese Mice

Ji-Hee Kang et al. PLoS One.

Abstract

Previously, we reported that Lactobacillus gasseri BNR17 (BNR17), a probiotic strain isolated from human breast milk, inhibited increases in body weight and adipocyte tissue weight in high-sucrose diet-fed Sprague-Dawley (SD) rats and reduced glucose levels in type 2 diabetes mice. In the current study, we conducted further experiments to extend these observations and elucidate the mechanism involved. C57BL/6J mice received a normal diet, high-sucrose diet or high-sucrose diet containing L. gasseri BNR17 (10(9) or 10(10) CFU) for 10 weeks. The administration of L. gasseri BNR17 significantly reduced the body weight and white adipose tissue weight regardless of the dose administered. In BNR17-fed groups, mRNA levels of fatty acid oxidation-related genes (ACO, CPT1, PPARα, PPARδ) were significantly higher and those of fatty acid synthesis-related genes (SREBP-1c, ACC) were lower compared to the high-sucrose-diet group. The expression of GLUT4, main glucose transporter-4, was elevated in BNR17-fed groups. L. gasseri BNR17 also reduced the levels of leptin and insulin in serum. These results suggest that the anti-obesity actions of L. gasseri BNR17 can be attributed to elevated expression of fatty acid oxidation-related genes and reduced levels of leptin. Additionally, data suggested the anti-diabetes activity of L. gasseri BNR17 may be to due elevated GLUT4 and reduced insulin levels.

Conflict of interest statement

Competing Interests: All authors are employed by the Bioneer Corporation. Bioneer Co. has patents for Lactobacillus gasseri BNR17. This does not alter the authors’ adherence to all the PLOS ONE policies on sharing data and materials, as detailed online in the guide for authors.

Figures

Figure 1
Figure 1. L. gasseri BNR17 supplementation decreases high-sucrose diet-induced body weight gain and fat mass accumulation.
(A) Change in body weight, (B) change in food intake, (C) representative CT scanning images of abdominal (left) and whole body (right) fat accumulation (in black) at 10 weeks (D) correspond to the volume of subcutaneous and abdominal fat, (E) representative adipose tissue-staining images in mice of four groups, (F) adipocyte mean area (µm2). Data represent the means ± SD. Pairwise t-test: *P<0.05, **P<0.01, ***P<0.001 versus the ND group; # P<0.05, ## P<0.01, ### P<0.001 versus the HSD group.
Figure 2
Figure 2. L. gasseri BNR17 affects mRNA expression in the liver.
C57BL/6J mice were given ND, HSD, or HSD containing BNR17 (109 or 1010 CFU) for 10 weeks. The liver was then removed and mRNA expression was measured by real-time RT-PCR using β-actin as a housekeeping gene. Data represent the means ± SD. Pairwise t-test: *P<0.05, **P<0.01, versus the ND group; # P<0.05, ## P<0.01 versus the HSD group.
Figure 3
Figure 3. L. gasseri BNR17 affects mRNA expression in white adipose tissue.
C57BL/6J mice were given ND, HSD, or HSD containing BNR17 (109 or 1010 CFU) for 10 weeks. The white adipose tissue was then removed and mRNA expression was measured by real-time RT-PCR using β-actin as a housekeeping gene. Data represent the means ± SD. Pairwise t-test: *P<0.05, **P<0.01 versus the ND group; # P<0.05 versus the HSD group.
Figure 4
Figure 4. L. gasseri BNR17 affects endocrine hormones.
C57BL/6J mice were given ND, HSD, or HSD containing BNR17 (109 or 1010 CFU) for 10 weeks. Serum was obtained by centrifugation of whole blood and analyzed. GIP, glucose-dependent insulinotropic polypeptide; GLP, glucagon-like peptide. Data represent the means ± SD. Wilcoxon rank-sum test: *P<0.05, **P<0.01, ***P<0.001 versus the ND group; # P<0.05, ## P<0.01 versus the HSD group.

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Grant support

This work was supported by High Value-Added Food Technology Development Program; Ministry for Food, Agriculture, Forestry and Fisheries, Republic of Korea. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
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