EFFECT OF BIFIDOBACTERIUM ANIMALIS SSP. LACTIS GCL2505, A PROBIOTIC STRAIN THAT PROLIFERATES IN THE GUT, ON VISCERAL FAT ACCUMULATION: EVIDENCE FROM HUMAN AND MICE STUDIES

Koga Y., Nishijima T., Aoki R., Anzawa D., Kamikado K.
Institute of Health Sciences, Ezaki Glico Co., Ltd., Japan

Introduction:
Gut microbiota currently has been recognized as the great contributor to the worldwide prevalence of metabolic syndrome (MS) which is based on the visceral fat accumulation. Numerous reports have indicated that gut bifidobacteria are associated with the improvement of MS, though the mechanism remains unclear. Bifidobacterium animalis ssp. lactis GCL2505 (GCL2505) was previously reported to proliferate in the gut and improve the fecal frequency in human study. The aims of present study were to investigate the preventive effect and its underlying mechanism of GCL2505 on visceral fat accumulation, a major risk factor of MS, in human and mice studies.

Methods:
The randomized, double-blind, placebo-controlled trial was carried out in 137 subjects with obese tendency. The subjects were assigned in two groups to receive fermented milk containing 8×1010 CFU of GCL2505 (GCL2505 group) or fermented milk without GCL2505 as placebo (Placebo group) for 12 weeks. To investigate the mechanism, we compared the effect of oral administration of GCL2505 (109 CFU/day) to that of Bifidobacterium longum JCM1217 (JCM1217: 109 CFU/day), a comparable Bifidobacterium strain, in a model of high-fat diet-induced C57BL/6 male mice.

Results:
In the human clinical study, visceral fat area in GCL2505 group at Week 8 and 12 was significantly reduced than that in Placebo group. Furthermore, GCL2505 administration significantly increased fecal bifidobacteria counts from Week 4 to the end of this study.
In the mice model study, similar preventive effect of GCL2505 on visceral fat accumulation was also observed while JCM1217 was not observed. Glucose tolerance was also improved only by GCL2505 administration. The 16S rRNA pyrosequencing analysis of mice cecal contents revealed that GCL2505 administration notably altered cecal microbiota from control and JCM1217 group mice and such alterations were characterized by the elevation of lactobacilli and bifidobacteria. GCL2505 administration resulted in an approximately 4-fold increase in cecal bifidobacteria counts as compared with JCM1217 administration. The cecal pool of acetate, a major metabolite of bifidobacteria, was also significantly elevated by GCL2505 administration, but not by JCM1217 administration. In accordance with this elevation, plasma acetate level and colonic GLP-1 expression, a gut hormone secreted by the short-chain fatty acids (SCFAs) stimulation, were significantly elevated only by GCL2505 administration.

Discussion:
We demonstrated that GCL2505 administration resulted in the increase of the gut bifidobacteria and the prevention of visceral fat accumulation in both human and mice studies. As the results of comparison with JCM1217 administration in mice study, it is suggested that GCL2505 was superior to JCM1217 on proliferative ability in the gut, which resulted in the cecal acetate elevation. It has been reported that SCFAs receptor signaling modulates insulin resistance and GLP-1 secretion, which leads to the improvement of visceral fat accumulation and glucose tolerance. Our findings in the present study therefore indicated that gut acetate elevation by GCL2505 administration could prevent the visceral fat accumulation through the SCFAs receptor reaction, which might be caused by a high proliferative ability of this probiotics.

Keywords: Human and Mice studies, Acetate, Proliferative ability, Bifidobacteria, Visceral fat accumulation, 16S rRNA pyrosequencing analysis, Probiotics

Citation:
Koga Y., et al. (2016). Effect of Bifidobacterium animalis ssp. lactis GCL 2505, a probiotic strain that proliferates in the gut, on visceral fat accumulation: Evidence from human and mice sudies. Conference Proceedings of IPC2016. Paper presented at the International Scientific Conference on Probiotics and Prebiotics, Budapest (p. 38.). IPC2016

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