A proliferative probiotic Bifidobacterium strain in the gut ameliorates progression of metabolic disorders via microbiota modulation and acetate elevation

Abstract

The gut microbiota is an important contributor to the worldwide prevalence of metabolic syndrome (MS), which includes obesity and diabetes. The anti-MS effects exerted by Bifidobacterium animalis ssp. lactis GCL2505 (BlaG), a highly proliferative Bifidobacterium strain in the gut, and B. longum ssp. longum JCM1217T (BloJ) were comparatively examined. BlaG treatment reduced visceral fat accumulation and improved glucose tolerance, whereas BloJ had no effect on these parameters. Gut microbial analysis revealed that BlaG exerted stronger effects on the overall bacterial structure of the gut microbiota than BloJ, including enrichment of the genus Bifidobacterium. The levels of acetate and glucagon-like peptide-1 were increased by BlaG treatment in both the gut and plasma, but not by BloJ treatment. Correlation analysis suggested that the elevation of gut acetate levels by BlaG treatment plays a pivotal role in the BlaG-induced anti-MS effects. These findings indicated that BlaG, a highly viable and proliferative probiotic, improves metabolic disorders by modulating gut microbiota, which results in the elevation of SCFAs, especially acetate.

Effects of synbiotics containing Bifidobacterium animalis subsp. lactis GCL2505 and inulin on intestinal bifidobacteria: A randomized, placebo‐controlled, crossover study

“…An improvement of the intestinal microbiota resulting from the intake of probiotics or prebiotics, especially an increase in the number of intestinal bifidobacteria, often leads to a higher frequency of defecation (Matsumoto et al, 2010;Yamano et al, 2006). The greater presence of bifidobacteria in the intestinal tract promotes the production of short-chain fatty acids, such as acetate (Aoki et al, 2017;Igarashi et al, 2017), which stimulate colonic motility (Fukumoto et al, 2003;Ono, Karaki, & Kuwahara, 2004). Some strains of B. lactis, including B. lactis strain GCL2505, were also reported to improve defecation frequency (Flach et al, 2018;Ishizuka et al, 2012;Tanaka et al, 2015;Yang et al, 2008).…”

PI 3‐kinase‐ and ERK‐MAPK‐dependent mechanisms underlie Glucagon‐Like Peptide‐1‐mediated activation of Sprague Dawley colonic myenteric neurons

“…In fact, the chemosensory properties of GLP‐1‐secreting L cells in the colon are likely to differ from those in more proximal regions, being activated by microbial products rather than nutrients . Indeed, specific commensal bacteria increase intestinal and circulating GLP‐1 . In the context of IBS pathophysiology, altered microbial profiles have been reported, which could result in modified circulating GLP‐1 .…”

“…29,30 Indeed, specific commensal bacteria increase intestinal and circulating GLP-1. 31,32 In the context of IBS pathophysiology, altered microbial profiles have been reported, 33 which could result in modified circulating GLP-1. 8 However, few studies have been carried out on the cellular mechanisms underlying the inhibitory effects of GLP-1 in the colon and how this may be impacted by other hormones in the context of bowel dysfunction.…”

Physical fitness in community‐dwelling older adults is linked to dietary intake, gut microbiota, and metabolomic signatures

“…Proinsulin was the most important feature of phenotype discrimination and corresponded inversely with the abundance of Bifidobacterium adolescentis and several species of Christensenella, and Ruminococcaceae (Figure a), strongly indicating that GM‐proinsulin interactions could be mediators of fitness phenotype. Bifidobacterium species (including B. adolescentis ) have previously been described as promoters of adiponectin and decreasing expression of interleukin‐6, both playing prominent roles in metabolic derangements associated with glucose regulation and fatty acid oxidation (Aoki et al, ; Straub & Scherer, ; Su et al, ). Christensenella minuta (another Clostridiales member) is enriched in individuals with low BMI and has been demonstrated to reduce weight gain and adiposity in mice (Goodrich et al, ).…”