Structural disruption of gut microbiota and associated inflammation are considered important etiological factors in high fat diet (HFD)-induced metabolic syndrome (MS). Three candidate probiotic strains, Lactobacillus paracasei CNCM I-4270 (LC), L. rhamnosus I-3690 (LR) and Bifidobacterium animalis subsp. lactis I-2494 (BA), were individually administered to HFD-fed mice (108 cells day−1) for 12 weeks. Each strain attenuated weight gain and macrophage infiltration into epididymal adipose tissue and markedly improved glucose–insulin homeostasis and hepatic steatosis. Weighted UniFrac principal coordinate analysis based on 454 pyrosequencing of fecal bacterial 16S rRNA genes showed that the probiotic strains shifted the overall structure of the HFD-disrupted gut microbiota toward that of lean mice fed a normal (chow) diet. Redundancy analysis revealed that abundances of 83 operational taxonomic units (OTUs) were altered by probiotics. Forty-nine altered OTUs were significantly correlated with one or more host MS parameters and were designated ‘functionally relevant phylotypes'. Thirteen of the 15 functionally relevant OTUs that were negatively correlated with MS phenotypes were promoted, and 26 of the 34 functionally relevant OTUs that were positively correlated with MS were reduced by at least one of the probiotics, but each strain changed a distinct set of functionally relevant OTUs. LC and LR increased cecal acetate but did not affect circulating lipopolysaccharide-binding protein; in contrast, BA did not increase acetate but significantly decreased adipose and hepatic tumor necrosis factor-α gene expression. These results suggest that Lactobacillus and Bifidobacterium differentially attenuate obesity comorbidities in part through strain-specific impacts on MS-associated phylotypes of gut microbiota in mice.

The influence of gender and obesity on the abundance of human colonic Feacalibacterium prausnitzii is currently unclear. We collected fecal samples from 54 obese and 54 sex- and age-matched normal-weight Chinese adults and quantified the fecal F. prausnitzii as percentage of 16S rRNA gene copies of F. prausnitzii accounting to that of total gut bacteria with quantitative PCR. The fecal F. prausnitzii amount was not significantly different between obese and lean subjects. Men possessed significantly lower level of fecal F. prausnitzii than women, and the significant and positive correlation of fecal F. prausnitzii quantity with fasting glucose level was observed in men, not in women. Our results suggest that the gender effect, in addition to other factors including the geographic location, ethnicity, diet and gut transit times of study subjects, has to be considered when studying the relationship between gut F. prausnitzii and diseases.

The transient disruption of gut microbiota in infancy by antibiotics causes adult adiposity in mice. Accelerated postnatal growth (A) leads to a higher risk of adult metabolic syndrome in low birth-weight (LB) humans than in normal birth-weight (NB) individuals, but the underlying mechanism remains unclear. Here, we set up an experiment using LB + A mice, NB + A mice, and control mice with NB and normal postnatal growth. At 24 weeks of age (adulthood), while NB + A animals had a normal body fat content and glucose tolerance compared with controls, LB + A mice exhibited excessive adiposity and glucose intolerance. In infancy, more fecal bacteria implicated in obesity were increased in LB + A pups than in NB + A pups, including Desulfovibrionaceae, Enterorhabdus, and Barnesiella. One bacterium from the Lactobacillus genus, which has been implicated in prevention of adult adiposity, was enhanced only in NB + A pups. Besides, LB + A pups, but not NB + A pups, showed disrupted gut microbiota fermentation activity. After weaning, the fecal microbiota composition of LB + A mice, but not that of NB + A animals, became similar to that of controls by 24 weeks. In infancy, LB + A mice have a more dysbiotic gut microbiome compared to NB + A mice, which might increase their risk of adult metabolic syndrome.

Lactic acid bacteria (LAB) are ubiquitous microorganisms that can colonize the intestine and participate in the phys-iological metabolism of the host. LAB can produce a variety of metabolites, including organic acids, bacteriocin, amino acids, exopolysaccharides and vitamins. These metabolites are the basis of LAB function and have a profound impact on host health. The intestine is colonized by a large num-ber of gut microorganisms with high species diversity. Me-tabolites of LAB can keep the balance and stability of gut microbiota through aiding in the maintenance of the intes-tinal epithelial barrier, resisting to pathogens and regulat-ing immune responses, which further influence the nutri-tion, metabolism and behavior of the host. In this review, we summarize the metabolites of LAB and their influence on the intestine. We also discuss the underlying regulatory mechanisms and emphasize the link between LAB and the human gut from the perspective of health promotion.

Background Gut microbiota is essential for providing colonization resistance against pathogens. Dietary sugars markedly shift the composition of the intestinal microbiota and alter host susceptibility to enteric infections. However, the role of dietary sugars in intestinal pathophysiology and colitis pathogenesis remains controversial.Results We demonstrate the effect of L-arabinose on bacterial infection by using Salmonella enterica serovar Typhimurium (S. Tm). L-arabinose triggers severe inflammation in the gut and aggravates systemic infection of S. Tm in conventional mice. In addition, L-arabinose represses the expression of Salmonella Pathogenicity Island 1 (SPI-1) genes by negatively regulating the activity of the cyclic 3’ 5’-AMP (cAMP)-cAMP receptor protein (CRP) complex. The cAMP-CRP complex activates yfiA to maintain the stability of HilD. In a streptomycin-pretreated mouse model, L-arabinose supplementation promotes S. Tm initial bloom and is unable to alter the disease progression of Salmonella infection. However, in the presence of microbiota, L-arabinose induces a dramatic expansion of Enterobacteriaceae, thereby decreasing the microbiota diversity and causing more severe systemic infections.Conclusions Our work reveals that a high intake of dietary L-arabinose disrupts gut homeostasis in response to enteric infections, which offers new perspectives for dietary strategies and supplementation for diabetics.