Consumption of RS modified the intestinal microbiota, stimulated intestinal immunity and endocrine-responses, and modified systemic metabolomes in obese mice consuming an otherwise obesogenic diet.

Lactobacillusplantarum bacteriocin is associated with intestinal and systemic improvements in diet-induced obese mice and maintains epithelial barrier integrity invitro, Gut Microbes,

Obesity is a prevalent chronic condition in many developed and developing nations that raises the risk for developing heart disease, stroke, and diabetes. Previous studies have shown that consuming particular probiotic strains of Lactobacillus is associated with improvement in the obese and diabetic phenotype; however, the mechanisms of these beneficial effects are not well understood. In this study, C57BL/6J male mice were fed a lard-based high fat diet for 15 weeks with Lactobacillus plantarum supplementation NCIMB8826 (Lp) between weeks 10 and 15 ( n = 10 per group). Systemic metabolic effects of supplementation were analyzed by NMR metabolomics, protein expression assays, gene transcript quantification, and 16S rRNA marker gene sequencing. Body and organ weights were not significantly different with Lp supplementation, and no microbiota community structure changes were observed in the cecum; however, L. plantarum numbers were increased in the treatment group according to culture-based and 16S rRNA gene quantification. Significant differences in metabolite and protein concentrations (serum, liver, and colon), gene expression (ileum and adipose), and cytokines (colon) were observed between groups with increases in the gene expression of tight junction proteins in the ileum and cecum and improvement of some markers of glucose homeostasis in blood and tissue with Lp supplementation. These results indicate Lp supplementation impacts systemic metabolism and immune signaling before phenotypic changes and without large-scale changes to the microbiome. This study supports the notion that Lp is a beneficial probiotic, even in the context of a high fat diet.

Intestinal microbes have important roles in the regulation of energy homeostasis, lipid and glucose metabolism, and immune system responses. Dysbiotic gut microbiota is associated with obesity, type 2 diabetes mellitus, and metabolic syndrome. Therefore, gut microbiota modulations by fermentable carbohydrates and/or probiotics might protect against these chronic diseases. In this study, male C57BL/6J mice received a high‐fat (HF) diet (45.9% energy from fat) for 9 weeks. Mice were then provided with either a HF diet modified to contain 20% (w/w) type 2 high‐amylose maize resistant starch (HF‐HAMRS) or remained on the control HF diet for another 6 weeks. During that time, half of the mice fed either HF‐HAMRS or HF received supplements of 10^9 cells of Lactobacillus plantarum WCFS1 (Lp) every other day (n=10/grp). HAMRS‐fed mice exhibited enhanced indicators of intestinal fermentation (cecum tissue and content weights and cecal proglucagon gene expression), increased serum adiponectin levels, and sensitized cecal and ileal responses to microbiota changes as indicated by increased expression of TLR genes and ileal antimicrobial Reg3g gene. Lp‐fed mice displayed significantly increased hepatic Cpt1a gene expression relative to HF controls, indicating increased fatty acid β‐oxidation. Combining HAMRS and Lp significantly enhanced gene expression of cecal tight junction protein occludin relative to HF control. These outcomes provide a rationale for developing nutritional strategies that prevent or treat obesity and its associated metabolic disorders. Funding: American Diabetes Association.

Incidence of obesity and type 2 diabetes mellitus (T2DM) is steadily increasing, and the contributions of diet and the gastrointestinal microbiota to these diseases are only partially understood. Enriching particular populations of microbes in a mouse model of pre‐diabetes and monitoring systemic metabolic effects will help to elucidate the mechanisms of obesity and T2DM progression. C57BL/6J mice were fed a 45% high fat diet for nine weeks and then supplemented with type 2 resistant starch (RS), Lactobacillus plantarum (Lp), or both for six weeks (n=10 per group). Urine was collected throughout the experiment; cecal contents and serum were obtained at the time of mouse sacrifice. All samples were analyzed using NMR‐based metabolomics. Unsupervised principal component analysis showed clear separation between RS and non‐RS groups for both cecal and serum samples. Significant differences were observed for microbial metabolites and amino acids when comparing RS groups to control, as well as when comparing Lp supplementation alone to RS supplementation alone. These results have implications for monitoring the effects of dietary supplementation on the gastrointestinal microbiota and overall host health. Funding was provided by the American Diabetes Association.

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