Obesity is associated with compromised intestinal barrier function and shifts in microbiota that may contribute to inflammation. Previous research suggests benefits of supplemental fiber, but the impacts of fermentable vs. non‐fermentable fibers are not well understood.OBJECTIVETo determine the impact of cellulose vs. fructan (short‐chain fructooligosaccharides [scFOS] or inulin) supplementation on fecal microbiota and gut physiology in obese mice.METHODS18‐wk old C57BL/6J mice (n=6/group) were fed high‐fat diets (45% kcal fat) containing 5% cellulose, 10% cellulose, 10% scFOS or 10% inulin for 4‐wk. Cecum and distal colon were collected to assess barrier function, histomorphology and gene expression. Fecal DNA was extracted, followed by 16S rRNA amplicon Illumina MiSeq sequencing and analysis with QIIME 1.8.0.RESULTSBoth fructans increased (p<0.05) intestinal transmural resistance and crypt depth but reduced (p<0.05) mRNA abundance of ZO‐1 and occludin. Principal coordinates analysis (PCoA) of weighted and unweighted UniFrac distances of fecal microbiota revealed a sharp separation (p<0.05) between fructan and cellulose groups. Alpha diversity measures revealed lower (p<0.05) species richness with fructan supplementation. Fructans reduced (p<0.05) the relative abundance of Firmicutes and increased (p<0.05) Actinobacteria and Verrucomicrobia (Akkermansia).CONCLUSIONFructan supplementation may modulate gut microbiota and physiological responses via multiple mechanisms.
Obesity commonly affects both humans and companion animals, and is often associated with altered blood glucose and hormone responses. Many studies have shown the ability of dietary fibers or prebiotics to curb postprandial glycemic responses, but some have suggested that certain prebiotics, when consumed at an early meal, can even curb the responses after a second meal consumed hours later. This response has been coined the ‘second‐meal effect’. Although it is known that dietary prebiotics can elicit shifts in the fecal microbiota composition, little research has been performed in dogs using modern high‐throughput DNA‐sequencing. In this study, our objective was to evaluate the (1) second‐meal effect of a commercial prebiotic blend of inulin‐type fructans, and (2) effects of the prebiotic on fecal microbiota, metabolites, and bile acids (BA). We hypothesized that the prebiotic would elicit a second‐meal effect in response to an oral glucose challenge, beneficially shift fecal microbiota by increasing Bifidobacterium, Faecalibacterium, and Lachnospira and decreasing Fusobacterium and Desulfovibrio, and shifting the fecal BA composition. Nine overweight dogs (4.2 ± 0.7 yr, 12.7 ± 2.4 kg, 7.8 ± 1.4 BCS) were used in a replicated 3×3 Latin Square design to test a non‐prebiotic control (cellulose) against low‐ (0.5% of diet) and high‐dose (1.0% of diet) prebiotic treatments. The study included three 14‐d treatment periods separated by 14‐d washouts. All dogs were fed the same experimental diet formulated to meet all nutrient needs as defined by AAFCO, with treatments provided orally via gelatin capsules prior to each meal. Dogs were fed twice daily (8 am; 4 pm) to maintain BW. At the end of each period, fresh fecal samples were collected for microbiota, metabolite, and BA analysis. On d13 or d14 of each period, dogs were fed at 8 am as usual, then dosed with 1 g/kg BW of maltodextrin as a 50% solution in place of the 4 pm meal. Blood samples were collected at baseline and 10, 20, 30, 45, 60, 90, 120, and 180 min after dosing, and analyzed for glucose, insulin, and active glucagon‐like peptide‐1 (GLP‐1) concentrations. Baseline and postprandial incremental area under the curve (IAUC) data were analyzed statistically. The prebiotic tended to attenuate postprandial blood glucose response to the oral glucose challenge (p=0.089), but did not affect (p>0.10) baseline glucose or baseline and postprandial active GLP‐1. The prebiotic also tended to increase the relative abundance of fecal Erysipelotrichi (p=0.089), particularly in the genus Eubacterium (p=0.075), the order Turicibacterales (p=0.066), the family Veillonellaceae (p=0.051), and the genus Megamonas (p=0.054). Fecal lithocholic acid, a secondary BA, tended to decrease (p=0.083) in dogs fed the prebiotic. Our results indicate that inulin‐type prebiotics may elicit a second‐meal effect and serve as a modulator of the gut microbiota in overweight dogs.Support or Funding InformationFunding provided by Beneo GmbH.
Objectives. Colorectal cancer (CRC) incidence is higher in post-industrial cultures, and the incidences varies among different populations. In the US, there is a higher incidence of CRC in African Americans (AAs) compared to non-Hispanic whites (NHWs). Recent evidence links consumption of a diet high in animal protein and fat as an environmental risk factor for the development of CRC. The intestinal microbiota is postulated to modulate the effects of diet in promoting or preventing CRC development. Hydrogen sulfide, which is produced by normal members of the colonic microenvironment (sulfidogenic bacteria), triggers pro-inflammatory and hyper-proliferative pathways, and it is genotoxic. We hypothesized that the production of hydrogen sulfide by sulfidogenic bacteria is a key environmental carcinogen contributing to CRC risk. Design. The abundance of sulfidogenic bacteria via quantitative PCR (qPCR) was compared in non-involved colonic mucosa of 97 AA and 56 NHW CRC patients and in 100 AA and 76 NHW healthy controls. In addition, we performed 16S rDNA sequencing in 61 AA cases and 94 AA controls. Additionally, we tested correlations among race, dietary intake, disease status, and sulfidogenic bacterial abundance. Results. Overall, the functional gene for hydrogen sulfide production in sulfate-reducing bacteria, dissimilatory sulfate reductase (dsrA), was more abundant in AAs than in NHWs, in both cases and controls. In addition, AA CRC cases exhibited a significantly higher abundance of Bilophila wadsworthia-specific dsrA. Linear discriminant analysis of 16S rDNA sequencing results revealed several taxa that differed between AA cases and controls, including the known butyrate producer Faecalibacterium that was more abundant in AA controls, and the sulfidogenic Pyramidobacter that was more abundant in AA CRC cases. Importantly, we found that dietary intake of protein and fat was higher in AAs compared to NHWs, and these dietary components correlated with a higher abundance of sulfidogenic bacteria. Conclusion. There were significant differences in sulfidogenic bacterial abundance between AAs and NHWs, in both cases and controls, and implicate sulfidogenic bacteria as an important diet-driven environmental exposure that contributes to the increased risk of CRC in AAs. Replication studies are needed to test that effectiveness of using B. wadsworthia as a biomarker for increased CRC risk. Citation Format: Cemal Yazici, Patricia G. Wolf, Tzu-Wen Liu, Karin Vermillion, Timothy Carroll, Ece Mutlu, Lisa Tussing-Humphreys, Carol Braunschweig, Rosa M. Xicola, Barbara Jung, Xavier Llor, Nathan A. Ellis, H. Rex Gaskins. Sulfidogenic bacteria are an important diet-driven exposure promoting colorectal cancer in African Americans. [abstract]. In: Proceedings of the Ninth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2016 Sep 25-28; Fort Lauderdale, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(2 Suppl):Abstract nr B31.
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