Irinotecan (CPT-11) Chemotherapy Alters Intestinal Microbiota in Tumour Bearing Rats

Intestinal microbiota mediate toxicity of irinotecan (CPT-11) cancer therapies and cause systemic infection after CPT-11-induced loss of barrier function. The intestinal microbiota and their functions are thus potential targets for treatment to mitigate CPT-11 toxicity. However, microbiota changes during CPT-11 therapy remain poorly described. This study analysed changes in intestinal microbiota induced by CPT-11 chemotherapy. Qualitative and quantitative taxonomic analyses, and functional analyses were combined to characterize intestinal microbiota during CPT-11-based chemotherapy, and in presence or absence of oral glutamine, a treatment known to reduce CPT-11 toxicity. In the first set of experiments tumour-bearing rats received a dose-intensive CPT-11 regimen (125 mg kg(-1)×3 days), with or without oral glutamine bolus (0.75 g kg(-1)). In a subsequent more clinically-oriented chemotherapy regimen, rats received two cycles of CPT-11 (50 mg kg(-1)) followed by 5-flurouracil (50 mg kg(-1)). The analysis of fecal samples over time demonstrated that tumours changed the composition of intestinal microbiota, increasing the abundance of clostrridial clusters I, XI, and Enterobacteriaceae. CPT-11 chemotherapy increased cecal Clostridium cluster XI and Enterobacteriaceae, particularly after the dose-intensive therapy. Glutamine treatment prevented the reduced abundance of major bacterial groups after CPT-11 administration; i.e. total bacteria, Clostridium cluster VI, and the Bacteroides-group. Virulence factor/toxin genes of pathogenic Escherichia coli and Clostridium difficile were not detected in the cecal microbiota. In conclusion, both colon cancer implantation and CPT-11-based chemotherapies disrupted the intestinal microbiota. Oral glutamine partially mitigated CPT-11 toxicity and induced temporary changes of the intestinal microbiota.     

Evaluation of Long-Term Toxicity of Oral Zinc Oxide Nanoparticles and Zinc Sulfate in Mice

The toxicological effects of zinc oxide nanoparticles (nano-ZnOs) are related to their dissolution and interference with zinc ion homeostasis. High-soluble zinc sources may produce more severe and acute toxicity; however, the evaluation of potential toxicity of long-term exposure to nano-ZnOs and high-soluble sources of zinc remains obscure. This study aimed at evaluating effects of nano-ZnOs and zinc sulfate on development, serum and hematological parameters, and mineral concentrations in selected tissues and intestinal microbiota in mice via gastrointestinal administration for 7 weeks. Results indicated that 250 mg/kg nano-ZnOs reduced the body weight from weeks 8 to 11, increased serum glutamic-pyruvic transaminase activity, and increased the zinc concentrations of the serum, liver, and kidney while did not affect the relative organ weight, intestinal microbiota, and other mineral concentrations (Fe, Cu, and Mn) in the kidney, liver, and thigh muscle. Oral administration with 250 mg/kg zinc sulfate seemed to show more severe and acute toxicity since mice in zinc sulfate group exhibited reduced body weight from weeks 5 to 11, decreased relative pancreas weight, and increased serum glutamic-oxalacetic transaminase activity and intestinal enteric group.     

Propionibacterium acidipropionici CRL1198 influences the production of acids and the growth of bacterial genera stimulated by inulin in a murine model of cecal slurries

Different attempts have been made to improve the health status of humans and animals by increasing the intestinal production of short-chain fatty acids (SCFA) derived from non-digestible carbohydrates fermentation. In this paper we investigate the in vitro production of short-chain fatty acids (SCFA) after addition of inulin, propionibacteria or a combination of both in an experimental model of mice cecal slurries. The development of bacterial genera which are usually stimulated by inulin addition was also investigated. According to our experimental data, acetic acid and butyric acids concentrations increased after incubation in slurries that had no supplements. By contrast, butyric acid concentrations remained in the basal value when supplements were used. Fermentation of only inulin did not increase the concentration of total SCFA. Propionibacterium acidipropionici CRL1198 improved the production of propionic acid in cecal slurries when it was added alone, but the effect was more noticeable in the combination with inulin. A modulation of the global fermentative activity of the cecal microbiota was evidenced by the increase on the ratio propionic acid/SCFA in supplementations with propionibacteria. Statistical analysis of data demonstrated that samples from homogenates with propionibacteria alone or combined with inulin belong to the same cluster. The presence of propionibacteria limited the growth of Bacteroides fragilis and Clostridium hystoliticum groups in slurries with and without inulin. The growth of Bifidobacterium was not modified and the stimulating effect of inulin on lactobacilli disappeared in the presence of propionibacteria. In conclusion, dairy propionibacteria are potential candidates to develop new functional foods helpful to ensure the intestinal production of SCFA during inulin supplementation and to control the overgrowth of bacteria belonging to Bacteroides and Clostridium genera.     

Butyrate and propionate protect against diet-induced obesity and regulate gut hormones via free fatty acid receptor 3-independent mechanisms

Short-chain fatty acids (SCFAs), primarily acetate, propionate, and butyrate, are metabolites formed by gut microbiota from complex dietary carbohydrates. Butyrate and acetate were reported to protect against diet-induced obesity without causing hypophagia, while propionate was shown to reduce food intake. However, the underlying mechanisms for these effects are unclear. It was suggested that SCFAs may regulate gut hormones via their endogenous receptors Free fatty acid receptors 2 (FFAR2) and 3 (FFAR3), but direct evidence is lacking. We examined the effects of SCFA administration in mice, and show that butyrate, propionate, and acetate all protected against diet-induced obesity and insulin resistance. Butyrate and propionate, but not acetate, induce gut hormones and reduce food intake. As FFAR3 is the common receptor activated by butyrate and propionate, we examined these effects in FFAR3-deficient mice. The effects of butyrate and propionate on body weight and food intake are independent of FFAR3. In addition, FFAR3 plays a minor role in butyrate stimulation of Glucagon-like peptide-1, and is not required for butyrate- and propionate-dependent induction of Glucose-dependent insulinotropic peptide. Finally, FFAR3-deficient mice show normal body weight and glucose homeostasis. Stimulation of gut hormones and food intake inhibition by butyrate and propionate may represent a novel mechanism by which gut microbiota regulates host metabolism. These effects are largely intact in FFAR3-deficient mice, indicating additional mediators are required for these beneficial effects.     

Chemically Defined Diet Alters the Protective Properties of Fructo-Oligosaccharides and Isomalto-Oligosaccharides in HLA-B27 Transgenic Rats

Non-digestible oligosaccharides (NDO) were shown to reduce inflammation in experimental colitis, but it remains unclear whether microbiota changes mediate their colitis-modulating effects. This study assessed intestinal microbiota and intestinal inflammation after feeding chemically defined AIN-76A or rat chow diets, with or without supplementation with 8 g/kg body weight of fructo-oligosaccharides (FOS) or isomalto-oligosaccharides (IMO). The study used HLA-B27 transgenic rats, a validated model of inflammatory bowel disease (IBD), in a factorial design with 6 treatment groups. Intestinal inflammation and intestinal microbiota were analysed after 12 weeks of treatment. FOS and IMO reduced colitis in animals fed rat chow, but exhibited no anti-inflammatory effect when added to AIN-76A diets. Both NDO induced specific but divergent microbiota changes. Bifidobacteria and Enterobacteriaceae were stimulated by FOS, whereas copy numbers of Clostridium cluster IV were decreased. In addition, higher concentrations of total short-chain fatty acids (SCFA) were observed in cecal contents of rats on rat chow compared to the chemically defined diet. AIN-76A increased the relative proportions of propionate, iso-butyrate, valerate and iso-valerate irrespective of the oligosaccharide treatment. The SCFA composition, particularly the relative concentration of iso-butyrate, valerate and iso-valerate, was associated (P≤0.004 and r≥0.4) with increased colitis and IL-1 β concentration of the cecal mucosa. This study demonstrated that the protective effects of fibres on colitis development depend on the diet. Although diets modified specific cecal microbiota, our study indicates that these changes were not associated with colitis reduction. Intestinal inflammation was positively correlated to protein fermentation and negatively correlated with carbohydrate fermentation in the large intestine.     

Differential influence of butyrate concentration on proximal and distal colonic mucosa in rats born germ-free and associated with a strain of Clostridium paraputrificum

In vivo influence of butyrate in colonic mucosa was studied using a model of gnotobiotic rats monoassociated with a Clostridium paraputrificum. Rats were fed a diet containing increasing amounts of non-digestible carbohydrates, the fermentation of which led to modulated amounts of butyrate in the large intestine. In the proximal colon, the increase in the butyrate concentration alters crypt depth and the number of mucus-containing cells; the increase in butyrate was highly correlated with the number of neutral-mucin-containing cells. Conversely, in the distal colon, no relation was found between the increase in butyrate concentration and crypt depth or number of mucin-containing cells. In both the proximal and distal colon, the mitotic index remained unchanged. In conclusion, in vivo production of physiological quantities of butyrate had a trophic effect on proximal colonic mucosa, but did not influence the distal epithelium.     

Dose-Dependent Effects of a Soluble Dietary Fibre (Pectin) on Food Intake,Adiposity, Gut Hypertrophy and Gut Satiety Hormone Secretion in Rats

Soluble fermentable dietary fibre elicits gut adaptations, increases satiety and potentially offers a natural sustainable means of body weight regulation. Here we aimed to quantify physiological responses to graded intakes of a specific dietary fibre (pectin) in an animal model. Four isocaloric semi-purified diets containing 0, 3.3%, 6.7% or 10% w/w apple pectin were offered ad libitum for 8 or 28 days to young adult male rats (n = 8/group). Measurements were made of voluntary food intake, body weight, initial and final body composition by magnetic resonance imaging, final gut regional weights and histology, and final plasma satiety hormone concentrations. In both 8- and 28-day cohorts, dietary pectin inclusion rate was negatively correlated with food intake, body weight gain and the change in body fat mass, with no effect on lean mass gain. In both cohorts, pectin had no effect on stomach weight but pectin inclusion rate was positively correlated with weights and lengths of small intestine and caecum, jejunum villus height and crypt depth, ileum crypt depth, and plasma total glucagon-like peptide-1 (GLP-1) and peptide tyrosine tyrosine (PYY) concentrations, and at 8 days was correlated with weight and length of colon and with caecal mucosal depth. Therefore, the gut’s morphological and endocrine adaptations were dose-dependent, occurred within 8 days and were largely sustained for 28 days during continued dietary intervention. Increasing amounts of the soluble fermentable fibre pectin in the diet proportionately decreased food intake, body weight gain and body fat content, associated with proportionately increased satiety hormones GLP-1 and PYY and intestinal hypertrophy, supporting a role for soluble dietary fibre-induced satiety in healthy body weight regulation.     

Physical Activity Differentially Affects the Cecal Microbiota of Ovariectomized Female Rats Selectively Bred for High and Low Aerobic Capacity

The gut microbiota is considered a relevant factor in obesity and associated metabolic diseases, for which postmenopausal women are particularly at risk. Increasing physical activity has been recognized as an efficacious approach to prevent or treat obesity, yet the impact of physical activity on the microbiota remains under-investigated. We examined the impacts of voluntary exercise on host metabolism and gut microbiota in ovariectomized (OVX) high capacity (HCR) and low capacity running (LCR) rats. HCR and LCR rats (age = 27wk) were OVX and fed a high-fat diet (45% kcal fat) ad libitum and housed in cages equipped with (exercise, EX) or without (sedentary, SED) running wheels for 11wk (n = 7-8/group). We hypothesized that increased physical activity would hinder weight gain, increase metabolic health and shift the microbiota of LCR rats, resulting in populations more similar to that of HCR rats. Animals were compared for characteristic metabolic parameters including body composition, lipid profile and energy expenditure; whereas cecal digesta were collected for DNA extraction. 16S rRNA gene-based amplicon Illumina MiSeq sequencing was performed, followed by analysis using QIIME 1.8.0 to assess cecal microbiota. Voluntary exercise decreased body and fat mass, and normalized fasting NEFA concentrations of LCR rats, despite only running one-third the distance of HCR rats. Exercise, however, increased food intake, weight gain and fat mass of HCR rats. Exercise clustered the gut microbial community of LCR rats, which separated them from the other groups. Assessments of specific taxa revealed significant (p<0.05) line by exercise interactions including shifts in the abundances of Firmicutes, Proteobacteria, and Cyanobacteria. Relative abundance of Christensenellaceae family was higher (p = 0.026) in HCR than LCR rats, and positively correlated (p<0.05) with food intake, body weight and running distance. These findings demonstrate that exercise differentially impacts host metabolism and gut microbial communities of female HCR and LCR rats without ovarian function.     

Disparate Metabolic Responses in Mice Fed a High-Fat Diet Supplemented with Maize-Derived Non-Digestible Feruloylated Oligo- and Polysaccharides Are Linked to Changes in the Gut Microbiota

Studies have suggested links between colonic fermentation of dietary fibers and improved metabolic health. The objectives of this study were to determine if non-digestible feruloylated oligo- and polysaccharides (FOPS), a maize-derived dietary fiber, could counteract the deleterious effects of high-fat (HF) feeding in mice and explore if metabolic benefits were linked to the gut microbiota. C57BL/6J mice (n = 8/group) were fed a low-fat (LF; 10 kcal% fat), HF (62 kcal% fat), or HF diet supplemented with FOPS (5%, w/w). Pronounced differences in FOPS responsiveness were observed: four mice experienced cecal enlargement and enhanced short chain fatty acid production, indicating increased cecal fermentation (F-FOPS). Only these mice displayed improvements in glucose metabolism compared with HF-fed mice. Blooms in the gut microbial genera Blautia and Akkermansia were observed in three of the F-FOPS mice; these shifts were associated with reductions in body and adipose tissue weights compared with the HF-fed control mice. No improvements in metabolic markers or weights were detected in the four mice whose gut microbiota did not respond to FOPS. These findings demonstrate that FOPS-induced improvements in weight gain and metabolic health in mice depended on the ability of an individual’s microbiota to ferment FOPS.     

Metabolomic analysis of amino acid metabolism in colitic rats supplemented with lactosucrose

Intestinal inflammation causes metabolic disorders. The purpose of this study was to determine the effect of dietary supplementation with lactosucrose (LS) on the serum metabolome and intestinal luminal content of fatty acids in colitic rats. Colitis was induced in rats using trinitrobenzene sulfonic acid. Subsequently, rats received intragastric administration of either 250 mg LS/kg body weight or saline (the control group) every day for 5 weeks. Short-chain fatty acids in the intestinal lumen, blood profile, and metabolites in serum were measured, respectively, using gas chromatography, biochemistry analyzer, and nuclear magnetic resonance-based metabolomics combined with multivariate statistics. Metabolic effects of LS included: (1) decreases in concentrations of branched-chain amino acids (isoleucine and valine), alanine, citric acid, trimethylamine oxide and taurine, and the abundance of aspartate aminotransferase in serum; (2) increases in concentrations of glucose metabolites (including succinate) in serum; and (3) altered concentrations of butyrate in the cecal content and of butyrate and acetate in the colon content. The results indicate that LS supplementation to colitic rats affects whole-body metabolism of amino acids and release of aspartate aminotransferase and alkaline phosphatase from tissues into the blood circulation, and enhances the production of short-chain fatty acids in the intestinal lumen.     

Age-related topographical metabolic signatures for the rat gastrointestinal contents

Symbiotic gut microbiota is essential for mammalian physiology and analyzing the metabolite compositions of gastrointestinal contents is vital for understanding the microbiome-host interactions. To understand the developmental dependence of the topographical metabolic signatures for the rat gastrointestinal contents, we systematically characterized the metabolite compositional variations of the contents in rat jejunum, ileum, cecum, and colon for two age-groups using (1)H NMR spectroscopy and multivariate analysis. Significant topographical metabolic variations were present for the jejunal, ileal, cecal, colonic contents, and feces, reflecting the absorption functions for each intestinal region and the gut microbiota therein. The concentrations of amino acids, lactate, creatine, choline, bile acids, uracil and urocanate decreased drastically from jejunal to ileal contents followed with steady decreases from cecal content to feces. Short-chain fatty acids (SCFAs) and arabinoxylan-related carbohydrates had highest levels in cecal content and feces, respectively. Such topographical metabolic signatures for the intestinal contents varied with animal age highlighted by the level changes for lactate, choline, taurine, amino acids, carbohydrates, keto-acids, and SCFAs. These findings provided essential information for the topographical metabolic variations in the gastrointestinal tract and demonstrated metabolic profiling as a useful approach for understanding host-microbiome interactions and functional status of the gastrointestinal regions.     

Oral administration of sodium butyrate attenuates inflammation and mucosal lesion in experimental acute ulcerative colitis

Butyrate is a four-carbon short-chain fatty acid that improves colonic trophism. Although several studies have shown the benefits of butyrate enemas in ulcerative colitis (UC), studies using the oral route are rare in the literature. In the present study, we evaluated the effect of butyrate intake in the immune response associated to UC. For that, mice were fed control or butyrate (0.5% sodium butyrate) diets for 14 days. Acute UC was induced by dextran sulphate sodium (DSS, 2.5%), replacing drinking water. The results showed that, in UC animals, oral butyrate significantly improved trophism and reduced leukocyte (eosinophil and neutrophil) infiltration in the colon mucosa and improved the inflammatory profile (activated macrophage, B and T lymphocytes) in cecal lymph nodes. In the small intestine, although mucosa histology was similar among groups, DSS treatment reduced duodenal transforming growth factor-β, increased interleukin-10 concentrations and increased memory T lymphocytes and dendritic cells in Peyer's patches. Butyrate supplementation was able to revert these alterations. When cecal butyrate concentration was analyzed in cecal content, it was still higher in the healthy animals receiving butyrate than in the UC+butyrate and control groups. In conclusion, our results show that oral administration of sodium butyrate improves mucosa lesion and attenuates the inflammatory profile of intestinal mucosa, local draining lymph nodes and Peyer's patches of DSS-induced UC. Our results also highlight the potential use of butyrate supplements as adjuvant in UC treatment.     

Isolation of lactate-utilizing butyrate-producing bacteria from human feces and in vivo administration of Anaerostipes caccae strain L2 and galacto-oligosaccharides in a rat model

Lactate-utilizing butyrate-producers were isolated from human feces and identified based on the sequences of 16S rRNA gene. Anaerostipes caccae strain L2, one of the seven human fecal isolates, was administered to rats with galacto-oligosaccharides (GOS) as bifidogenic carbohydrates for stimulating lactate formation in the hindgut. Ingestion of GOS alone increased concentrations of cecal lactate and butyrate compared with control rats (P<0.05). Additional administration of strain L2 on GOS tended to enhance the promoting effect of GOS on cecal butyrate formation (P=0.06) and lowered the mean value of cecal lactate concentration (P=0.32). Consequently, cecal and fecal butyrate concentrations in rats administered with both strain L2 and GOS were significantly higher than those in the control rats (P<0.01 and P<0.05, respectively). Significant changes were observed in the other fermentation acids, such as succinate, acetate, and propionate, depending on the ingestion of strain L2. Administered strain L2 was retrieved from the cecal content of a rat based on randomly amplified polymorphic DNA analysis. The results suggest that synbiotic ingestion of lactate-utilizing butyrate-producers and GOS alters the microbial fermentation and promotes the formation of beneficial fermentation acids, including butyrate, in the gut.     

The Short-Chain Fatty Acid Uptake Fluxes by Mice on a Guar Gum Supplemented Diet Associate with Amelioration of Major Biomarkers of the Metabolic Syndrome

Studies with dietary supplementation of various types of fibers have shown beneficial effects on symptoms of the metabolic syndrome. Short-chain fatty acids (SCFAs), the main products of intestinal bacterial fermentation of dietary fiber, have been suggested to play a key role. Whether the concentration of SCFAs or their metabolism drives these beneficial effects is not yet clear. In this study we investigated the SCFA concentrations and in vivo host uptake fluxes in the absence or presence of the dietary fiber guar gum. C57Bl/6J mice were fed a high-fat diet supplemented with 0%, 5%, 7.5% or 10% of the fiber guar gum. To determine the effect on SCFA metabolism, ¹³C-labeled acetate, propionate or butyrate were infused into the cecum of mice for 6 h and the isotopic enrichment of cecal SCFAs was measured. The in vivo production, uptake and bacterial interconversion of acetate, propionate and butyrate were calculated by combining the data from the three infusion experiments in a single steady-state isotope model. Guar gum treatment decreased markers of the metabolic syndrome (body weight, adipose weight, triglycerides, glucose and insulin levels and HOMA-IR) in a dose-dependent manner. In addition, hepatic mRNA expression of genes involved in gluconeogenesis and fatty acid synthesis decreased dose-dependently by guar gum treatment. Cecal SCFA concentrations were increased compared to the control group, but no differences were observed between the different guar gum doses. Thus, no significant correlation was found between cecal SCFA concentrations and metabolic markers. In contrast, in vivo SCFA uptake fluxes by the host correlated linearly with metabolic markers. We argue that in vivo SCFA fluxes, and not concentrations, govern the protection from the metabolic syndrome by dietary fibers.     

Construction of a model of the human proximal colon

The objective of the present study was to construct a system that re-creates the conditions of fermentation and absorption of the human proximal colon. The model was constructed using a glass tube with an internal dialysis membrane tube. The food substrate was fed into the dialysis membrane three times a day simulating a typical human feeding. The substrate contained 58% carbohydrates, 35% proteins, 3% fiber, 3% starch, and 1% lipids on dry weight base, with 90% moisture. The inoculum was a fecal culture propagated in TSB. The intestinal absorption was simulated using a polyethylene glycol (PEG) solution running continuously outside the dialysis membrane. All microorganisms increased their counts after inoculation, and reached higher counts generally after substrate feed. The most important short chain fatty acids (SCFA: acetic, propionic and butyric acids) were analyzed, and their concentrations inside and outside the membrane were significantly different due to the extraction efficiency of the PEG solution. The greatest production occurred at 48 h. SCFA ratios showed that at the beginning, acetate was the predominant compound, but after 12 h the proportion of butyrate increased and the acetate was decreased. This SCFA production pattern is similar to that reported for the proximal colon in live systems. Continuous operation of the colon model for 48 h was enough to reveal the development of microorganisms and SCFA production. This model reproduced the conditions of the human proximal colon adequately and can be used to study the development of colonic microbiota.     

Impact of dietary protein on microbiota composition and activity in the gastrointestinal tract of piglets in relation to gut health: a review

In pigs, the microbial ecosystem of the gastrointestinal tract (GIT) is influenced by various factors; however, variations in diet composition have been identified as one of the most important determinants. Marked changes in fermentation activities and microbial ecology may occur when altering the diet, for example, from milk to solid feed during weaning. In that way, access of pathogens to the disturbed ecosystem is alleviated, leading to infectious diseases and diarrhea. Thus, there is increasing interest in improving intestinal health by use of dietary ingredients suitable to beneficially affect the microbial composition and activity. For example, fermentable carbohydrates have been shown to promote growth of beneficial Lactobacillus species and bifidobacteria, thereby enhancing colonization resistance against potential pathogens or production of short-chain fatty acids, which can be used as energy source for epithelial cells. On the other hand, fermentation of protein results in the production of various potentially toxic products, such as amines and NH₃, and is often associated with growth of potential pathogens. In that way, excessive protein intake has been shown to stimulate the growth of potentially pathogenic species such as Clostridium perfringens, and to reduce fecal counts of beneficial bifidobacteria. Therefore, it seems to be a promising approach to support growth and metabolic activity of the beneficial microbiota by developing suitable feeding strategies. For example, a reduction of dietary CP content and, at the same time, dietary supplementation with fermentable carbohydrates have proven to successfully suppress protein fermentation. In addition, the intestinal microbiota seems to be sensible to variations in dietary protein source, such as the use of highly digestible protein sources may reduce growth of protein-fermenting and potentially pathogenic species. The objective of the present review is to assess the impact of dietary protein on microbiota composition and activity in the GIT of piglets. Attention will be given to studies designed to determine the effect of variations in total protein supply, protein source and supplementation of fermentable carbohydrates to the diet on composition and metabolic activity of the intestinal microbiota.     

Carbohydrate-Free Peach (Prunus persica) and Plum (Prunus domestica) Juice Affects Fecal Microbial Ecology in an Obese Animal Model

Background

Growing evidence shows the potential of nutritional interventions to treat obesity but most investigations have utilized non-digestible carbohydrates only. Peach and plum contain high amounts of polyphenols, compounds with demonstrated anti-obesity effects. The underlying process of successfully treating obesity using polyphenols may involve an alteration of the intestinal microbiota. However, this phenomenon is not well understood.

Methodology/Principal Findings

Obese Zucker rats were assigned to three groups (peach, plum, and control, n = 10 each), wild-type group was named lean (n = 10). Carbohydrates in the fruit juices were eliminated using enzymatic hydrolysis. Fecal samples were obtained after 11 weeks of fruit or control juice administration. Real-time PCR and 454-pyrosequencing were used to evaluate changes in fecal microbiota. Over 1,500 different Operational Taxonomic Units at 97% similarity were detected in all rats. Several bacterial groups (e.g. Lactobacillus and members of Ruminococcacea) were found to be more abundant in the peach but especially in the plum group (plum juice contained 3 times more total polyphenolics compared to peach juice). Principal coordinate analysis based on Unifrac-based unweighted distance matrices revealed a distinct separation between the microbiota of control and treatment groups. These changes in fecal microbiota occurred simultaneously with differences in fecal short-chain acids concentrations between the control and treatment groups as well as a significant decrease in body weight in the plum group.

Conclusions

This study suggests that consumption of carbohydrate-free peach and plum juice has the potential to modify fecal microbial ecology in an obese animal model. The separate contribution of polyphenols and non-polyphenols compounds (vitamins and minerals) to the observed changes is unknown.     

Genetics of efficient feed utilization and national cattle evaluation: a review

Selection for the wide range of traits for which most beef breed associations calculate expected progeny differences focus on increasing the outputs of the production system, thereby increasing the genetic potential of cattle for reproductive rates, weights, growth rates, and end-product yield. Feed costs, however, represent a large proportion of the variable cost of beef production and genetic improvement programs for reducing input costs should include traits related to feed utilization. Feed conversion ratio, defined as feed inputs per unit output, is a traditional measure of efficiency that has significant phenotypic and genetic correlations with feed intake, growth rate, and mature size. One limitation is that favorable decreases in feed to gain either directly or due to correlated response to increasing growth rate do not necessarily relate to improvement in efficiency of feed utilization. Residual feed intake is defined as the difference between actual feed intake and that predicted on the basis of requirements for maintenance of body weight and production. Phenotypic independence of residual feed intake with growth rate, body weight, and other energy depots can be forced. However, genetic associations may remain when a phenotypic prediction approach is used. Heritability estimates for phenotypic residual feed intake have been moderate, ranging from 0.26 to 0.43. Genetic correlations of phenotypic residual feed intake with feed intake have been large and positive, suggesting that improvement would produce a correlated response of decreased feed intake. Residual feed intake estimated by genetic regression results in a zero genetic correlation with its predictors, which reduces concerns over long-term antagonistic responses such as increased mature size and maintenance requirements. The genetic regression approach requires knowledge of genetic covariances of feed intake with weight and production traits. Cost of individual feed intake measurements on potential replacements must be considered in implementation of national cattle evaluations for efficiency of feed utilization. These costs need to be compared to expected, and, if possible, realized rates of genetic change and the associated reduction in feed input requirements.     

Effects of nitro compounds and feedstuffs on in vitro methane production in chicken cecal contents and rumen fluid

Short-chain volatile fatty acids (VFA) and methane are the products from a wide variety of microorganisms living in the gastrointestinal tract. The objective of this study was to examine effects of feedstuff and select nitro compounds on VFA and methane production during in vitro incubation of laying hen cecal contents and rumen fluid from cattle and sheep. In the first experiment, one of the three nitro compound was added to incubations containing cecal contents from laying hens supplemented with either alfalfa (AF) or layer feed (LF). Both feed material influenced VFA production and acetic acid was the primary component. Incubations with nitro ethanol and 2-nitropropanol (NP) had significantly (P<0.05) higher propionate concentrations than incubations with added nitroethane (NE). The results further indicated that incubations containing LF produced significantly (P<0.05) more butyrate than incubations with added AF. Addition of NP and LF to incubations of avian cecal flora may promote Gram-positive, saccharolytic, VFA-producing bacteria, especially Clostridium spp. which is the predominant group in ceca. Similar to VFA production, both feed materials fostered methane production in the incubations although methane was lower (P<0.05) in incubations with added nitro compound, particularly NE. In experiments 3-8, NE was examined in incubations of bovine or ovine rumen fluid or cecal contents containing either AF or LF. Unlike cecal contents, LF significantly (P<0.05) supported in vitro methane production in incubations of both rumen fluids. The results show that NE impedes methane production, especially in incubations of chicken cecal contents.     

Bromochloromethane,a Methane Analogue,Affects the Microbiota and Metabolic Profiles of the Rat Gastrointestinal Tract

Bromochloromethane (BCM), an inhibitor of methanogenesis, has been used in animal production. However, little is known about its impact on the intestinal microbiota and metabolic patterns. The present study aimed to investigate the effect of BCM on the colonic bacterial community and metabolism by establishing a Wistar rat model. Twenty male Wistar rats were randomly divided into two groups (control and treated with BCM) and raised for 6 weeks. Bacterial fermentation products in the cecum were determined, and colonic methanogens and sulfate-reducing bacteria (SRB) were quantified. The colonic microbiota was analyzed by pyrosequencing of the 16S rRNA genes, and metabolites were profiled by gas chromatography and mass spectrometry. The results showed that BCM did not affect body weight and feed intake, but it did significantly change the intestinal metabolic profiles. Cecal protein fermentation was enhanced by BCM, as methylamine, putrescine, phenylethylamine, tyramine, and skatole were significantly increased. Colonic fatty acid and carbohydrate concentrations were significantly decreased, indicating the perturbation of lipid and carbohydrate metabolism by BCM. BCM treatment decreased the abundance of methanogen populations, while SRB were increased in the colon. BCM did not affect the total colonic bacterial counts but significantly altered the bacterial community composition by decreasing the abundance of actinobacteria, acidobacteria, and proteobacteria. The results demonstrated that BCM treatment significantly altered the microbiotic and metabolite profiles in the intestines, which may provide further information on the use of BCM in animal production.