Abstract  High-mobility group box 1 protein (HMGB1), a ubiquitous nuclear protein, drives proinflammatory responses when released extracellularly. It plays a key role as a distal mediator in the development of acute lung injury (ALI). Sodium butyrate, an inhibitor of histone deacetylase, has been demonstrated to inhibit HMGB1 expression. This study investigates the effect of sodium butyrate on burn-induced lung injury. Sprague-Dawley rats were divided into three groups: 1) sham group, sham burn treatment; 2) burn group, third-degree burns over 30% total body surface area (TBSA) with lactated Ringer's solution for resuscitation; 3) burn plus sodium butyrate group, third-degree burns over 30% TBSA with lactated Ringer's solution containing sodium butyrate for resuscitation. The burned animals were sacrificed at 12, 24, and 48 h after burn injury. Lung injury was assessed in terms of histologic changes and wet weight to dry weight (W/D) ratio. Tumor necrosis factor (TNF)-α and interleukin (IL)-8 protein concentrations in bronchoalveolar lavage fluid (BALF) and serum were measured by enzyme-linked immunosorbent assay, and HMGB1 expression in the lung was determined by Western blot analysis. Pulmonary myeloperoxidase (MPO) activity and malondialdehyde (MDA) concentration were measured to reflect neutrophil infiltration and oxidative stress in the lung, respectively. As a result, sodium butyrate significantly inhibited the HMGB1 expressions in the lungs, reduced the lung W/D ratio, and improved the pulmonary histologic changes induced by burn trauma. Furthermore, sodium butyrate administration decreased the TNF-α and IL-8 concentrations in BALF and serum, suppressed MPO activity, and reduced the MDA content in the lungs after severe burn. These results suggest that sodium butyrate attenuates inflammatory responses, neutrophil infiltration, and oxidative stress in the lungs, and protects against remote ALI induced by severe burn, which is associated with inhibiting HMGB1 expression.

Abstract  Nicotinamide phosphoribosyl transferase (Nampt) is the rate-limiting enzyme for the salvage biosynthesis of nicotinamide adenine dinucleotide (NAD). Although elevated level of Nampt expression has been observed in various cancers, the involvement of Nampt promoter regulation was not well understood. We have identified a cluster of MEF2 recognition sites upstream of the functional hypoxia response elements (HREs) within the human Nampt promoter, and demonstrated that the two MEF2 sites at -1272 and -1200 were functional to upregulate the promoter activity by luciferase reporter assays. The Nampt promoter was able to be activated cooperatively following hypoxic stimulation by CoCl2 treatments with associated MEF2C overexpression. During the investigation on MEF2C regulation of endogenous Nampt expression in HeLa cells, the most significant enhancement of Nampt expression observed was by overexpression of MEF2C in combination with sodium butyrate exposure. By chromatin immunoprecipitation with a MEF2C anti-body, we found that the MEF2C indeed interacted with endogenous Nampt promoter. The requirement of HDAC inhibition for the MEF2C enhancement of Nampt transcription was verified by RNAi of HDAC. Our results were in support of reports indicating that MEF2 family transcription factors interacted with HDACs and regulated downstream gene expression at the epigenetic levels. Our study provided important evidence to demonstrate the sophisticated mechanism of endogenous Nampt promoter regulation, and therefore, will help to better understand the Nampt overexpression in cancer progression, especially in the context of MEF2C upregulation which frequently occurred in cancer development and drug resistance.

Abstract  OBJECTIVE: Bacteria play an important role in the onset and perpetuation of intestinal inflammation in inflammatory bowel disease (IBD). Unlike in Crohn's disease (CD), in which dysbiosis has been better characterised, in ulcerative colitis (UC), only small cohorts have been studied and showed conflicting data. Therefore, we evaluated in a large cohort if the microbial signature described in CD is also present in UC, and if we could characterise predominant dysbiosis in UC. To assess the functional impact of dysbiosis, we quantified the bacterial metabolites.

DESIGN: The predominant microbiota from 127 UC patients and 87 age and sex-matched controls was analysed using denaturing gradient gel electrophoresis (DGGE) analysis. Differences were quantitatively validated using real-time PCR. Metabolites were quantified using gas chromatography-mass spectrometry.

RESULTS: Based on DGGE analysis, the microbial signature previously described in CD was not present in UC. Real-time PCR analysis revealed a lower abundance of Roseburia hominis (p<0.0001) and Faecalibacterium prausnitzii (p<0.0001) in UC patients compared to controls. Both species showed an inverse correlation with disease activity. Short-chain fatty acids (SCFA) were reduced in UC patients (p=0.014), but no direct correlation between SCFA and the identified bacteria was found.

CONCLUSIONS: The composition of the fecal microbiota of UC patients differs from that of healthy individuals: we found a reduction in R hominis and F prausnitzii, both well-known butyrate-producing bacteria of the Firmicutes phylum. These results underscore the importance of dysbiosis in IBD but suggest that different bacterial species contribute to the pathogenesis of UC and CD.

Abstract  INTRODUCTION: Travellers' diarrhoea (TD) remains a considerable concern among international travellers. Known methods of prevention include dietary precautions, administration of vaccines and antibiotic agents.

AIM: To assess the efficacy of sodium butyrate (SB) and short-chain fatty acids (SCFA) in prevention of TD.

MATERIAL AND METHODS: 67 adult patients planning to travel to subtropical countries were originally enrolled in the study. After eliminating 7 patients for not fulfilling the inclusion criteria, 60 patients were randomized into a study group receiving SB with SCFA and a placebo group. Patients were requested to complete previously distributed questionnaire daily. After elimination of 18 patients who did not return questionnaires, 42 patients completed the study (22 study, 20 placebo).

RESULTS: In comparison to the control arm, the study arm noted significantly reduced occurrence of TD (4.5% vs. 40%, p = 0.008), was associated with a significant decrease in number of stools per day in travellers (1.9 vs. 4.2, p = 0.04), as well as a decrease in gastrointestinal symptoms including pain, bloating and nausea with fevers (0.7 vs. 1.4, p = 0.01). We recorded a trend towards decrease in diarrhoea related utilization of medical care in subjects from the study arm. There were no adverse effects noted regarding the use of SB and SCFA.

CONCLUSIONS: Administration of SB with SCFA decreases occurrence of travellers' diarrhoea. It is safe and may constitute a new method of travellers' diarrhoea prevention.

Abstract  Bacterial vaginosis (BV), a common condition in women, is associated with increased shedding of HIV in the female genital tract. While the Lactobacillus species that comprise a healthy vaginal microbiota produce lactic acid, the bacteria common in BV produce high concentrations of short chain fatty acids (SCFAs) and succinic acid. Macrophages are abundant in the lower genital tract mucosa and are thought to play an important role in HIV infection. In this study, we investigated whether SCFAs and succinic acid impacted HIV expression in monocyte-derived macrophages. Monocytes differentiated with either granulocyte-macrophage colony-stimulating factor (GM-CSF) or macrophage colony-stimulating factor (M-CSF) were infected with either HIVBal or an HIV-luciferase reporter virus and treated with SCFAs, succinic acid, or lactic acid. Butyric acid suppressed HIV expression while succinic acid significantly increased expression in macrophages differentiated with either GM-CSF or M-CSF. Acetic, propionic, and lactic acids had no effect on HIV expression. Only succinic acid resulted in a significant increase in interleukin-8 production by infected macrophages. Our results suggest that succinic acid present in increased concentrations in the genital tract of women with BV plays a pro-inflammatory role and increases HIV expression. This could be one factor contributing to increased virus shedding seen in women with BV.

Abstract  Dietary modulation of the synthesis of endogenous host defense peptides (HDPs) represents a novel antimicrobial approach for disease control and prevention, particularly against antibiotic-resistant infections. However, HDP regulation by dietary compounds such as butyrate is species-dependent. To examine whether butyrate could induce HDP expression in pigs, we evaluated the expressions of a panel of porcine HDPs in IPEC-J2 intestinal epithelial cells, 3D4/31 macrophages, and primary monocytes in response to sodium butyrate treatment by real-time PCR. We revealed that butyrate is a potent inducer of multiple, but not all, HDP genes. Porcine β-defensin 2 (pBD2), pBD3, epididymis protein 2 splicing variant C (pEP2C), and protegrins were induced markedly in response to butyrate, whereas pBD1 expression remained largely unaltered in any cell type. Additionally, a comparison of the HDP-inducing efficacy among saturated free fatty acids of different aliphatic chain lengths revealed that fatty acids containing 3-8 carbons showed an obvious induction of HDP expression in IPEC-J2 cells, with butyrate being the most potent and long-chain fatty acids having only a marginal effect. We further investigated a panel of butyrate analogs for their efficacy in HDP induction, and found glyceryl tributyrate, benzyl butyrate, and 4-phenylbutyrate to be comparable with butyrate. Identification of butyrate and several analogs with a strong capacity to induce HDP gene expression in pigs provides attractive candidates for further evaluation of their potential as novel alternatives to antibiotics in augmenting innate immunity and disease resistance of pigs.

Abstract  AIM: This study aimed to assess the role of HCO3- in the transport of acetate and butyrate across the basolateral membrane of rumen epithelium and to identify transport proteins involved.

METHODS: The effects of basolateral variation in HCO3- concentrations on acetate and butyrate efflux out of the epithelium and the transepithelial flux of these short-chain fatty acids were tested in Ussing chamber experiments using (14) C-labelled substrates. HCO3--dependent transport mechanisms were characterized by adding specific inhibitors of candidate proteins to the serosal side.

RESULTS: Effluxes of acetate and butyrate out of the epithelium were higher to the serosal side than to the mucosal side. Acetate and butyrate effluxes to both sides of rumen epithelium consisted of HCO3--independent and -dependent parts. HCO3--dependent transport across the basolateral membrane was confirmed in studies of transepithelial fluxes. Mucosal to serosal fluxes of acetate and butyrate decreased with lowering serosal HCO3- concentrations. In the presence of 25 mm HCO3-, transepithelial flux of acetate was inhibited effectively by p-hydroxymercuribenzoic acid or α-cyano-4-hydroxycinnamic acid, while butyrate flux was unaffected by the blockers. Fluxes of both acetate and butyrate from the serosal to the mucosal side were diminished largely by the addition of NO3- to the serosal side, with this effect being more pronounced for acetate.

CONCLUSION: Our results indicate the existence of a basolateral short-chain fatty acid/HCO3- exchanger, with monocarboxylate transporter 1 as a primary candidate for acetate transfer.

Abstract  BACKGROUND & AIMS: Short-chain fatty acids (SCFAs), the most abundant microbial metabolites in the intestine, activate cells via G-protein-coupled receptors (GPRs), such as GPR41 and GPR43. We studied regulation of the immune response by SCFAs and their receptors in the intestines of mice.

METHODS: Inflammatory responses were induced in GPR41(-/-), GPR43(-/-), and C57BL6 (control) mice by administration of ethanol; 2, 4, 6-trinitrobenzene sulfonic-acid (TNBS); or infection with Citrobacter rodentium. We examined the effects of C rodentium infection on control mice fed SCFAs and/or given injections of antibodies that delay the immune response. We also studied the kinetics of cytokine and chemokine production, leukocyte recruitment, intestinal permeability, and T-cell responses. Primary colon epithelial cells were isolated from GPR41(-/-), GPR43(-/-), and control mice; signaling pathways regulated by SCFAs were identified using immunohistochemical, enzyme-linked immunosorbent assay, and flow cytometry analyses.

RESULTS: GPR41(-/-) and GPR43(-/-) mice had reduced inflammatory responses after administration of ethanol or TNBS compared with control mice, and had a slower immune response against C rodentium infection, clearing the bacteria more slowly. SCFAs activated intestinal epithelial cells to produce chemokines and cytokines in culture and mice after administration of ethanol, TNBS, or C rodentium. These processes required GPR41 and GPR43 and were required to recruit leukocytes and activate effector T cells in the intestine. GPR41 and GPR43 activated extracellular signal-regulated kinase 1/2 and p38 mitogen-activated protein kinase signaling pathways in epithelial cells to induce production of chemokines and cytokines during immune responses.

CONCLUSIONS: SCFAs activate GPR41 and GPR43 on intestinal epithelial cells, leading to mitogen-activated protein kinase signaling and rapid production of chemokines and cytokines. These pathways mediate protective immunity and tissue inflammation in mice.

Abstract  Small molecules (SM) can greatly enhance the efficiency of induced pluripotent stem (iPS) cell generation, but the mechanisms by which they act have not been fully explored. We show here that an SM cocktail (NaB, PD03259, and SB431542) significantly promotes iPS cell generation from human fibroblasts, and NaB is more potent than the other two common histone deacetylase inhibitors (valproic acid and Trichostatin A) in promoting cellular reprogramming. Our data indicate that the SM cocktail substantially upregulates the miR302/367 cluster expression by increasing the stability and transcriptional level of this microRNA (miRNA) cluster in a manner dependent on the four defined transcription factors (TFs). Among the four TFs, Oct4 in particular appears to be required for the induction of the miR302/367 cluster by the SM cocktail. We also found that NaB alone can enhance the TFs-dependent upregulation of the miR302/367 cluster. Using a promoter reporter assay, we show that the SM cocktail remarkably enhanced the transcriptional activity of the four TFs in the miR302/367 promoter. Notably, attenuation of miRNA302/367 using a miRZip impairs the ability of the SM cocktail in promoting reprogramming. Collectively, these findings suggest that the SM cocktail promotes reprogramming at least partly through the induction of the miR302/367 cluster expression. Further insights into this process may pave the way for the generation of iPS cells using only SM cocktails.

Abstract  Cancer stem cells (CSCs) also known as cancer-initiating cells (CICs) show high tumorigenic activity and high chemo- and radiation resistance. It is, therefore, important to identify CSCs reliably to develop novel curative cancer treatments. In this study, we re-evaluated CSC markers of colorectal cancer for their cellular differentiation and tumorigenic activity, with the aim to identify reliable CSC markers. The rates of change in CD44, CD133, CD166, CD24, CD49f and CXCR4 expression during sodium butyrate (NaBT)-induced cell differentiation were assessed in HT29 and Caco2 colon cancer cell lines. Expression levels of target markers were assessed in clinical CRC samples. Tumorigenic activity was assessed on isolated cell fractions identified by multicolor flow cytometric analysis. In the cell differentiation assay, the average percent change was higher in CD44 (-98.2%) and CD49f (-74.4%) compared to CD133 (-17.9%) and CD166 (-49.4%). Expression of CD24 and CXCR4 appeared random in HT29 and Caco2. Expression of CD44, CD49f, CD133 and CD166 was confirmed in all four clinical CRC samples. Limiting dilution assay of CD44- and CD133-expressing cells revealed that only the CD133⁺CD44⁺ population possessed tumorigenic activity. Tumorigenesis was not affected by CD166 expression. Highly tumorigenic cells could be enriched in samples with higher CD49f expression; CD49f⁺ cells showed high tumorigenesis, whereas CD133⁺ and CD44⁺ cells that were negative for CD49f exhibited no tumorigenic activity. Multicolor analysis revealed that CD49f⁺ cells localized in CD44⁺ and CD133⁺ cell fractions. These findings demonstrated that CD49f is an important marker for identifying colorectal CSCs and suggest that the CD49f⁺ cell fraction may be the best candidate for colorectal CSCs.

Abstract  Low-temperature nonthermal plasma has been used to prepare solid-phase microextraction (SPME) fibers with high adsorbability. long-term serviceability, and high reproducibility. Graphite rods serving as fiber precursors were treated by an air plasma discharged at 15.2-15.5 kV for a duration of 8 min. Sampling results revealed that the adsorptive capacity of the homemade fiber was 2,5-34.6 times that of a polyacrylate (PA) fiber for alcohols (methanol, ethanol, isopropyl alcohol, n-butyl alcohol), and about 1.4-1.6 times and 2.5-5.1 times that of an activated carbon fiber(ACF) for alcohols and BTEX (benzene, toluene, ethylbenzene, and xylenes), respectively. It is confirmed from FTIR (Fourier transform infrared spectrophotometer) and SEM (scanning electron microscope) analyses that the improvement in the adsorptive performance attributed to increased Surface energy and toughness of the graphite fiber. Using gas chromatography (GC)-flame-ionization detector (FID), the limits of detection (LODs) of the alcohols and BTEX ranged between 0.19 and 3.75 mu g L-1, the linear ranges were between 0.6 and 35619 mu g L-1 with good linearity (R-2 =0.9964-0.9997). it was demonstrated that nonthermal plasma offers a fast and simple method for preparing an efficient graphite SPME fiber, and that SPME using the homemade fiber represents a sensitive and selective extraction method for the analysis of a wide range of organic compounds. (C) 2008 Elsevier B.V. All rights reserved.

Abstract  Background: Metabolomic studies have been applied to disease biomarkers selection. With the metabolomic technique, gas chromatography/mass spectrometry (GC/MS), human serum metabolites can be detected and identified. The purpose of this study was to investigate the serum metabolic profile of hepatitis B virus (HBV) infected cirrhosis patients and to detect disease biomarkers. Methods: HBV infected non-cirrhosis male subjects (n=20) and HBV infected cirrhosis male patients (n=20) participated in this experiment. Serum metabolome was detected through chemical derivatization followed by GC/MS. The high-flux metabolomic data were analyzed by stepwise discriminant analysis. Results: Out of the 41 metabolites detected in serum, we selected metabolites, including acetic acid, sorbitol, D-lactic acid, hexanoic acid, 1-naphthalenamine, butanoic acid, phosphoric acid, D-glucitol, and glucose, which in combination with each other could segregate the two groups. The error count was 0% for the non-cirrhosis group and 25% for the cirrhosis group. Conclusions: This technique can be used to select biomarkers for hepatic cirrhosis. Clin Chem Lab Med 2009;47.

Abstract  ABSTRACT: Volatile hydrocarbon production by Ascocoryne sacroides was studied over its growth cycle. Gas-phase compounds were measured continuously with a proton transfer reaction-mass spectrometry (PTR-MS) and at distinct time points with gas chromatography-mass spectrometry (GC-MS) using head space solid phase microextraction (SPME). The PTR-MS ion signal permitted temporal resolution of the volatile production while the SPME results revealed distinct compound identities. The quantitative PTR-MS results showed the volatile production was dominated by ethanol and acetaldehyde, while the concentration of the remainder of volatiles consistently reached 2,000 ppbv. The measurement of alcohols from the fungal culture by the two techniques correlated well. Notable compounds of fuel interest included nonanal, 1-octen-3-ol, 1-butanol, 3-methyl- and benzaldehyde. Abiotic comparison of the two techniques demonstrated SPME fiber bias toward higher molecular weight compounds, making quantitative efforts with SPME impractical. Together, PTR-MS and SPME GC-MS were shown as valuable tools for characterizing volatile fuel compound production from microbiological sources.

Abstract  Four butyrate-producing isolates were obtained from the caecal content of a 4-week-old broiler chicken. The 16S rRNA gene sequences were determined and confirmed the close relatedness of the four isolates, which suggested that they were derived from a single bacterial clone. Phylogenetic analysis based on 16S rRNA gene sequences showed that its closest relatives were members of cluster XIVa of the Clostridium subphylum of Gram-positive bacteria and that the closest related type strain was Anaerostipes caccae L1-92(T) (94.5 % similarity). Similarity levels of 96-98 % with sequences from uncultured bacteria from human stool samples were observed. On the basis of morphological, biochemical and phylogenetic characteristics, this strain is assigned to a novel species in the genus Anaerostipes, for which the name Anaerostipes butyraticus sp. nov. is proposed. The type strain is 35-7(T) (=LMG 24724(T) =DSM 22094(T)). An emended description of the genus Anaerostipes is also provided.

Abstract  Sphingosine kinases (SphKs) have been recognized as important proteins regulating cell proliferation and apoptosis. Of the two isoforms of SphK (SphK1 and SphK2), little is known about the functions of SphK2. Sodium butyrate (NaBT) has been established as a promising chemotherapeutic agent, but the precise mechanism for its effects is unknown. In this study, we investigated the role of SphK2 in NaBT-induced apoptosis of HCT116 colon cancer cells. The results indicated that following NaBT treatment SphK2 was translocated from the nucleus to the cytoplasm, leading to its accumulation in the cytoplasm; in the meantime, only mild apoptosis occurred. However, downregulation of SphK2 resulted in sensitized apoptosis, and overexpression of SphK2 led to even lighter apoptosis; these strongly indicate an inhibitory role of SphK2 in cell apoptosis induced by NaBT. After knocking down protein kinase D (PKD), another protein reported to be critical in cell proliferation/apoptosis process, by using siRNA, blockage of cytoplasmic accumulation of SphK2 and sensitized apoptosis following NaBT treatment were observed. The present study suggests that PKD and SphK2 may form a mechanism for the resistance of cancer cells to tumor chemotherapies, such as HCT116 colon cancer cells to NaBT, and these two proteins may become molecular targets for designation of new tumor-therapeutic drugs.

Abstract  BACKGROUND: In eukaryotic cells, the genomic DNA is packed with histones to form the nucleosome and chromatin structure. Reversible acetylation of the histone tails plays an important role in the control of specific gene expression. Mounting evidence has established that histone deacetylase inhibitors selectively induce cellular differentiation, growth arrest and apoptosis in variety of cancer cells, making them a promising class of anticancer drugs. However, the molecular mechanisms of the anti-cancer effects of these inhibitors have yet to be understood.

RESULTS: Here, we report that a key determinant for the susceptibility of cancer cells to histone deacetylase inhibitors is their ability to maintain cellular Akt activity in response to the treatment. Also known as protein kinase B, Akt is an essential pro-survival factor in cell proliferation and is often deregulated during tumorigenesis. We show that histone deacetylase inhibitors, such as valproic acid and butyrate, impede Akt1 and Akt2 expression, which leads to Akt deactivation and apoptotic cell death. In addition, valproic acid and butyrate induce apoptosis through the caspase-dependent pathway. The activity of caspase-9 is robustly activated upon valproic acid or butyrate treatment. Constitutively active Akt is able to block the caspase activation and rescues cells from butyrate-induced apoptotic cell death.

CONCLUSION: Our study demonstrates that although the primary target of histone deacetylase inhibitors is transcription, it is the capacity of cells to maintain cellular survival networks that determines their fate of survival.

Abstract  BACKGROUND: Combination therapy is usually desirable for successful cancer treatment, especially in cancers that are resistant to single forms of therapy.

METHODS: To achieve an optimal therapeutic effect against glioblastoma, we tested a strategy that combines baculovirus-mediated transfer of the p53 tumor suppressor gene with the use of sodium butyrate, a histone deacetylase inhibitor. This strategy was designed based on the findings that the transduction efficiency of baculovirus in mammalian cells can be markedly enhanced by the addition of histone deacetylase inhibitors and that these inhibitors are effective in inducing cell cycle arrest, differentiation, or apoptosis in tumor cells.

RESULTS: We observed a synergistic effect of the combination of the two treatments in provoking apoptosis in glioblastoma cells with mutant p53. In a mouse glioma xenograft model, the tumor inhibitory effect of baculovirus-expressed p53 was significantly enhanced by co-administration of sodium butyrate.

CONCLUSIONS: These findings suggest a new approach to treat glioblastoma using baculovirus-mediated gene transfer in combination with administration of histone deacetylase inhibitor.

Abstract  Given the trillions of microbes that inhabit the mammalian intestines, the host immune system must constantly maintain a balance between tolerance to commensals and immunity against pathogens to avoid unnecessary immune responses against otherwise harmless bacteria. Misregulated responses can lead to inflammatory bowel diseases such as ulcerative colitis or Crohn's disease. The mechanisms by which the immune system maintains this critical balance remain largely undefined. Here, we demonstrate that the short-chain fatty acid n-butyrate, which is secreted in high amounts by commensal bacteria, can modulate the function of intestinal macrophages, the most abundant immune cell type in the lamina propria. Treatment of macrophages with n-butyrate led to the down-regulation of lipopolysaccharide-induced proinflammatory mediators, including nitric oxide, IL-6, and IL-12, but did not affect levels of TNF-α or MCP-1. These effects were independent of toll-like receptor signaling and activation of G-protein-coupled receptors, two pathways that could be affected by short-chain fatty acids. In this study, we provide several lines of evidence that suggest that these effects are due to the inhibition of histone deacetylases by n-butyrate. These findings elucidate a pathway in which the host may maintain tolerance to intestinal microbiota by rendering lamina propria macrophages hyporesponsive to commensal bacteria through the down-regulation of proinflammatory effectors.

Abstract  A concern about enhancing the natural defense mechanisms of animals and reducing the massive use of antibiotics led to the banning of studies in this field. So, this research was done to investigate the effect of butyric acid glycerides and salinomycin sodium on the performance of the broiler chickens (strain Ross 308). A total of 800 chickens were reared for 42 days. A 3 factor statistical design was conducted with 4 replicates, and each factor contained 2 levels (25 broilers in each pen). The factors were butyric acid glycerides (0 and 0.3% of diet), salinomycin sodium - an anticoccidial drug (0 and 0.5% of diet) - and litter moisture (normal litter with average moisture of 35% and wet litter with average moisture of 75%). Data were collected and analyzed by SAS with GLM procedure. The results showed that butyric acid glycerides had no significant effect on feed intake. Weight gain and feed conversion ratio were not significantly affected by the mentioned factors. The effect of the treatments on the number of Eimeria oocytes excreta in the second and fourth week of breeding and feed intake were significant (p<0.05). Diet acidification with butyric acid glycerides caused an increase in ash, calcium and phosphorus of the chicken tibia, but this increase was not significant (p>0.05). Considering the result of this experiment, the use of butyric acid glycerides and salinomycin sodium in the aforementioned levels had no positive effect on the performance of broiler chickens (p>0.05).

Abstract  BACKGROUND: Cecal or distal colonic concentration of butyrate has been used as an index of butyrate production from various fermentable carbohydrates. However, we previously found that cecal concentration of butyrate does not correlate with the rate of synthesis of butyrate in the cecal lumen. As part of a larger study of the cellular effects of cecal infusions of butyrate, we sought to rule out the null hypothesis that cecal infusion of butyrate also would not alter butyrate concentration in the cecum.

METHODS: Piglets (n = 10) were fed sow milk replacement formula plus inulin (3 g x L(-1)). After 6 days of oral feeding, the piglets were randomly assigned into 2 equal groups: (I) Cecal infusion of phosphate-buffered NaCl and (II) cecal infusion of butyrate (2.13 micromol x kg(-1) x min(-1)). The concentration of butyrate was measured by gas chromatography in the cecum and distal colon.

RESULTS: There was no effect of cecal butyrate infusion on butyrate concentration (mM; I vs II) in the cecum (5.7 +/- 0.4 vs 5.3 +/- 1.1) or distal colon (3.3 +/- 0.6 vs 4.1 +/- 0.8) or on the ratio of cecal butyrate concentration to the sum of the concentrations of butyrate, acetate, propionate, and valerate (0.101 +/- 0.004 vs 0.083 +/- 0.011). There was no effect of cecal butyrate infusion on the concentration of any of these short chain fatty acids.

CONCLUSIONS: At an entry rate into the cecum within the physiological range, butyrate had no effect on cecal or distal colonic luminal concentration of butyrate.

Abstract  Carbohydrates of laminin, a family of large multidomain glycoproteins, have been implicated in various cellular activities including maintaining the protein structure, its function and also basement membrane integrity. During the course of our investigation, we observed that purified laminin from kidneys of control, diabetic, and dietary fiber- and butyric acid-treated diabetic rats showed differences in binding to extracellular matrix components. This prompted us to determine whether there are structural changes in laminin oligosaccharides. In this study, we have characterized a few major N-linked oligosaccharides isolated from purified laminin in various experimental groups, viz. normal, diabetic and diabetic rats fed with dietary fiber and butyric acid. Sugar composition, as identified by GLC, revealed the presence of mannose, galactose and N-acetylglucosamine. In order to study fine structures of the oligosaccharides, N-linked oligosaccharides of laminin were released by Peptide-N-glycosidase F digestion, end-labeled with 2-anthranilic acid and fractionated by lectin affinity chromatography. Furthermore, structural elucidation carried out by MALDI-TOF MS/MS analysis showed variations in the oligosaccharide sequence of laminin during diabetes which were altered by the feeding of dietary fiber and butyric acid.