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PubMed2000

Mechanism(s) of butyrate transport in Caco-2 cells: role of monocarboxylate transporter 1.

The short-chain fatty acid butyrate was readily taken up by Caco-2 cells. Transport exhibited saturation kinetics, was enhanced by low extracellular pH, and was Na(+) independent. Butyrate uptake was unaffected by DIDS; however, alpha-cyano-4-hydroxycinnamate and the butyrate analogs propionate and L-lactate significantly inhibited uptake. These results suggest that butyrate transport by Caco-2 cells is mediated by a transporter belonging to the monocarboxylate transporter family. We identified five isoforms of this transporter, MCT1, MCT3, MCT4, MCT5, and MCT6, in Caco-2 cells by PCR, and MCT1 was found to be the most abundant isoform by RNase protection assay. Transient transfection of MCT1, in the antisense orientation, resulted in significant inhibition of butyrate uptake. The cells fully recovered from this inhibition by 5 days after transfection. In conclusion, our data showed that the MCT1 transporter may play a major role in the transport of butyrate into Caco-2 cells.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2000

Butyrate upregulates stromelysin-1 production by intestinal mesenchymal cells.

Nutritional factors and resident bacteria participate in the pathogenesis of intestinal inflammation. However, the ways in which bacteria and complex diets might modulate matrix metalloproteinase (MMP) production are unknown. We hypothesized that butyrate might enhance production of MMPs, thus amplifying their response to signals in inflammatory conditions. Human mesenchymal cells were incubated with butyrate and then stimulated with cytokines. MMPs and inhibitors were studied by Western blotting and quantitative RT-PCR. Acetylation of histones was examined in Triton X acetic acid-urea gels by PAGE. We showed that butyrate selectively enhanced the protein production and mRNA expression of stromelysin-1 in tumor necrosis factor-alpha- or interleukin-1beta-stimulated mesenchymal cells. Butyrate alone did not induce any change in MMP production or mRNA expression. It increased the acetylation of histones in mesenchymal cells. Furthermore, acetylation of histones (induced by trichostatin A) reproduced the effects of butyrate. Although butyrate is a major source of nutrient for the colonic epithelial cells, it modulates intestinal inflammation through the secretion of stromelysin-1 in stimulated stromal cells via the inhibition of histone deacetylase.

Acetylation↗
PubMedDate not supplied

Lipopolysaccharide exhibits synergistic enhancement of butyrate-induced and retinoic acid-mediated alkaline phosphatase activity on small intestinal epithelial cell line, IEC-6.

Although both lipopolysaccharide (LPS) and sodium butyrate are major bacterial products and bioactive chemicals with multiple functions on mucosal cells in the gut, their interaction effects on epithelial cells are not well understood. The purpose of the present study was to investigate whether LPS modulates butyrate-induced and retinoic acid-mediated alkaline phosphatase (ALP) activity of IEC-6 cells - a rat nontransformed small intestinal epithelial cell line. When cells reached confluency, various combinations of sodium butyrate, retinoic acid and LPS were added to the cultures. Cells were then harvested for the measurement of ALP activities. Sodium butyrate, but not retinoic acid or LPS alone, enhanced ALP activity. When LPS was additionally used with butyrate or retinoic acid, synergistic induction of ALP activities was demonstrated. No additive effect for ALP activity was observed when muramyl peptides or N-formylmethionyl-leucyl-phenylalanine was used with these acids. The present study clearly demonstrated that the specific combination of butyrate and LPS synergistically increased ALP activity, an epithelial differentiation-associated marker, of an intestinal epithelial cell line.

Alkaline Phosphatase↗
PubMedDate not supplied

Physiological and anti-inflammatory roles of dietary fiber and butyrate in intestinal functions.

BACKGROUND: We investigated the effects of pectin, a soluble dietary fiber, on the morphological parameters of the small intestine. In addition, we tested the effects of butyrate enemas on dextran sulfate sodium (DSS)-induced experimental colitis. METHODS: Male Wistar rats were fed an elemental diet containing 2.5% pectin for 14 days, and several parameters were then determined. DSS-induced colitis was evoked by the oral administration of water containing 3% DSS for 10 days. The butyrate enema (3 mL of 100 mmol/L butyrate per day) was begun 7 days before the DSS treatment. Interleukin (IL)-8 secretion in the human intestinal epithelial cell line HT-29 was determined by enzyme-linked immunosorbent assay (ELISA). RESULTS: Pectin feeding induced a significant increase in the villus height and crypt depth in the small intestine. These effects correlated with a significant increase in plasma enteroglucagon levels. Pretreatment with a butyrate enema significantly blocked the development of DSS-induced experimental colitis. In the in vitro experiment, sodium butyrate dose-dependently inhibited tumor necrosis factor (TNF)-alpha-induced IL-8 secretion in HT-29 cells. CONCLUSIONS: A trophic effect due to dietary fiber was directly observed. The generation of short-chain fatty acids and the induction of enteroglucagon release might play an important role in this process. Butyrate, one of the major metabolites of dietary fiber, exerted a potent anti-inflammatory effect both in vivo and in vitro. Dietary fiber may therefore play important roles in the regulation of normal and pathological conditions in the intestine.

Adenocarcinoma↗
PubMed1980

Effects of sodium butyrate and 5-bromo-2'-deoxyuridine on the synthesis of human chorionic gonadotropin in human placental cells transformed by tsA mutants of simian virus 40.

The synthesis of hCG and its subunits was studied in simian virus 40 (SV40) tsA mutant-transformed human first trimester and term placental cells at 33 C (the temperature at which the cells have the transformed phenotype) and 40 C (the temperature at which the temperature-sensitive tsA transformants regain their nontransformed phenotype). In the presence of sodium butyrate at 33 C, synthesis of both hCG and hCG alpha was greatly induced in the tsA transformants. at 40 C, hCG synthesis was induced by sodium butyrate, although to a lesser extent than at 33 C. Yet, hCG alpha synthesis was inhibited by sodium butyrate at 40 C. In the presence of 5-bromo-2'-deoxyuridine (BrdUrd) at 33 C, hCG synthesis was not affected in the transformed first trimester placental cells and was induced in the transformed term placental cells. In the presence of BrdUrd at 40 C, hCG synthesis was induced in both forms of placental cells. The synthesis of the free hCG alpha-subunit appeared to be controlled differently. At 33 C, hCG alpha synthesis was also induced by BrdUrd. At 40 C, however, hCG alpha synthesis was inhibited by BrdUrd. hCG synthesis was induced and hCG alpha synthesis was inhibited by sodium butyrate and BrdUrd in the tsA-transformed placental cells grown at 40 C. Whereas the synthesis of both hCG and hCG alpha in choriocarcinoma cells has been reported to be inhibited by both sodium butyrate and BrdUrd. Our data indicate that the effects of sodium butyrate and BrdUrd on the production of hCG, but not hCG alpha, were different in the SV40 tsA-transformed placental cells and choriocarcinoma cells.

Bromodeoxyuridine↗
PubMed1981

Sodium butyrate blocks HeLa cells preferentially in early G1 phase of the cell cycle.

The effects of sodium butyrate on the cell-cycle transverse of HeLa cells was re-examined using the kinetic and the premature chromosome condensation methods of cell-cycle analysis. The results of this study indicate that the sodium butyrate effects are dose-dependent and cell-cycle phase-specific. Cells in the early G1 period are the most sensitive to the inhibitory effects of the drug. When HeLa cells in exponential growth were exposed to a 5 mM concentration of butyrate for 48 h. 67% of the cell population was preferentially arrested in the early G1 period as indicated by the condensed morphology of the prematurely condensed chromosomes (PCC). There was no accumulation of cells in the G2 period. The results of this study suggest that hyperacetylation of histones induced by sodium butyrate does not necessarily result in decondensation of chromatin and the butyrate-enhanced protein, which has been reported to be present in butyrate-treated cells, may have a role in the regulation of the transition of cells from early G1 to the subsequent phases of the cells cycle.

Butyrates↗
PubMed1989

Effect of butyrate on the expression of the human preprourokinase gene introduced into Chinese hamster ovary cells.

A plasmid containing the human preprourokinase gene cDNA under the control of the simian virus 40 early region promoter was introduced into CHO-K1 cells and recombinant cell lines secreting a relatively high level of urokinase were obtained. In the course of studying the effects of various agents on the recombinant cell lines, we found that exposure of recombinant cells to 5 mM butyrate for 24 hours resulted in a 2-3 fold increase in urokinase production. The induction by butyrate was dose-dependent. The half maximal dose was approximately 2 mM; maximal stimulation occurred at 5-10 mM. Cell growth, on the other hand, was inhibited by butyrate concentrations greater than 2.5 mM. The response of cells to butyrate was rapid: a significant increase in urokinase production was observed 6 hours after exposure to 5 mM butyrate. Butyrate treatment increased not only the extracellular level but also the intracellular level of urokinase.

Animals↗
PubMed1994

Butyrate enhances the in vitro anti-SRBC (sheep red blood cell) antibody responses in murine splenocytes.

Butyrate at concentrations of 200-600 microM markedly enhanced the in vitro antibody productions against sheep red blood cells (SRBC) in murine splenocytes. However, other saturated short-chain fatty acids, including acetate, propionate and valeric acid, and 4-carbon compounds such as butanol, acetoacetate and beta- and gamma-hydroxybutyrate had no such effects. The presence of butyrate in the early phase of the cell culture was crucial for enhancement of the response. Butyrate also augmented the antibody production in T-cell-depleted splenocytes supplemented with the culture supernatant of concanavalin A (Con A)-stimulated lymphocytes. Interleukin (IL)-2 secreted from splenocytes in response to SRBC was increased by adding butyrate to the culture, but IL-1 secretion was not affected. On the other hand, Con A or lipopolysaccharide-stimulated proliferation of splenocytes was partly depressed by the addition of butyrate, while Con A-induced IL-2 production was not effected. These findings suggest that butyrate may act on T and B cells to promote their differentiation during the process of antibody production.

Animals↗
PubMed2003

Characteristics of an anaerobic, syntrophic, butyrate-degrading bacterium in paddy field soil.

The number of syntrophic butyrate-degrading bacteria in a flooded paddy field soil was 1.7 x 10(3) MPN/g dry soil. Butyrate was degraded to acetate and methane when paddy soils were incubated anaerobically with the addition of butyrate. However, butyrate degradation was completely suppressed by the addition of the specific inhibitor of methanogenesis, 2-bromoethanesulfonate (BES) to the soil. A hydrogen-using methanogen, strain TM-8, was isolated from flooded paddy field soil. Strain TM-8 was identified as Methanobacterium formicicum based on its physiology and phylogeny. Syntrophic butyrate-degrading bacteria were enumerated and isolated using strain TM-8. A syntrophic butyrate-degrading bacterium, strain TB-6, was isolated in coculture with strain TM-8 from paddy soil. The strain was Gram-negative, had curved rods, and grew on crotonate. Sulfate was not used as an electron acceptor. Strain TB-6 was closely related to S. wolfei subsp. wolfei. The relation between strain TB-6 and the members of Syntrophomonas are discussed.

Bacteria, Anaerobic↗
PubMed2001

Colonic delivery of sodium butyrate via oral route: acrylic coating design of pellets and in vivo evaluation in rats.

Few pharmaceutical studies, with the exception of those on rectal solutions, are described on short chain fatty acid (SCFA) formulations-especially for sodium butyrate, which is a colonocyte preferential substrate. Highly dosed butyrate pellets (90%) were prepared and their coating was designed for colonic delivery. In vivo determination (pH and transit time of pellets in rats) allowed to respectively choose the grade and thickness (resistance of 6 h) of the pH-dependent coating (Eudragi L+S, 1:1). The coated pellets were administered to naturally butyrate-deprived rats. The rats' colonic mucosa had the particularity to weakly express mitochondrial HMG-CoA synthase, an enzyme that responds to luminal butyrate. The results did not show early absorption of butyrate, but a probable cecal loss in the rat cecum as cecal residence time of the pellets was important and as pH was propitious for the coating hydrolysis. It seemed that butyrate, given daily for 7 days without the other main SCFA. was unable to induce the enzyme and/or that the dose (0.32 mmol/day) was insufficient.

Administration, Oral↗
PubMed2002

Butyrate induces apoptosis in murine macrophages via caspase-3, but independent of autocrine synthesis of tumor necrosis factor and nitric oxide.

We demonstrated that 4 mM butyrate induces apoptosis in murine peritoneal macrophages in a dose- and time-dependent manner as indicated by studies of cell viability, flow cytometric analysis of annexin-V binding, DNA ladder pattern and the determination of hypodiploid DNA content. The activity of caspase-3 was enhanced during macrophage apoptosis induced by butyrate and the caspase inhibitor z-VAD-FMK (100 microM) inhibited the butyrate effect, indicating the major role of the caspase cascade in the process. The levels of butyrate-induced apoptosis in macrophages were enhanced by co-treatment with 1 microg/ml bacterial lipopolysaccharide (LPS). However, our data indicate that apoptosis induced by butyrate and LPS involves different mechanisms. Thus, LPS-induced apoptosis was only observed when macrophages were primed with IFN-gamma and was partially dependent on iNOS, TNFR1 and IRF-1 functions as determined in experiments employing macrophages from various knockout mice. In contrast, butyrate-induced macrophage apoptosis was highly independent of IFN-gamma priming and of iNOS, TNFR1 and IRF-1 functions.

Amino Acid Chloromethyl Ketones↗
PubMed2007

Hepatic differentiation and transcriptional profile of the mouse liver epithelial progenitor cells (LEPCs) under the induction of sodium butyrate.

The liver regenerates by progenitor cells when it is damaged in chronic liver diseases and extensive damage. The progenitor cells, also termed "oval cells" according to their morphological traits, can differentiate into hepatocytes and bile duct cells in vivo. To better understand the transcriptional pattern that accompanies the hepatic differentiation of oval cells, we applied cDNA microarray to analyze the oval cell-derived liver epithelial progenitor cells (LEPCs) during in vitro induced differentiation. Upon exposure to sodium butyrate, a histone deacetylase inhibitor, cultured LEPCs differentiate and express functional hepatocyte markers albumin, tryptophan 2, 3-dioxygenase and alcohol dehydrogenase. For expression profiling, cells were harvested at 6 h, 12 h, 1 d, 3 d and 7 d after exposure to sodium butyrate. After analyzing the microarray data by SOM clustering, total of 796 differentially regulated genes were grouped into 48 clusters. Consistent with the phenotype change of LEPCs after sodium butyrate treatment, many hepatocyte functional genes are revealed by analyzing the clusters containing genes up-regulated through all the time points. The clusters, containing down-regulated genes immediately after the induction, are also analyzed. The microarray data was validated by analyzing the expression of selected genes by quantitative real-time PCR. A set of genes expressed synergistically in these clusters may play a central role during the process of differentiation. Sodium butyrate decreases cyclin B1 and Cdk4 expression, which would be associated with LEPCs growth arrest shortly after treatment. Bmi1, a polycomb group protein, is also down-regulated immediately after treatment and remains at a low level during the induction. These findings highlight the key molecular mechanisms by which sodium butyrate, mediates its effects on cell growth arrest and induction of differentiation. In conclusion, our data reflect a global view of gene expression during hepatic differentiation of LEPCs induced by sodium butyrate.

Animals↗
PubMed2004

Modulation of Wnt-specific colon cancer cell kill by butyrate and lithium.

Colorectal cancer (CRC) may be particularly amenable to gene therapy because CRCs exhibit constitutive upregulation of Wnt signaling. We have previously demonstrated that butyrate, found in the colonic lumen, modulates Wnt signaling and nonspecifically upregulates transcription from minimal promoters. Because both of these actions may influence the efficiency and specificity of Wnt-targeted expression, the effects of butyrate on Wnt-targeted gene therapy were determined. Lithium is another agent known to upregulate Wnt activity in HCT-116 CRC cells and therefore may induce Wnt-targeted CRC cell kill. CRC cells were cotransfected with an expression vector for green fluorescent protein (GFP) and different versions of vectors coupling Wnt-sensitive promoters to FADD or diphtheria toxin A-chain (DT) effector genes. Cells were treated with butyrate and/or lithium chloride and flow cytometry was used to determine the percentage of remaining transfected (GFP-positive) cells. We demonstrate that promoter and cell type-specific differences occur in Wnt-specific cell kill induced by FADD and DT. A Wnt-sensitive version of the CMV promoter (TcfCMV) exhibited the optimum combination of efficient SW620 CRC cell kill and Wnt specificity; in addition, treatment with a physiologically relevant concentration of butyrate enhanced cell kill induced by TcfCMV-FADD while maintaining specificity. In HCT-116 CRC cells, optimum results were achieved utilizing TcfFos-DT constructs and cotreatment with both butyrate and lithium. The findings suggest that effective CRC cell kill can be achieved by gene therapy through modulation of Wnt signaling by butyrate and/or lithium.

Apoptosis↗
PubMed1999

Increased growth of Bifidobacterium and Eubacterium by germinated barley foodstuff, accompanied by enhanced butyrate production in healthy volunteers.

Germinated barley foodstuff (GBF) derived from the aleurone and scutellum fractions of germinated barley mainly consists of low-lignified hemicellulose and glutamine-rich protein. GBF improves the proliferation of intestinal epithelial cells and defecation, through the bacterial production of short chain fatty acids (SCFA), especially butyrate. In this study we investigated the mechanism of production of butyrate by microflora in humans and in vitro. Daily administration of 9 g GBF for 14 successive days significantly increased fecal butyrate content. Fecal Bifidobacterium and Eubacterium were also significantly increased by GBF administration in healthy volunteers. Ten anaerobic micro-organisms selected from intestinal microflora were cultured in vitro in the medium containing GBF as a sole carbon source (GBF medium). After a 3-day incubation, 7 strains (Bifidobacterium breve, Bifidobacterium longum, Lactobacillus acidophilus, Lactobacillus casei subsp. casei, Bacteroides ovatus, Clostridium butyricum, and Eubacterium limosum) lowered the medium pH producing SCFA. Eubacterium grown together with Bifidobacterium in GBF medium efficiently produced butyrate. On the other hand, GBF changed the intestinal microflora and increased probiotics such as Bifidobacterium in the intestinal tract. As a result, butyrate was produced by the mutual action of Eubacterium and Bifidobacterium. This butyrate is considered to enhance the proliferation of colonic epithelial cells.

Adult↗
PubMed1999

Induction of differentiation and apoptosis in the prostate cancer cell line LNCaP by sodium butyrate and galectin-1.

Galectin-1 has been implicated in the process of vertebrate developmental regulation. Sodium butyrate is an established differentiation-inducing agent and has been shown to increase galectin-1 expression in colon carcinoma cells. We studied the roles of butyrate and galectin-1 in the induction of differentiation and apoptosis in the prostate cancer cell line LNCaP. Treatment of LNCaP cells with butyrate resulted in induction of galectin-1 expression in a time- and dose-dependent manner. Treatment with butyrate also resulted in inhibition of proliferation, morphologic changes consistent with a differentiated phenotype, and induction of apoptosis. Prostate specific antigen expression was transiently reduced. To determine which of these effects might be secondary to the induction of galectin-1, LNCaP cells were transfected with a galectin-1 expression vector. The transfected cells displayed growth inhibition and an increased rate of apoptosis. PSA expression was not affected. We conclude that galectin-1 may be responsible for many of the phenotypic changes resulting from butyrate treatment and may function downstream in the pathway of butyrate-induced differentiation. We also found PSA to be somewhat inconsistent as an indicator of differentiation of LNCaP cells, likely due to other factors influencing its expression.

Apoptosis↗
PubMed1999

Butyrate-induced apoptotic cascade in colonic carcinoma cells: modulation of the beta-catenin-Tcf pathway and concordance with effects of sulindac and trichostatin A but not curcumin.

Short-chain fatty acids play a critical role in colonic homeostasis because they stimulate pathways of growth arrest, differentiation, and apoptosis. These effects have been well characterized in colonic cell lines in vitro. We investigated the role of beta-catenin-Tcf signaling in these responses to butyrate and other well-characterized inducers of apoptosis of colonic epithelial cells. Unlike wild-type APC, which down-regulates Tcf activity, butyrate, as well as sulindac and trichostatin A, all inducers of G0-G1 cell cycle arrest and apoptosis in the SW620 colonic carcinoma cell line, up-regulate Tcf activity. In contrast, structural analogues of butyrate that do not induce cell cycle arrest or apoptosis and curcumin, which stimulates G2-M arrest without inducing apoptosis, do not alter Tcf activity. Similar to the cell cycle arrest and apoptotic cascade induced by butyrate, the up-regulation of Tcf activity is dependent upon the presence of a mitochondrial membrane potential, unlike the APC-induced down-regulation, which is insensitive to collapse of the mitochondrial membrane potential. Moreover, the butyrate-induced increase in Tcf activity, which is reflected in an increase in beta-catenin-Tcf complex formation, is independent of the down-regulation caused by expression of wild-type APC. Thus, butyrate and wild-type APC have different and independent effects on beta-catenin-Tcf signaling. These data are consistent with other reports that suggest that the absence of wild-type APC, associated with the up-regulation of this signaling pathway, is linked to the probability of a colonic epithelial cell entering an apoptotic cascade.

Animals↗
PubMedDate not supplied

[Changes in the K562 cell sensitivity to nonspecific lysis by human and rat leukocytes under the influence of sodium butyrate, dimethyl sulfoxide and phorbol-12-myristate-13-acetate].

We studied the ability of inducers and inhibitors of erythroid differentiation of K562 leukemia cells, such as sodium butyrate, dimethyl sulfoxide, and phorbol-12-myristate-13-acetate, respectively, to modulate sensitivity of these cells to non-specific lysis (non-restricted with respect to antigens of the major histocompatibility complex) mediated by natural human or rat killer cells. Unfractionated leukocytes from human peripheral blood or rat splenocytes were used as sources of natural killers. The induction of erythroid differentiation by sodium butyrate was accompanied by a significant increase in cell sensitivity to lysis with human peripheral blood lymphocytes; incubation of K562 cells in the mixture of sodium butyrate and dimethyl sulfoxide did not change cell sensitivity to lysis by both types of effector cells. The inhibition of sodium butyrate-induced erythroid differentiation with high doses of phorbol-12-myristate-13-acetate (100 nM; incubation was in the presence of both these agents simultaneously) resulted in an increased cell sensitivity to lysis with rat splenocytes. Incubation of K562 cells in a mixture of sodium butyrate, dimethyl sulfoxide, and phorbol-12-myristate-13-acetate (100 nM) produced greater lysis by human leukocytes, as compared with incubation in the mixture of sodium butyrate and dimethyl sulfoxide.

Animals↗
PubMedDate not supplied

[Experience on clinical application of positron emission tomography with a new radiopharmaceutical preparation sodium 11C-butyrate in differential diagnosis of pathological volume in brain formation].

The study was aimed to investigate the possibilities of the application of a new radiopharmaceutical--"Sodium butyrate, [1-(11)C]" (11C-Butyrate) for differential diagnosis of pathological volume brain formations. Positron emission tomography (PET) ("Ecat Exact 47", Siemens) of the brain was performed in 24 patients (14 male & 10 female, aged 19-56). The scanning was carried out as static scan 4-5 min after intravenous administration of 250-350 Mbq 11C-Butyrate and proceeded within 15-20 min. In addition PET with 18F-FDG was performed in all patients. The data had been verified histologically and morphologically. In 15 out of 24 patients the brain malignant tumor has been discovered, in 4 patients--benign tumors, in 5--postoperative cysts. Results of the studies showed that the ratio tumor/normal tissue in case of 11C-Butyrate and 18F-FDG application proved to be comparable for all studied hystological types of tumors. Malignant tumors in these cases had been visualized as a hot sports-fokci of increased uptake 11C-Butyrate (ratio > 1). The obtained data testify to the possibility of 11C-Butyrate application for differential diagnosis of the pathological volumic brain formation.

Adult↗