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At least 1,207 records · Page 67Linked to original sources
PubMed1995

Heparan-dependent endothelial antithrombin binding is increased by butyrate.

Heparin biosynthesis involves a critical early step of N-deacetylation which is inhibited by the short chain fatty acid n-butyrate. Such inhibition causes mast cells to produce heparins with high affinity for antithrombin (AT). We have cultured endothelial cells in media supplemented with short chain fatty acids and have found that isobutyric, propionic and valeric acids cause significant increases in endothelial binding of AT measured by flow cytometry, but n-butyric acid was the most effective fatty acid to increase AT binding. Such binding,was heparan sulfate-dependent, for it was decreased significantly by pre-treatment of the cells with heparinase. These findings suggest that inhibition of N-deacetylation in heparan biosynthesis affects sulfation and results in the distribution of negative charges and conformation changes within the heparan domain that binds AT to endothelial plasma membranes. These changes also were associated with up-regulation of the intercellular adhesion molecule-1, which is a marker of endothelial activation.

Anticoagulants↗
PubMed1987

Differentiation of PC12 pheochromocytoma cells by sodium butyrate.

PC12 pheochromocytoma cells cease dividing and show increased cell-cell and cell-substratum adhesion in response to treatment with sodium butyrate. These changes are accompanied by the rapid appearance of neuron-specific enolase, an APUD cell marker. However, neurofilament proteins, markers for neuronal differentiation, are not induced. These results suggest that sodium butyrate induces differentiation in the PC12 cell line, perhaps along the chromaffin cell pathway.

Adrenal Gland Neoplasms↗
PubMed1989

Sodium butyrate induces major morphological changes in C6 glioma cells that are correlated with increased synthesis of a spectrin-like protein.

Butyrate induced flattening and development of cell processes in rat glioma (C6) cells and this change was correlated with an increase in the synthesis of a polypeptide doublet with an apparent molecular weight of about 200 kDa. Blot analysis revealed that at least one of these polypeptides was a spectrin-like protein. Indirect immunofluorescence studies with the spectrin antiserum indicated that the antigen was present in the cell bodies, and also in the cell processes. Thus fodrin may be one the major targets for the action of butyrate on C6 cells.

Autoradiography↗
PubMed1990

Effects of sodium butyrate and 5-azacytidine on DNA methylation in human tumor cell lines: variable response to drug treatment and withdrawal.

The effect of butyrate (Btr) and 5-azacytidine (azaC) on genomic DNA methylation was examined in a variety of human tumor cell lines. Butyrate treatment differentially affected 5-methylcytosine (m5C) content in a cell type-specific manner. For example, incubation of CBT cells (glioblastoma multiforme) for 48 h in medium containing 2 mM Btr resulted in the hypomethylation of their DNA; after removal of the drug, the m5C content was rapidly (24 h) restored to its original level. In contrast, when HeLa cells (cervical carcinoma) were cultured for 48 h in 3 mM Btr, their genomic DNA became more extensively methylated relative to the untreated control, and the hypermethylated state was maintained for long periods in culture. Treatment of HeLa cell lines with azaC resulted in extensive demethylation of their DNA. Following removal of the drug, the DNA was rapidly remethylated to levels equal to or greater than those of the untreated cells. The hypermethylated state has remained stable for over 180 generations. Together, the data suggest that cells respond rapidly to alter drug-induced reductions in the m5C content of their DNA, and this response can subsequently result in overmethylation. In contrast, when drug-induced hypermethylation of genomic DNA occurs, it may persist for many cell generations.

5-Methylcytosine↗
PubMed1983

Preferential alkaline phosphatase isoenzyme induction by sodium butyrate.

SW-620, a continuous cell line derived from a poorly differentiated human colon carcinoma, produces two alkaline phosphatases. Under basal conditions the heat-stable, term-placental is the major isoenzyme and the heat-labile, liver/bone/kidney form represents a minor component. Exposing SW-620 cells to sodium butyrate causes induction of increased levels of activity accompanied by a striking shift in isoenzyme distribution not observed heretofore. The activity increase is accounted for entirely by augmentation of the liver/bone/kidney isoenzyme, with the term-placental form not being affected. Two other known alkaline phosphatase inducers, prednisolone and hyperosmolality, do not influence specific activity and isoenzyme distribution. The preferential induction of the liver/bone/kidney form of alkaline phosphatase in SW-620 cells may reflect a butyrate-elicited expression of a more differentiated state.

Alkaline Phosphatase↗
PubMed1987

Regulation of nerve growth factor gene expression in primary brain monolayer cultures: effects of dibutyryl cyclic AMP and sodium butyrate.

Primary brain cultures composed of a heterogeneous population of cells, most of which reacted with anti-fibronectin and only few with anti-GFAP antiserum, were found to synthesize a mRNA indistinguishable from mouse submandibular gland nerve growth factor (NGF) mRNA in hybridization characteristics and electrophoretic behavior in agarose gels. The levels of this mRNA were increased 2.5-10 fold by 1 mM dibutyryl cyclic AMP (db-cAMP) and sodium butyrate within 24 h, but not by 10 microM forskolin, and were unaffected by serum in the culture medium. These observations demonstrate that brain cells synthesize a NGF mRNA in primary culture and that the butyrate moiety of db-cAMP enhances NGF gene expression in these cells, probably by a modification of chromatin structure in and around the NGF gene.

Animals↗
PubMed1987

Modulation of secreted plasminogen activator activity of human renal carcinoma cells by dimethylsulfoxide, butyrate and retinoate.

Dimethylsulfoxide, butyrate and retinoic acid, agents which induce differentiation of certain malignant cells, were examined for their effect on the activity of plasminogen activator (PA) of serumless conditioned medium (CM) of two human renal carcinoma cell lines. All three agents produced a decrease in PA activity. More than 90% of the PA was secreted in latent form, and this was not altered by the agents. Active PA components of Mr 52,000 and 93,000 were identified in cell secretions by zymography. In the presence of DMSO or butyrate the Mr 52,000 component was markedly reduced. Reversibility of the effect on PA was demonstrated for both DMSO and retinoic acid with activity of CM returning to control level after removal of the agent. That the effect was temporary agrees with most observations of the effects of these and similar agents on cells from solid tumors.

Butyrates↗
PubMed1993

Potentiation of butyrate-induced differentiation in human colon tumor cells by deoxycholate.

Human colon adenocarcinoma cells, treated with deoxycholate for 24 h prior to exposure to 1 mM butyrate, exhibited dose-dependent increases in the activities of three markers of colonic differentiation (alkaline phosphatase, lactase and CEA). Treatment with deoxycholate alone, for 24 h or longer, did not increase the secretion of CEA or the activities of either of the brush border-associated enzyme activities. Increases in differentiation markers were found to be bile acid-specific. Pretreatment with either dehydrocholic acid or cholic acid, even at cytotoxic concentrations, led to no significant butyrate-induced increases in brush-border associated hydrolase activities. The addition of a bacterial superoxide dismutase decreased the short-term cytotoxicity of deoxycholate and increased the maturation-potentiating effects of the bile acid in HCT-116 DO cells. The results of these studies demonstrate that bile acids, which are commonly thought to have tumor promoting activities in vivo, may also have physiological effects which serve to limit carcinogenic processes in the human colon by potentiating tumor cell differentiation.

Adenocarcinoma↗
PubMed1996

Differential effects of butyrate and dibutyryl cAMP on mRNA levels of muscarinic acetylcholine receptor subtypes expressed in neurohybrid cell lines.

NCB-20 cells expressed m1- and m4-muscarinic acetylcholine receptor (mAChR) mRNAs, while NG108-15 cells expressed only m4-mAChR mRNA. Butyrate induced a time-dependent increase in the level of m1-mAChR mRNA with no change in the m4-mAChR mRNA level in NCB-20 cells. Similarly, butyrate did not affect the m4-mAChR mRNA level in NG108-15 cells. In contrast, dibutyryl cAMP caused a significant time-dependent decrease in the level of m4-mAChR mRNA in NCB-20 and NG108-15 cells as well as m1-mAChR mRNA in NCB-20 cells. Our results suggest that these two differentiating agents are important physiological regulators of the transcription and/or stability of the mRNA of certain mAChR subtypes expressed in these two neurohybrid cell lines.

Animals↗
PubMed1992

Differential and coordinate responses of the human genes encoding the heat stable alkaline phosphatases to cAMP and sodium butyrate in the choriocarcinoma line JEG-3.

Human heat stable alkaline phosphatases are encoded by two closely related genes: the PLAP-1, which specifies the term placental enzyme, and the PLAP-2, which is expressed primarily in germ cells. In the choriocarcioma line JEG-3, 8-Br-cAMP induced the accumulation of the mRNA of both genes, while sodium butyrate induced the accumulation of PLAP-2 transcripts only. Each agent increased the transcription rate of one or both of the genes, as assayed by run-on transcription. In transfection of JEG-3 cells with PLAP promoters fused to the firefly luciferase gene, the activity of the PLAP-2 promoter (but not PLAP-1) was induced with sodium butyrate, while both promoters were induced by 8-Br-cAMP. Inducibility of the PLAP-2 promoter by 8-Br-cAMP was still observed when the promoter was shortened to -103, leaving intact a sequence resembling a cAMP response element. The extent of transcriptional activation by either agent was not sufficient to explain the accumulation of PLAP mRNA. These studies suggest that both transcriptional and posttranscriptional processes are involved in the induction of the PLAP-1 and PLAP-2 gene in JEG-3 cells.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1990

Alpha-fetoprotein mRNA: variation of half-life in rat hepatoma cell lines and destabilization by sodium butyrate.

The half-life of alpha-fetoprotein (AFP) mRNA was determined in two rat hepatoma cell lines. In the 7777 cell line, AFP mRNA half-life is 30-35 h, consistent with earlier observations (Innis and Miller, 1979). However, the half-life in McA-RH8994 cells is only 14-16 h. Dexamethasone does not affect AFP mRNA half-life in either cell line, indicating that glucocorticoid-mediated alterations in AFP mRNA levels in these cells is at the transcriptional level. The naturally-occurring fatty acid sodium butyrate did, however, cause significantly more rapid degradation of AFP mRNA in McA-RH8994 cells, decreasing the half-life from 14-16 h to only 5-6 h. The ability of sodium butyrate to block glucocorticoid action on AFP gene expression in this cell line is therefore due to both transcriptional and post-transcriptional effects.

Animals↗
PubMed1992

Sodium butyrate selectively induces transcription of promoters adjacent to the MoMSV viral enhancer.

The long terminal repeat region of the Moloney murine sarcoma virus (MoMSV) was cloned upstream from the Chinese hamster ovary adenine phosphoribosyltransferase (APRT)-encoding gene (APRT) in order to enhance synthesis of the APRT protein. The replacement of the native promoter with the viral enhancer-promoter increased the enzymatic activity of APRT two- to threefold. Addition of sodium butyrate (NaBu) to the cell growth medium induced APRT activity ten- to 20-fold above wild-type levels in both transient and stable transfectants. The introduction of the APRT native promoter between the MoMSV enhancer-promoter and structural gene reduced the magnitude of the NaBu response. The bacterial cat gene was also stimulated by NaBu when linked to the viral enhancer-promoter. No NaBu response was found in constructs lacking the MoMSV enhancer region. Northern analysis and nuclear run-on experiments indicated that NaBu enhanced transcription of APRT mRNA in both transiently and stably transfected cells, but not in cells inhibited by cycloheximide. Thus, a butyrate-response element (BRE) is associated with the MoMSV enhancer and the action of the MoMSV BRE is promoter-dependent.

Adenine Phosphoribosyltransferase↗
PubMed1988

Fibroblast-like transformation and c-myc gene alteration of human hepatocytes induced by novobiocin and butyrate.

Topoisomerase II inhibitor novobiocin and deacetylase inhibitor sodium butyrate synergistically transformed Chang liver cells into fibroblast-like cells. In these fibroblast-like cells, the production of type III procollagen was increased and the DNase I hypersensitivity of c-myc gene was reduced. In addition, these changes were associated with an increased acetylation of nuclear proteins, especially those of DNase I sensitive nucleosomes. Therefore, it is suggested that chemical modulation of nuclear proteins by novobiocin and butyrate may be responsible, at least partly, for the alteration of the chromatin structure of c-myc gene and the fibroblast-like transformation of Chang liver cells.

Butyrates↗
PubMed1998

Sodium butyrate suppresses apoptosis in human Burkitt lymphomas and murine plasmacytomas bearing c-myc translocations.

We report that sodium butyrate, a natural product of fiber degradation by colonic bacteria, markedly suppresses c-Myc-mediated apoptosis induced in murine plasmacytomas and human Burkitt lymphomas by growth factor deprivation, but not in cell lines devoid of c-myc translocations. Attenuation of cell death is associated with downregulation of the rearranged c-myc and activation of pRb via its dephosphorylation. We suggest that in vivo sodium butyrate may play an important role in plasmacytomagenesis by supporting the survival of cells with c-myc translocations, which otherwise would be eliminated by the lack of growth factors.

Animals↗
PubMed1996

Supplementation of enteral nutrition with butyrate leads to increased portal efflux of amino acids in growing pigs with short bowel syndrome.

Previously, short-chain fatty acids (SCFAs) infused into the hindgut or administered intravenously have been shown to stimulate intestinal adaptation after massive small bowel resection. To study the effects of enterally supplemented n-butyrate on food digestion and absorption in growing pigs with short bowel syndrome, the authors examined the portal efflux of glucose and amino acids during a meal. In 12 growing pigs, 75% of the small intestine was resected. Five control (CONT) animals underwent transection and reanastomosis of the small bowel. A splenic vein, the aorta, the portal vein, and the stomach were catheterized. Postoperatively, seven enterectomized (ENT) pigs and the CONT pigs were fed by infusion of a liquid diet, without SCFAs, through the gastrostomy catheter. Five enterectomized animals received the same diet, supplemented with butyrate (ENTB) (0.26 g/kg body weight/d). After 3 weeks, the portal efflux of amino acids and glucose was measured after 2 hours of constant feeding. The portal efflux of glucose expressed per kilogram of body weight in the ENT group was 10% of that in the CONT group, and in the ENTB group it was 42%. No significant difference in portal glucose efflux between the ENT and the ENTB groups was found. The portal efflux of amino acids during a meal in the ENT group in relation to the CONT groups was 34%; in the ENTB group it was 63%. These data suggest that enteral supplementation with SCFAs leads to improvement of intestinal food digestion and absorption during short bowel syndrome, possibly related to improved intestinal adaptation.

Amino Acids↗
PubMed1997

Transient transcriptional activation of gastrin during sodium butyrate-induced differentiation of islet cells.

Transient expression of pancreatic gastrin corresponds to a period of rapid islet cell development. After birth gastrin expression silencing is coincidental with islet cell terminal differentiation, while persistent expression is accompanied with nesidioblastosis and reexpression observed in islet cell tumors. Experiments with transgenic animals suggested that gastrin might act synergistically with growth factors to stimulate islet cell development. The present study intended to establish an in vitro cell culture model to analyse the molecular events controlling gastrin gene activation and repression dependent on islet cell differentiation. Sodium butyrate, a proliferation-arresting compound has previously been shown to differentiate insulinoma cells while increasing insulin production. The present paper demonstrates concomitant transient increase in gastrin mRNA, intracellular and secreted gastrin during sodium butyrate treatment. Increased gastrin expression was due to activation or derepression of gastrin promoter activity as revealed by promoter analyses. This in vitro model mimics the expression pattern of gastrin and insulin observed during fetal islet cell development and provides an excellent tool to analyse the molecular mechanisms controlling gastrin gene activation and selective repression during islet cell differentiation.

Animals↗
PubMed1997

Fiber-derived butyrate and the prevention of colon cancer.

Inhibition of the enzyme histone deacetylase by butyrate results in the direct transcriptional upregulation of the cyclin-dependent kinase inhibitor p21/Cip1/WAF1. We discuss a small-molecule-mediated signaling pathway to explain the suspected anti-colon-cancer properties of fiber-derived butyrate.

Binding Sites↗
PubMed1992

Scaffold-attached regions (SAR elements) mediate transcriptional effects due to butyrate.

The expression of certain genes has been reported to respond positively to sodium butyrate. This study demonstrates the same feature for two marker genes under the control of five different promoters. In all examples, the stimulatory effect is largest if one or especially two scaffold/matrix-attached regions (SAR/MAR elements) are present adjacent to the gene, and in one case, the stimulation depends entirely upon this situation. These results are observed with several SAR sequences including those obtained by oligomerizing short stretches of DNA surrounding a core motif. It is suggested that butyrate exerts important actions at the level of the chromatin structure.

Animals↗