Resistant Starch Modulates In Vivo Colonic Butyrate Uptake and Its Oxidation in Rats with Dextran Sulfate Sodium-Induced Colitis
Noëlle M. MoreauMartine ChampStéphane M. GoupryBruno J. Le BizecMichel KrempfPatrick NguyenH. DumonLucile Martin
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Sodium butyrate
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The effect of sodium butyrate on various bodily parameters of broilers such as performance, gut microflora, gut morphology, and immunity is reviewed in order to highlight its importance as an alternative to antibiotic growth promoters. Sodium butyrate is used as a source of butyric acid, which is known for its beneficial effects in the gut in monogastrics. Sodium butyrate is available in uncoated and enteric-coated forms protected with fat or fatty acid salts. Varying results in productive performance, gut microbes, and gut morphology have been reported in the literature in response to supplementation of broiler diets with uncoated and fat-coated types of sodium butyrate. However, sodium butyrate has shown pronounced effects on immunity of chickens that are not fully understood yet. Although there are contrasting results of sodium butyrate in chicken, further research is needed using the sodium butyrate coated with the salts of fatty acids.
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To evaluate the preventive effect of sodium butyrate in the appearance of aberrant crypt foci (ACF) in rats after induction with the carcinogen 1,2-dimethylhydrazine (DMH).Forty Wistar rats were separated into four groups (n=10) distributed as follows: control 1, control 2, butyrate 1 and butyrate 2. The groups control 1 and butyrate 1 remained under experimentation for 4 weeks, while the groups control 2 and butyrate 2 remained for 8 weeks. In the first four weeks, the animals of the control groups received water ad libitum and the animals of the butyrate groups received a sodium butyrate solution (3.4%) ad libitum. Injections of the drug 1,2-dimethylhydrazine were applied during the two first weeks of the experiment in all the animals, concurrently with the application of sodium butyrate. The large intestine of the animals was removed, for the analysis of the ACF and of the content of polyamines. The animal feces were collected for the analysis of the SCFA profile.The spermidine presented a higher concentration in the group butyrate 2 in comparison to the group control 2. There was a significant difference in the concentration value (µmol/mL) of acetate in comparison to the groups control 2 and butyrate 2.The use of sodium butyrate together with the induction of colorectal cancer was not effective in the prevention of the disease progression.
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Abstract We investigated whether sodium butyrate, administered orally as gastroresistant slow‐release pellets to rats, could affect markers of colon carcinogenesis. F344 male rats were fed a high‐fat diet (230 g/kg corn oil, wt/wt) and treated with two injections (1 wk apart) of azoxymethane (15 mg/kg sc) or saline. Rats were then divided into two groups: one received the diet with 1.5% (wt/wt) sodium butyrate for 10 weeks to provide 150 mg butyrate/day, and one group received no butyrate. At the end of this period, rats were sacrificed, and colonic proliferative activity, number of aberrant crypt foci (ACF), and apoptosis were assessed in the colon. The proliferative activity and A CF induction were not affected by butyrate pellet administration. On the contrary, in rats treated with butyrate, apoptotic index increased from 0.12 ± 0.12 to 0.81 ± 0.10 (means ± SE, p < 0.05). The short‐chain fatty acid concentration was significantly increased in the feces of rats treated with butyrate. In conclusion, the increase in the mucosal apoptotic index suggests that gastroresistant butyrate pellets have a beneficial effect against colon carcinogenesis. However, because butyrate pellets did not modify proliferation or ACF induction, this conclusion should be confirmed in long‐term carcinogenesis experiments.
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Friend erythroleukemia cells can be induced to undergo erythroid differentiation by a variety of unrelated compounds. The fact that sodium butyrate causes reversible alterations in growth, morphology, and biochemistry in many cell systems prompted us to reexamine its pattern of induction of differentiation and to compare it to that of dimethyl sulfoxide (DMSO) and hexamethylbisacetamide (HMBA). By the fourth day of induction, a peak in hemoglobin accumulation was reached in the cultures treated with each of these potent inducers. Differences, however, were noted in cultures in which there had been no change of medium for 7 days. Whereas DMSO or HMBA induced cultures reached a stationary stage of growth and maintained a high percentage of benzidine positive cells, butyrate treated cultures resumed active growth and showed a marked decrease in the percentage of benzidine positive cells. However, the actual number of terminally differentiated cells remained relatively constant. The addition of fresh butyrate to 4-day treated cultures prevented the decrease in the percentage of benzidine positive cells. Measurement of [14C]butyrate uptake into the cells showed a decrease in the incorporation of the inducer with time coincident with the decrease in the percentage of benzidine positive cells and of the butyrate in the medium. Incorporation of [3H]thymidine into cells undergoing differentiation for 4 days indicated that butyrate treated cells, but not cells treated with DMSO or HMBA were capable of active DNA synthesis and growth after removal of the inducers. These data suggest that butyrate, a natural fatty acid, is metabolized by the cells and with time its concentration is reduced to a level below that required to stimulate differentiation. Additional evidence to support this notion are the results obtained with conditioned medium (CM) from induced cultures. CM-DMSO and CM-HMBA retained the capacity to induce differentiation whereas CM-butyrate lost its potency with time.
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Sodium butyrate or glucose deprivation induce a more differentiated phenotype in many cancer cells. The aim of this study was to determine whether the induction effect of butyrate and/or glucose deprivation is dependent, in some way, on the differentiation state of individual cell lines. Sodium butyrate enhanced alkaline phosphatase activity and induced formation of an ultrastructurally more differentiated phenotype in both HT29 and HT115 cell lines. Interestingly, the more invasive HT115 cells responded more strongly to butyrate treatment. On the other hand, the differentiation effect of glucose deprivation was much less prominent in the HT115 cell line in comparison with HT29 cells. Our data confirm the influence of the malignant potential of the cells on their response to treatment with differentiation and apoptosis-inducing agents. Butyrate treatment also enhanced the adhesiveness of HT115 cells. Since E-cadherin was not found in these cells, while the level of CEACAM1 was increased, it is obvious that the CEACAM1 molecules are involved in HT115 cell-cell adhesion.
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Recombinant CHO cells were cultured in CHO-S-SFM II. The effects of sodium butyrate on cell growth, glucose metabolism and EPO expression were investigated. Cell growth decreased with the addition of sodium butyrate in the serum-free medium and was entirely inhibited at 2 mmol/L sodium butyrate. The specific rate of glucose utilization was also reduced by 30% in the presence of sodium butyrate. In addition, EPO expression was not facilitated by the addition of sodium butyrate, but its addition may be helpful to maintain the stability of EPO productivity.
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Butyrate exerts anti-tumour effects in vitro, but not consistently in vivo. We previously demonstrated that the administration of slow-release gastro-resistant pellets of sodium butyrate increases apoptosis in the colon mucosa of rats, an effect which may protect against carcinogenesis. Therefore, we studied whether the administration of butyrate pellets could protect rats against experimental colon carcinogenesis. Four to 5 week old male F344 rats were fed a high-fat (HF) diet (230 g/kg corn oil w/w) and treated s.c. with two injections (one week apart) of azoxymethane (AOM) at a dose rate of 15 mg/kg body weight or saline. Rats were then divided into two groups: one group received sodium butyrate pellets mixed into the diet (1.5% w/w) for 33 weeks (150 mg butyrate/day) and the second group received the high-fat diet with no butyrate. Administration of sodium butyrate pellets in the diet did not significantly affect colon carcinogenesis: the number of intestinal tumours/rat was 1.6 ± 0.2 in controls and 2.1 ± 0.2 in butyrate-fed rats (means ± SE; P = 0.22, by ANOVA), while the incidence of intestinal tumours was 79 (23/29) and 90% (27/30) in controls and in butyrate-fed rats, respectively (P = 0.29 by Fisher's exact test). The level of apoptosis in the tumours was not affected by butyrate, nor was the expression of p21CIP, a cell cycle-related protein. In conclusion, the current study indicates that butyrate does not protect against AOM-induced colon carcinogenesis in rats.
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Butyrate, in relatively low concentrations, has been shown to induce synthesis of enzymes, cause changes in cell morphology, and inhibit growth of a variety of mammalian cells in tissue culture (reviewed in [1]). In this communication, we report our observations on the effect of butyrate on lymphocyte activation. Butyrate completely and reversibly inhibits mitogen-induced blast formation. We present evidence that it does not interfere with the binding of mitogens, that it does not inhibit a number of the early reactions involved in activation, and that it does not affect ongoing DNA synthesis for an extended period of time. However, butyrate rapidly inhibits any increase in the rate of DNA synthesis.
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Objective:To investigate the effects of sodium butyrate on cell growth inhibition and apoptosis in cell of gastric carcinoma and to explore its mechanism.Methods:MTT assay was used to observe the inhibitory complexion of sodium butyrate on SGC-7901 cells at various concentrations.The expression of apoptosis-related gene protein p21WAF1 was detected by immunohistochemical staining.Results:SGC-7901 cells growth was significantly inhibited by sodium butyrate and the inhibitory affect was in time and dose-dependent manner;The level of p21WAF1 was higher in the sodium butyrate treated cell than the cell without treatment.Conclusion:Sodium butyrate can inhibit the cell growth and induce apoptosis in SGC-7901.Therefore,to explore the mechanism of sodium butyrate in the human cell of gastric carcinoma can provide a new mentality to the gastric carcinoma chemotherapy.
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