• Journal of Life Science
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• v.22 no.11
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• pp.1571-1586
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• 2012

On earth, there are about 5,400 kinds of mammals, of which about 1,000 kinds are herbivores. Among herbivores, about 250 kinds are known to be ruminants. As for cattle and sheep, which are ruminants, fermentation takes places mainly in their rumen; in contrast, for pigs and men, which are non-ruminants, fermentation takes place mainly in their caecum, colon, and rectum. As for the kind and dominance of rumen microorganisms, Bacteroidetes account for 51% and Firmicutes for 43%. As for the dominance of the large intestine microorganisms in men, Firmicutes account for 65% and Bacteroidetes for 25%. Cell wall components are decomposed by microorganisms, and short chain fatty acids (SCFAs) are generated through fermentation; the ratio of acetate, propionate, and butyrate generate is 60:25:15. Butyrate absorbed through the primary butyrate transporter MCT1 (mono carboxylate transports-1) in the intestines activates such SCFA receptors as GPR43 and GPR41. Butyrate has a strong anti-tumorigenic function. Butyrate is characterized by the fact that it has an effect on many cancer cells, contributes to the coordination of functions in the cells, and induces cancer apoptosis. Butyrate activates caspase but inhibits the activity of HDAC (histone deacetylase), so as to induce apoptosis. In addition, it increases p53 expression, so as to induce cell cycle arrest and apoptosis. Anti-inflammation actions of SCFA include the reduction of IL-8 expression in intestinal epithelial cells, the inhibition of NO synthesis, and the restraint of the activity of NF-${\kappa}B$ (nuclear factor ${\kappa}B$), so as to suppress the occurrence of cancers caused by inflammation. Butyrate plays an important role in maintaining physiological functions of intestinal mucous membranes and is used as a cure for inflammatory bowel disease (IBD).

• Nutrition Research and Practice
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• v.9 no.4
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• pp.343-349
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• 2015

BACKGROUND/OBJECTIVES: Fermentation of dietary fiber results in production of various short chain fatty acids in the colon. In particular, butyrate is reported to regulate the physical and functional integrity of the normal colonic mucosa by altering mucin gene expression or the number of goblet cells. The objective of this study was to investigate whether butyrate modulates mucin secretion in LS174T human colorectal cells, thereby influencing the adhesion of probiotics such as Lactobacillus and Bifidobacterium strains and subsequently inhibiting pathogenic bacteria such as E. coli. In addition, possible signaling pathways involved in mucin gene regulation induced by butyrate treatment were also investigated. MATERIALS/METHODS: Mucin protein content assay and periodic acid-Schiff (PAS) staining were performed in LS174T cells treated with butyrate at various concentrations. Effects of butyrate on the ability of probiotics to adhere to LS174T cells and their competition with E. coli strains were examined. Real time polymerase chain reaction for mucin gene expression and Taqman array 96-well fast plate-based pathway analysis were performed on butyrate-treated LS174T cells. RESULTS: Treatment with butyrate resulted in a dose-dependent increase in mucin protein contents in LS174T cells with peak effects at 6 or 9 mM, which was further confirmed by PAS staining. Increase in mucin protein contents resulted in elevated adherence of probiotics, which subsequently reduced the adherent ability of E. coli. Treatment with butyrate also increased transcriptional levels of MUC3, MUC4, and MUC12, which was accompanied by higher gene expressions of signaling kinases and transcription factors involved in mitogen-activated protein kinase (MAPK) signaling pathways. CONCLUSIONS: Based on our results, butyrate is an effective regulator of modulation of mucin protein production at the transcriptional and translational levels, resulting in changes in the adherence of gut microflora. Butyrate potentially stimulates the MAPK signaling pathway in intestinal cells, which is positively correlated with gut defense.

• The Korean Journal of Food And Nutrition
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• v.28 no.2
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• pp.171-177
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• 2015

Sodium butyrate is a short-chain fatty acid derivative found in foods, such as Parmesan cheese and butter and is produced by anaerobic bacteria fermentation of dietary fibers in the large intestine. There have been reports that butyrate prevented obesity, protected insulin sensitivity, and ameliorated dyslipidemia in dietary obese mice. This study investigated the effects of sodium butyrate on fasting blood glucose level and serum lipid profile in streptozotocin(STZ)-induced diabetic mice. Male C57BL/6 mice were fed AIN-93G for four weeks prior to intraperitoneal injections with STZ (100 mg/kg body weight). Diabetic mice had supplements of 5% sodium butyrate for four weeks. The 5% sodium butyrate diet significantly improved fasting blood glucose level and lipid profile in STZ-induced diabetic mice. Inflammation has been recognized to decrease beta cell insulin secretion and increase insulin resistance. Circulating cytokines can directly affect beta cell function, leading to secretory dysfunction and increased apoptosis. Thus, anti-inflammatory therapies represented a potential approach for the therapy of diabetes and its complications. In this animal study, the 5% sodium butyrate supplementation also inhibited inflammatory cytokine production in STZ-induced diabetic mice. These results suggested that sodium butyrate can be a potential candidate for the prevention of diabetes and its complications.

• Journal of Life Science
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• v.31 no.5
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• pp.464-474
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• 2021

Inflammation induced by metabolic syndromes, cancers, injuries, and sepsis can alter cellular metabolism by reducing mitochondrial function via oxidative stress, thereby resulting in neuropathy and muscle atrophy. In this study, we investigated whether butyrate, a short chain fatty acid produced by gut microbiota, could prevent mitochondrial dysfunction and muscle atrophy induced by lipopolysaccharide (LPS) in the C2C12 cell line. LPS-activated MAPK signaling pathways increased the levels of the mitochondrial fission signal, p-DRP1 (Ser616), and the muscle atrophy marker, atrogin 1. Interestingly, butyrate significantly inhibited the phosphorylation of JNK and p38 and reduced the atrogin 1 level in LPS-treated C2C12 cells while increasing the phosphorylation of DRP1 (Ser637) and levels of mitofusin2, which are both mitochondrial fusion markers. Next, we investigated the effect of MAPK inhibitors, finding that butyrate had the same effect as JNK inhibition in C2C12 cells. Also, butyrate inhibited the LPS-induced expression of pyruvate dehydrogenase kinase 4 (PDK4), resulting in decreased PDHE1α phosphorylation and lactate production, suggesting that butyrate shifted glucose metabolism from aerobic glycolysis to oxidative phosphorylation. Finally, we found that these effects of butyrate on LPS-induced mitochondrial dysfunction were caused by its antioxidant effects. Thus, our findings demonstrate that butyrate prevents LPS-induced muscle atrophy by improving mitochondrial dynamics and metabolic stress via the inhibition of JNK phosphorylation. Consequently, butyrate could be used to improve LPS-induced mitochondrial dysfunction and myopathy in sepsis.

• Tuberculosis and Respiratory Diseases
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• v.45 no.3
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• pp.587-595
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• 1998

Background: Recombinant adenovirus hold promise as vectors to carry therapeutic genes for several reasons: 1) they can infect both dividing and non-dividing cells; 2) they have the ability to directly transduce tissues in vivo; 3) they can easily be produced in high titer; and 4) they have an established record of safety as vaccination material. However, one of the major limitation in the use of adenoviruses is that transgene expression is quite short because adenovirusees insert their DNA genome episomally rather than by chromosomal integration, and an immune response against the virus destroys cells expressing the therapeutic gene. Since sodium butyrate has been reported to induce adenovirus-mediated gene expression, we hypothesized that treatment of tumor cells, transduced with herpes simples virus thymidine kinase(HSVtk) gene using adenoviral vector, with butyrate could augment the effect of gene therapy. Methods: We transduced HSVtk gene, driven by the cytomegalovirus promoter, into REN cell line(human mesothelioma cell line). Before proceeding with the comparison of HSVtk/ganciclovir mediated bystander killing, we evaluated the effect of butyrate on the growth of tumor cells in order to rule out a potential antitumor effect of butyrate alone, and also on expression of HSVtk gene by Western blot analysis. Then we determined the effects of butyrate on bystander-mediated cell killing in vitro. Results: There was no inhibition of growth of cells exposed to butyrate for 24 hours at a concentration of 1.5mM/L. Toxic effects were seen when the concentration of butyrate was greater than 2.0mM/L. Gene expression was more stable and bystander effect was augmented by butyrate treatment of a concentration of 1.5mM/L. Conclusion: These results provide evidence that butyrate can augment the efficiency of cell killing with HSVtk/GCV system by inducing transgene expression and may thus by a promising new approach to improve responses in gene therapy using adenoviral vectors.

• Journal of Life Science
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• v.9 no.2
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• pp.160-168
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• 1999

Butyrate is one of the short-chain fatty acids that are present in the colon of mammals in millimolar concentration as a result of microbial anaerobic fermentation of dietary fiber, undigested starch, and proteins. In this study, sodium butyrate was examined in HT29 cell, human colonic cancer cell line, on cell viability, alkaline phosphatase activity, PLC-${\gamma}$1 expression and complex sphingolipid biosynthesis. Treatment with butyrate showed that the decrease of cell adhesion and viability was time-dependent. Sodium butyrate also induced to increase the activity of alkaline phosphatase which is a differentiation marker enzyme and decrease the expression of PLC-${\gamma}$1. Biosynthesis of sphingomyelin and galactosylceramide by butyrate treatment were decreased so fast but ceramide was increased 680dpm/mg protein% more than untreated group on first day and then decreased fast. In addition, acid ceramidase and neutral ceramidase activity were inhibited early stage by sodium butyrate. These results suggest that sodium butyrate causes cell differentiation or cell growth arrest of HT29 cell accompanied by early increase of ceramide content and alkaline phosphatase activity and decrease of galactosylceramide content and PLC-r1 expression.

• 한국생물공학회:학술대회논문집
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• 2005.04a
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• pp.214-217
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• 2005

Mammalian cell culture in the presence of sodium butyrate has been shown to enhance protein biosynthesis. In the present study, the effect of sodium butyrate on growth of recombinant Chinese Hamster Ovary cells and on the production of Iduronate 2-sulphatase were investigated in serum-containing and serum-free media. The culture with addition of 0-5mM sodium butyrate showed enhancement of both intracellular and extracellular IDS production. But, Cell death was observed in a dose-dependent manner. The optimal sodium butyrate concentration was observed to be 5mM. Also, The relative productivity of IDS was significantly increased when sodium butyrate was added to medium at 48 hour, the rapid growth phase. These results suggest that sodium butyrate are efficient agent for increasing the productivity of IDS with recombinant CHO cells.

• Applied Biological Chemistry
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• v.44 no.4
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• pp.215-218
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• 2001

To examine the expression of foreign protein in Polygonum tinctorium cells, plasmid pCAMBIA1302 encoding Green Fluorescent Protein(GFP) was used to transform the cells and the expression was confirmed using Western blot analysis. When the effect of sodium buryrate on the formation of GFP was examined, cell growth was retarded at the addition of 10 mM and was stalled at more than 15 mM. The amount of GFP production was increased by 15% when 5 mM of sodium butyrate was added at three-days after inoculation as compared to at 0-day. Moreover, when sodium butyrate was added at three-days after inoculation, the amount of GFP was increased by 50% at the addition of 5 mM of sodium butyrate as compared to 10 mM.

• Membrane Journal
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• v.10 no.4
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• pp.186-191
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• 2000

The recovery of three ethyl esters (aroma model compounds; ethyl acetate, ethyl propionate. ethyl butyrate) from aqueous solutions was studied for vapor permeation with surface-modified hydrophobic alumina membrane, Although the driving force of ethyl butyrate is the highest, the ethyl butyrate concentration in permeate is lower than those of propionate and acetate. Since the solubility of aroma compounds for water is very low, phase separation occurred in permeate, and we could obtain pure ethyl esters. The experimental results showed that the porous hydrophobic alumina membrane had high selectivity and permeation flux on the ester-model compounds.

• Asian-Australasian Journal of Animal Sciences
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• v.22 no.7
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• pp.1026-1031
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• 2009

An experiment was conducted to study the effect of graded levels of butyric acid (butyrate) on performance, gastrointestinal tract health and carcass characteristics in young broiler chickens. Control starter (0-3 wk) and finisher (4-5 wk) diets were formulated to contain 2,900 kcal ME/kg and 22% CP, and 3,000 kcal ME/kg and 20% CP, respectively. Subsequently, four other experimental diets were formulated to contain 0.05% antibiotic (furazolidone) or 0.2, 0.4 and 0.6% butyric acid. Each diet was fed at random to 8 replicates of 6 chicks each throughout the experimental period (0-5 wk). The results showed that 0.4% butyrate in the diet was similar to antibiotic in maintaining body weight gain and reducing E. coli numbers but superior for feed conversion ratio. No added advantage on these parameters was obtained by enhancing the concentration of butyrate from 0.4 to 0.6% in the diet. Feed intake and mortality were not influenced by the dietary treatments. A reduction in pH of the upper GI tract (crop, proventiculus and gizzard) was observed by inclusion of butyrate in the diets of broilers compared to either control or antibiotic-fed group. Butyrate at 0.4% was more effective in reducing the pH than 0.2% butyrate. Within the lower GI tract, 0.4 and 0.6% butyrate was effective in lowering pH in the duodenum, but no effect was found in either the jejunum or ileum. The villus length and crypt depth in the duodenum increased significantly in all the butyrate treated diets irrespective of the level tested. Carcass yield was higher and abdominal fat content was lower significantly in all the butyrate treatment groups compared to the control or antibiotic group. From these findings, it is concluded that 0.4% butyric acid supplementation maintained performance, intestinal tract health, and villi development and carcass quality in broiler chickens.