Review article: the role of butyrate on colonic function

Hamer, Henrike M.; Jonkers, Daisy; Venema, Koen; Vanhoutvin, Steven; Troost, Freddy J.; Brummer, Robert Jan

doi:10.1111/j.1365-2036.2007.03562.x

Cited by 2,221 publications

(1,784 citation statements)

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“…Several studies showed that butyrate functions as a HDI, reduces proliferation and induces apoptosis as well as differentiation. Butyrate regulates the expression of genes and proteins involved in cell cycle control like p21 and Cyclin D1, leading to a cell cycle arrest in human colon cancer cells (Hamer et al 2008;Hinnebusch et al 2002;Siavoshian et al 2000). Lately, Hu et al (2011) as well as Humphreys et al (2013) showed that butyrate also influences miRNA expression in HCT116 and HT29 colon cancer cells, respectively.…”

Section: Discussionmentioning

confidence: 99%

Influence of miRNA-106b and miRNA-135a on butyrate-regulated expression of p21 and Cyclin D2 in human colon adenoma cells

et al. 2015

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Epigenetic and posttranslational modifications of the expression of cell cycle-relevant genes or proteins like p21, e.g., by miRNAs are crucial mechanisms in the development or prevention of colon cancer. The present study investigated the influence of butyrate and trichostatin A (TSA) as histone deacetylase inhibitors on the expression of colon cancer-relevant miRNA (miR-135a, miR-135b, miR-24, miR-106b, miR-let-7a) in LT97 colon adenoma cells as a model of an early stage of colon carcinogenesis. The impact of distinct miRNAs (miR-106b, miR-135a) on butyrate-mediated regulation of p21 and Cyclin D2 gene and protein expression as well as the effect on LT97 cell proliferation (non-transfected, miR-106b and miR-135a mimic transfected) was analyzed. Butyrate and partial TSA reduced the expression of miR-135a, miR-135b, miR-24 and miR-let-7a (*0.5-fold, 24 h) and miR-24, miR-106b and miR-let-7a (*0.5-0.7-fold, 48 h) in LT97 cells. Levels of p21 mRNA and protein were significantly increased by butyrate and TSA (*threefold and 4.5-fold, respectively, 24 h) in non-transfected but not in miR-106b transfected LT97 cells. Levels of Cyclin D2 mRNA were significantly reduced by butyrate and TSA (*0.3-fold, 24 h) in non-transfected and miR-135a-transfected LT97 cells, whereas protein levels were predominantly not influenced. MiR-106b and miR-135a significantly reduced butyrate-/TSA-mediated inhibition of LT97 cell proliferation (72 h). These results indicate that butyrate is able to modify colon cancer-relevant miRNAs like miR-106b and miR-135a which are involved in the regulation of cell cycle-relevant genes like p21 and might influence inhibition of adenoma cell proliferation.

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Section: Discussionmentioning

confidence: 99%

Influence of miRNA-106b and miRNA-135a on butyrate-regulated expression of p21 and Cyclin D2 in human colon adenoma cells

et al. 2015

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“…SCFAs increase cell metabolism by more than 80% and the production and secretion of mucins by the colon epithelium more than twentyfold 8,33 . Experimental models that inhibit the oxidation of SCFAs or that use animals that have been silenced for the MUC-2 gene are capable of causing inflammation of the colon mucosa to appear, with histological similarities to diversion colitis 10,27,37,34 . All these points reinforce the important role played by SCFAs in relation to the capacity of the colon epithelium to produce mucins and consequently to protect the mucosa against aggression coming from the intestinal lumen 8 .…”

Section: Discussionmentioning

confidence: 99%

“…Reductions in the supply of SCFAs, as occurs during intestinal diversion operations, are accompanied by morphological and functional changes, thereby causing reductions in protein synthesis capacity 26 . The mechanisms through which shortages of SCFAs lead to lower capacity for mucin production are still not completely clear 9,27 . Studies have shown that intestinal diversion reduces the quantities of dietary fiber and modifies the bacterial populations in the segment excluded and it decreases the production of SCFAs, thereby causing a state of nutritional deficiency for the cells of the colon mucosa [28][29][30] .…”

Section: Discussionmentioning

confidence: 99%

Quantification by computerized morphometry of tissue levels of sulfomucins and sialomucins in diversion colitis in rats

et al. 2010

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PURPOSE: To quantify the intensity of sulfomucin and sialomucin expression in the colon mucosa, by means of computer-assisted image processing, comparing segments with and without fecal stream and correlating with the duration of fecal transit exclusion. METHODS: Forty-five Wistar rats were subjected to diversion of the fecal stream in the left colon by means of constructing a proximal colostomy and distal mucosal fistula. They were distributed randomly into three experimental groups of 15 animals, of which 10 were subjected to colon diversion (experimental subgroup) and five were only subjected to laparotomy, without colon diversion (control subgroup). The three experimental groups were formed according to the sacrifice date, which was to be performed six weeks after the surgical procedure (Group A), 12 weeks (Group B) and 18 weeks (Group C). The sulfomucin and sialomucin expression in the colon mucosa was evaluated using the histochemical technique of high iron diamine-alcian blue (HID-AB). The tissue expression was quantified for each animal, in the segments with and without fecal stream, at a location where there were four complete contiguous crypts in two random fields, with the aid of the computer-assisted image analysis software. The final value was taken to be the mean reading from the two fields selected, in the segments with and without fecal stream. To compare the expressions of the two mucin subtypes in the segments with and without fecal stream, the paired Student t test was used. To analyze variance according to duration of exclusion, ANOVA with the Newman-Keuls post-test was used, setting the significance level at 5% (p<0.05). RESULTS: There were significant reductions in tissue sulfomucin and sialomucin content in the colon without fecal stream, independent of the duration of exclusion considered. There was increased tissue sulfomucin content and decreased tissue sialomucin in the segments without fecal stream, with increasing duration of exclusion. CONCLUSIONS: Diversion of the fecal transit decreased the tissue sulfomucin and sialomucin content in the segments without fecal stream. Notwithstanding the reduction in the levels of both subtypes of acid mucin in the segments without fecal stream, there was increased tissue sulfomucin content and decreased tissue sialomucin with increasing duration of intestinal diversion.

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“…Members of E. rectale, Roseburia, and R. bromii are main producers of butyrate in the colon (71,107,109). It has been shown that increasing butyrate-producing bacteria and butyrate production is closely linked with prevention of the progression from steatosis to hepatocarcinogenesis and improving hepatic inflammatory and oxidative stress indexes and gut integrity (74,110,111). This would appear to indicate that there is a mutualistic relation between the gut microbiota and the host; dietary ingredients such as RS could induce special species of bacteria that produce metabolic products such as butyrate.…”

Section: Introductionmentioning

confidence: 99%

“…Akkermansia municiphila has been known as a major propionate-producing bacterium (70) and Eubacterium hallii, Eubacterium rectale, Roseburia inulinivorans, Faecalibacterium prausnitzii, Clostridium lavalense, Bacteroides uniformis, and Ruminococcus bromii appear to be responsible for most of butyrate production (70)(71)(72). Butyrate and propionate at low amounts exert multiple advantageous effects on the host, including the prevention of colonic carcinogenesis, inflammation, and oxidative stress; improvement in intestinal barrier function; and stimulation of satiety and lipid oxidation in hepatocytes (73,74). Acetate may be more important for modulating insulin sensitivity and metabolic disease (75) and the development of diabetes (76).…”

Section: Introductionmentioning

confidence: 99%

Nonalcoholic Fatty Liver Disease, the Gut Microbiome, and Diet

Mokhtari

Gibson

Hekmatdoost

2017

Advances in Nutrition

134

100

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Nonalcoholic fatty liver disease (NAFLD) is the most common liver disorder in the world, yet the pathogenesis of the disease is not well elucidated. Due to the close anatomic and functional association between the intestinal lumen and the liver through the portal system, it is speculated that the gut microbiome may play a pivotal role in the pathogenesis of NAFLD. Furthermore, diet, which can modulate the gut microbiome and several metabolic pathways involved in NAFLD development, shows a potential tripartite relation between the gut, diet, and the liver. In this review, we summarize the current evidence that supports the association between NAFLD, the gut microbiome, and the role of diet. Adv Nutr 2017;8:240-52.

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Review article: the role of butyrate on colonic function

Abstract: SUMMARY BackgroundButyrate, a short-chain fatty acid, is a main end-product of intestinal microbial fermentation of mainly dietary fibre. Butyrate is an important energy source for intestinal epithelial cells and plays a role in the maintenance of colonic homeostasis.

Cited by 2,221 publications

References 210 publications

Influence of miRNA-106b and miRNA-135a on butyrate-regulated expression of p21 and Cyclin D2 in human colon adenoma cells

Influence of miRNA-106b and miRNA-135a on butyrate-regulated expression of p21 and Cyclin D2 in human colon adenoma cells

Quantification by computerized morphometry of tissue levels of sulfomucins and sialomucins in diversion colitis in rats

Nonalcoholic Fatty Liver Disease, the Gut Microbiome, and Diet

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