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PubMed1992

Oat bran increases serum acetate of hypercholesterolemic men.

Mechanisms for the hypocholesterolemic effects of oat bran remain unclear. Soluble fibers such as oat bran are fermented in the colon to short-chain fatty acids (SCFAs), which may enter the portal vein and attenuate hepatic cholesterol synthesis. To compare effects of oat bran and wheat bran on serum SCFA concentrations, 20 hypercholesterolemic men entered a metabolic ward and received control diets for 1 wk followed by oat-bran or wheat-bran diets for 3 wk. Oat bran decreased serum cholesterol 12.8% (P less than 0.001) whereas wheat bran had no effect. Peripheral serum SCFA concentrations were measured seven times over 14 h at the end of each diet. Serum acetate values from 1200 to 2200 were significantly higher in subjects fed oat-bran vs wheat-bran diets. Peak and incremental peak acetate values were also significantly higher than control values in subjects fed oat bran but not in subjects fed wheat bran. SCFA responses may contribute to the hypocholesterolemic effects of oat bran.

Acetates↗

PubMed1998

Prevention of colonic aberrant crypt foci and modulation of large bowel microbial activity by dietary coffee fiber, inulin and pectin.

The present experiments were aimed at developing novel dietary fibers to aid in reduction of colon cancer risk. We assessed the effects of coffee (non-fiber fraction), coffee fiber (arabino-galactose polymer) and inulin (oligo-fructose) in male F344 rats using formation of azoxymethane (AOM)-induced aberrant crypt foci (ACF) in the colon as the measure of preventive efficacy (or lack of such). At 5 weeks of age, groups of rats were fed the AIN-76A (control) and experimental diets that contained 1% coffee, 10% coffee fiber, 10% inulin, 10% pectin (positive control for fiber) or 200 p.p.m. piroxicam (a known ACF inhibitor). At 7 weeks of age, all animals were s.c injected with AOM (15 mg/kg body wt) once weekly for 2 weeks. All rats were killed 8 weeks after the last AOM injection and ACF were counted. The contents of the cecum were analyzed for bacterial beta-glucuronidase activity and short-chain fatty acids (SCFAs). Dietary administration of coffee fiber significantly suppressed AOM-induction of colonic ACF, in terms of total number, as well as crypt multiplicity and number of ACF/cm2 colon (P < 0.01-0.001). Inulin diet had no significant effect on total ACF, but had reduced the number of ACF/cm2 (P < 0.05). Whereas coffee had no effect on ACF formation, 10% pectin diet and 200 p.p.m. piroxicam significantly suppressed colonic ACF (P < 0.001) as had been expected. A significant reduction of cecal beta-glucuronidase activity was observed in the rats fed coffee, coffee fiber and pectin diets. Further, coffee fiber, inulin and pectin increased cecal SCFA levels 3- to 5-fold. These results suggest that coffee fiber can prevent colon cancer risk. Further studies are warranted to determine the full potential of this fiber in pre-clinical efficacy studies.

Animals↗

PubMed2003

Effect of resistant starch on genotoxin-induced apoptosis, colonic epithelium, and lumenal contents in rats.

The effect of different doses of a type-2 resistant starch (RS) in the form of high amylose cornstarch (HAS) on the intralumenal environment and the acute-apoptotic response to a genotoxic carcinogen (AARGC) in the colon was assessed to determine if changes in lumenal conditions were associated with an enhanced apoptotic response to DNA damage. The control diet was a modified form of the AIN-76 diet containing fully digestible starch but no dietary fibre. HAS was added to the control diet at the expense of digestible starch to give 10% HAS, 20% HAS and 30% HAS. Rats were fed the different experimental diets for a period of 4 weeks, after which a single injection of azoxymethane was given to induce DNA damage in the colonic epithelium; 6 h later AARGC was measured. Other measures included fecal and cecal short chain fatty acids (SCFA) and pH, and cell proliferation in the colonic epithelium. In HAS-supplemented rats, fermentation events were significantly increased in both cecum and feces. There was a progressive decrease in pH in both the cecum and feces as the amount of HAS in the diet increased. SCFA concentrations, including butyrate, were significantly elevated by HAS with higher levels being observed in the cecum than in the feces. There was a significant increase in colonic AARGC with HAS doses of 20 and 30% (P < 0.01) but not with 10% HAS. Cell proliferation was not affected by any dose of HAS. Correlations with AARGC, independent of dietary group, were seen for fecal SCFAs and pH, suggesting that fermentation events, might explain the effect of RS on AARGC. Altering amounts of dietary RS changes fermentative activity in the colon. Increased RS is associated with enhanced AARGC. Changes in amount of fermentable substrate are capable of changing the biological response to DNA damage.

Amylose↗

PubMed2006

Effect of dietary resistant starch and protein on colonic fermentation and intestinal tumourigenesis in rats.

Protein as well as starch is fermented in the colon, but the interaction between protein and starch fermentation and the impact on colonic oncogenesis is unknown. High-protein diets increase delivery of protein to the colon and might promote oncogenesis through generation of toxic products. We investigated the interaction of resistant starch (RS) with digestion-resistant potato protein (PP) on colonic fermentation events and their relationship to intestinal tumourigenesis. Male Sprague-Dawley rats were fed an AIN-76A-based diet for 4 weeks and intestinal neoplasms were induced by azoxymethane. Experimental diets included the following: no added RS or PP, 10% high amylose maize starch (source of RS) replacing digestible starch, 15% PP replacing casein and 10% high amylose maize starch+15% PP. Rats were maintained on diets until killed at 30 weeks. Feeding RS significantly increased short-chain fatty acid (SCFA) levels (P<0.001) in the caecum and colon. Importantly, butyrate concentration was significantly increased in the distal colon with RS (P<0.001). Feeding PP increased protein fermentation products, but this effect was reduced by adding RS to the diet. Intestinal neoplasms and colorectal adenocarcinomas were reduced by feeding RS (P<0.01) regardless of whether PP was fed, whereas PP alone increased the incidence and number of small intestinal neoplasms including the adenocarcinomas (P<0.01). In conclusion, RS altered the colonic luminal environment by increasing the concentration of SCFAs including butyrate and lowering production of potentially toxic protein fermentation products. These effects of RS not only protected against intestinal tumourigenesis but also ameliorated the tumour-enhancing effects of feeding indigestible protein.

Animals↗

PubMedDate not supplied

Preservation of colonization resistance parameters during empiric therapy with aztreonam in the febrile neutropenic patient.

The role of the anaerobic intestinal flora in maintaining colonization resistance was examined in a study of empiric therapy in febrile neutropenic patients who received aztreonam plus tobramycin, aztreonam plus cloxacillin, or moxalactam plus tobramycin, regimens with differential effects on the anaerobic intestinal flora. Surveillance cultures showed that all regimens eradicated fecal carriage of enteric gram-negative bacilli but that fecal acquisition of fungi occurred in 4 (27%) of 15 aztreonam/tobramycin, 6 (43%) of 14 aztreonam/cloxacillin, and 13 (81%) of 16 moxalactam/tobramycin recipients. Fungi were acquired at 11 (22%) of 49 sites in aztreonam/tobramycin, 15 (31%) of 48 sites in aztreonam/cloxacillin, and 28 (54%) of 52 sites in moxalactam/tobramycin recipients. Aztreonam/tobramycin reduced fecal anaerobe counts by less than 1 log10; aztreonam/cloxacillin, by a mean of 2.5 log10; and moxalactam/tobramycin, by 5.1 log10 colony-forming units (cfu)/g of feces by day 10 +/- 3 of therapy. Elimination of the anaerobes was reflected by a reduction in concentrations of short-chain fatty acids (SCFAs) in fecal supernatants. Fecal specimens containing greater than or equal to 10(6) cfu of Bacteroides fragilis group organisms/g (dry weight) contained significantly higher concentrations of succinic, propionic, and isobutyric acids. Flat SCFA chromatograms were observed in 90% of fecal samples from which no anaerobes were recovered. Preservation of the anaerobic flora appears critical in the prevention of fungal acquisition in neutropenic patients.

Adolescent↗

PubMed2004

Ingestion of guar gum hydrolysate, a soluble and fermentable nondigestible saccharide, improves glucose intolerance and prevents hypertriglyceridemia in rats fed fructose.

Fructose feeding provides a dietary model of insulin resistance accompanied by hypertriglyceridemia. We examined the effects of guar gum hydrolysate (GGH), a soluble and fermentable nondigestible saccharide with low viscosity, on glucose intolerance and hypertriglyceridemia in rats fed high-fructose diets. Rats were fed either a dextrin-based or a fructose-based diet with or without GGH (75 g/kg) for 30 d. Oral glucose tolerance tests (OGTTs) were performed 0, 14, and 28 d after feeding. High-fructose feeding negatively affected glucose tolerance on d 14 and 28. The addition of GGH to the diets improved glucose intolerance on d 28. Fructose feeding induced hyperinsulinemia after an oral glucose load; this was also improved by GGH on d 28. The glycogen concentration in the gastrocnemius muscles of rats was lowered by dietary fructose, and GGH supplementation abolished this decrease. Triglycerides in the plasma and livers of rats fed fructose diets were elevated, and the increases were ameliorated by supplemental GGH. Regardless of the type of carbohydrate, GGH enlarged the cecum and increased the cecal SCFA pools. In conclusion, supplemental feeding of GGH to rats improved the glucose intolerance and hypertriglyceridemia induced by a high-fructose diet. Possible mediators of these beneficial effects of GGH are the SCFAs produced by microbial fermentation of GGH in the large intestine.

Animals↗

PubMed2004

Short chain fatty acid regulation of signaling genes expressed by the intestinal epithelium.

Changes in diet greatly affect the mucosal immune system, particularly in diseases such as Crohn's disease and necrotizing enterocolitis. This review examines the hypothesis that alterations in the luminal environment of the intestine regulate the expression of genes in the epithelium responsible for signaling to immune cells. Increasing chemokine expression in the mouse intestinal epithelium using transgenic techniques enhances the recruitment of neutrophils and lymphocytes into the intestine. Furthermore, SCFA concentrations in the intestinal lumen vary markedly with diet. SCFAs alter chemokine expression by inhibiting histone deacetylase activity in the enterocyte. The review therefore describes a molecular pathway explaining how changes in diet may alter leukocyte recruitment by regulating enterocyte gene expression. It is likely that other similar pathways remain to be discovered.

Animals↗

PubMed2000

Partially hydrolyzed guar gum-supplemented oral rehydration solution in the treatment of acute diarrhea in children.

BACKGROUND: Partially hydrolyzed guar gum (Benefiber; Novartis Nutrition, Minneapolis, MN, U.S.A.) is fermented by colonic bacteria liberating short-chain fatty acids (SCFAs), which accelerate colonic absorption of salt and water. The purpose of this study was to evaluate the effect of Benefiber (BF)-supplemented World Health Organization Oral Rehydration Solution (WHO ORS) in the treatment of acute noncholera diarrhea in children. METHODS: A double-blind, randomized, controlled clinical trial was performed at ICDDR,B in 150 male children aged 4 to 18 months who had watery diarrhea of less than 48 hours' duration. After admission, children were assigned to receive either WHO ORS or BF-supplemented WHO ORS until recovery. Major outcome measures, such as duration of diarrhea and amount of stool output, were compared between the treatment groups. RESULTS: Patients receiving BF-supplemented WHO ORS had significantly reduced duration of diarrhea compared with the control group (mean +/- SD, 74 +/- 37 vs. 90 +/- 50 hours, P = 0.03). Survival analysis for duration of diarrhea also showed a reduction the BF-supplemented WHO ORS-treated group (P = 0.025, log rank test). There was also less stool output daily from days 2 through 7 in the patients treated with BF-supplemented WHO ORS compared with that in the children treated with WHO ORS; the reduction was significant on day 7 only. CONCLUSION: Benefiber added to standard WHO ORS substantially reduces the duration of diarrhea and modestly reduced stool output in acute noncholera diarrhea in young children, indicating its potential as a new antidiarrheal therapy for acute diarrhea in children.

Acute Disease↗

PubMed2003

Increasing fecal butyrate in ulcerative colitis patients by diet: controlled pilot study.

Topical butyrate has been shown to be effective in the treatment of ulcerative colitis (UC). Butyrate is derived from colonic fermentation of dietary fiber, and our aim was to study whether UC patients could safely increase the fecal butyrate level by dietary means. We enrolled 22 patients with quiescent UC (mean age, 44 years; 45% women; median time from last relapse, 1 year) in a controlled pilot trial lasting 3 months. The patients were instructed to add 60 g oat bran (corresponding to 20 g dietary fiber) to the daily diet, mainly as bread slices. Fecal short-chain fatty acids (SCFAs) including butyrate, disease activity, and gastrointestinal symptoms were recorded every 4 weeks. During the oat bran intervention the fecal butyrate concentration increased by 36% at 4 weeks (from 11 +/- 2 (mean +/- SEM) to 15 +/- 2 micromol/g feces) (p < 0.01). The mean butyrate concentration over the entire test period was 14 +/- 1 micromol/g feces (p < 0.05). Remaining fecal SCFA levels were unchanged. No patient showed signs of colitis relapse. Unlike controls, the patients showed no increase in gastrointestinal complaints during the trial. Yet patients reporting abdominal pain and reflux complaints at entry showed significant improvement at 12 weeks that returned to baseline 3 months later. This pilot study shows that patients with quiescent UC can safely take a diet rich in oat bran specifically to increase the fecal butyrate level. This may have clinical implications and warrants studies of the long-term benefits of using oat bran in the maintenance therapy in UC.

Adult↗

PubMed2005

Bicarbonate secretion: a neglected aspect of colonic ion transport.

Understanding of the mechanism of colonic electrolyte transport has markedly increased over the past three decades. This article provides a brief summary of the critical features of Na, Cl, and K transport in the large intestine and how these processes may be altered in diarrhea. Less understood is the mechanism of colonic HCO3 secretion. Recent progress in the regulation of HCO3 secretion in the distal colon is summarized with emphasis on the interrelationship between Cl-dependent, short-chain fatty acid (SCFA)-dependent, and cAMP-induced HCO3 secretion. cAMP down-regulates Cl-dependent HCO3 secretion, while SCFA stimulates HCO3 secretion but also inhibits both Cl-dependent and cAMP-induced HCO3 secretion. As SCFAs are the primary anions in stool, it is likely that SCFA-dependent HCO3 secretion is the primary mechanism of HCO3 secretion in the mammalian colon. Future studies will undoubtedly provide increased understanding of the mechanism of HCO3 secretion in health and disease.

Animals↗

PubMed2006

Nutritional supplementation with transforming growth factor-beta, glutamine, and short chain fatty acids minimizes methotrexate-induced injury.

OBJECTIVE: Gastrointestinal (GI) damage caused by methotrexate (MTX) results in mucosal injury, bacterial invasion, and activation of an immune system that is reduced in function. Diets enriched with glutamine, short chain fatty acids (SCFAs), and transforming growth factor (TGF)-beta have demonstrated decreased infection, weight loss, and GI damage in Crohn disease. We, therefore, sought to study the cytoprotective effects of a diet enriched in glutamine, TGF-beta, and SFCAs (Modulen) in Fischer 344 rats exposed to MTX. METHODS: Rats were divided into five groups: two receiving normal saline and three receiving MTX and fed either normal chow, Modulen supplemented chow starting with the first MTX dose, or Modulen supplemented chow beginning 3 days before MTX injection. Rats were weighed daily. On day 5, albumin and bicarbonate levels were drawn, and rats were killed for examination of their intestinal mucosa by a pathologist unaware of groupings. RESULTS: Rats pretreated with Modulen supplemented chow maintained weight (2.6 vs, 12.3 g weight loss), albumin levels (3.13 vs, 2.43 mg/dL), and bicarbonate levels (23.8 vs. 18.1 mg/dL) as compared with rats fed normal chow throughout MTX treatment (P < 0.05). Pretreatment with Modulen also protected against crypt cell loss, villus atrophy, crypt abscesses, crypt/villus ratio, and overall histologic damage (P < 0.05). CONCLUSION: When administered before and during MTX treatment, Modulen supplementation provided statistically significant protection against weight loss, hypoalbuminemia, acidosis, and GI damage in a rat model. Future animal research of Modulen's protective effects with other chemotherapeutic agents is needed before human trials.

Animals↗

PubMed2005

Lactate is mainly fermented to butyrate by human intestinal microfloras but inter-individual variation is evident.

AIM: To assess the role of lactate as a precursor for butyrate biosynthesis in human colonic microflora. METHODS AND RESULTS: Three human faecal microfloras were incubated in vitro with media supplemented with 30 mmol l(-1) unenriched or 13C-enriched lactate. Lactate metabolism and short-chain fatty acid (SCFA) production were quantified. Lactate conversion to butyrate was investigated by gas chromatography-mass spectrometry and the pathways involved were identified by 13C nuclear magnetic resonance spectroscopy. All human faecal microfloras rapidly and completely fermented lactate, yielding approx. 19 mmol l(-1) total SCFAs. However, the SCFA composition varied markedly between microfloras. Butyrate was the main end-product for two microfloras but not for the third (60 and 61%vs 27% of the net concentration of SCFA produced respectively). The latter was typified by its ability to produce propionate as a major product (37%), and valerate (3%). 13C-Labelling showed that butyrate was produced through the acetyl-CoA pathway and that the three microfloras possessed significant differences in their metabolic pathways for lactate consumption. CONCLUSIONS: In contrast to the ruminal microflora, the human intestinal microflora can utilize both d- and l-lactate as precursors for butyrate synthesis. Inter-individual variation is found. SIGNIFICANCE AND IMPACT OF THE STUDY: This study suggests that the butyrogenic capability of colonic prebiotics could be related to lactate availability. These findings will direct the development of selection strategies for the isolation of new butyrate-producing bacteria among the lactate-utilizing bacteria present in the human intestinal microfloras.

Adult↗

PubMed1994

Sodium and chloride transport across the rumen epithelium of cattle in vitro: effect of short-chain fatty acids and amiloride.

Isolated mucosal sheets of cattle rumen were studied in vitro in Ussing chambers using a computer-controlled voltage clamp. Unidirectional fluxes of Na+ and Cl- were measured in standard (short-chain fatty acid (SCFA)-free) or SCFA-containing Ringer solution under zero voltage clamp conditions. Net NaCl absorption was observed under zero voltage clamp conditions, was stimulated by SCFAs and was not reduced by 1 mmol l-1 amiloride, although short-circuit current was significantly reduced by this concentration of the blocker. A constant coupling ratio of Na+ and Cl- absorption was observed.

Amiloride↗

PubMed1988

Luminal propionate-induced secretory response in the rat distal colon in vitro.

1. The stimulatory action of propionate on colonic electrolyte transport and involvement of the enteric reflex in this was studied in vitro using an Ussing chamber in the rat. The short-circuit current (Isc) and bidirectional fluxes of Na+ and Cl- were measured. Mucosa-submucosa preparations, containing the submucosal nerve, from the distal colon were used in most cases. 2. Mucosal application of propionate caused transient increases in the transmural potential difference, with the mucosal side negative, Isc and conductance. Serosal application of the acid had no effect. 3. Adaptation of the Isc response occurred when the acid was applied to the bathing solution cumulatively without washing out the first dose. If tissues were washed and held more than 20 min before the next application, the response was almost completely restored. 4. The increase in Isc in response to propionate was concentration dependent, with a 50% effective concentration of approximately 7 x 10(-5) M. 5. Two other short-chain fatty acids (SCFAs), n-butyrate and n-valerate, but not acetate, increased Isc when added to the mucosal bathing solution. 6. Bumetanide (3 x 10(-5) M) and the serosal chloride-free condition, but not amiloride (10(-4) M), inhibited the responses of Isc to propionate. Propionate-stimulated Cl- secretion resulted mainly from an increase in unidirectional serosal-to-mucosal Cl- movement. Propionate did not affect the Na+ flux. 7. Tetrodotoxin (10(-7) M), somatostatin (10(-7) M) and hexamethonium (10(-4) M) inhibited the propionate-evoked increase in Isc by 40, 70 and 30%, respectively. 8. Atropine (10(-5) M) also inhibited the Isc-increase response to propionate more than 90%. 9. Pre-treatment (2 min) of the mucosal surface with procaine (5 x 10(-4) M) inhibited the propionate-evoked increase in Isc by 90%. 10. The results suggest that luminal propionate transiently stimulated the colonic chloride secretory response that is not due to direct action on colonocytes, but due in large part to release of acetylcholine at neuro-colonocyte junctions, probably via an enteric reflex involving a mucosal sensory mechanism, cholinergic motor nerves and submucosal ganglia.

Action Potentials↗

PubMed1994

Functional role of bicarbonate in propionate transport across guinea-pig isolated caecum and proximal colon.

1. Unidirectional fluxes of propionate across isolated epithelia from the guinea-pig caecum and proximal colon were measured under short-circuit current conditions. In the caecum and proximal colon the serosal-to-mucosal propionate flux (JPrsm) was higher than mucosal-to-serosal flux (JPrms), resulting in a net secretory flux of propionate. 2. HCO3(-)-CO2-free solution reduced JPrms in the caecum and proximal colon markedly; JPrsm was not (caecum) or little (proximal colon) affected. The subsequent addition of acetazolamide caused a further decrease in JPrms in the proximal colon, but not in the caecum. 3. In HCO3(-)-containing solutions acetazolamide or ethoxzolamide inhibited JPrms; JPrsm was not affected. A macromolecular carbonic anhydrase inhibitor, prontosil-dextran, had no effect on propionate fluxes, indicating that the intracellular carbonic anhydrase is of importance for short-chain fatty acid transport. 4. Subsequent to carbonic anhydrase inhibition, mucosal addition of amiloride caused a slight further decrease of JPrms in the caecum and proximal colon; JPrsm was not affected. 5. Results support the view that a considerable proportion of short-chain fatty acids (SCFAs) is absorbed via a SCFA(-)-HCO3- exchange.

Acetazolamide↗

PubMed1996

Non-ionic diffusion and carrier-mediated transport drive extracellullar pH regulation of mouse colonic crypts.

1. Extracellular pH (pHo) regulation within mouse colonic crypt lumens is stimulated by transepithelial gradients of short-chain fatty acids (SCFAs). Current work assesses underlying mechanisms contributing to pHo regulation. 2. Crypt luminal alkalinization was saturable by apical SCFA (substrate concentration activating half-maximal transport (KT) of isobutyrate = 45 mM). However, saturation was consistent with either carrier-mediated SCFA flux or non-ionic diffusion, because the non-ionized form was titrated by luminal alkalinization. Direct acidification of apical perfusates increased the magnitude of SCFA-induced luminal alkalinization, roughly in the same proportion to the increased concentration of non-ionized SCFA in the crypt lumen. 3. Transepithelial gradients of an alternative weak acid (CO2) produce pHo changes similar to SCFA. In contrast, a weak base (NH3) changes pHo with reverse dependence on the orientation of the transepithelial gradient compared with SCFA. Results implicate non-ionic diffusion in pHo regulation, and suggest that pHo changes may underly SCFA-stimulated bicarbonate secretion and ammonium absorption. 4. SCFA metabolism plays a minor role in extracellular pH regulation. An avidly metabolized SCFA (N-butyrate) augments crypt luminal alkalinization only slightly (0.08 pH units) versus a poorly metabolized SCFA (isobutyrate). 5. Apical addition of 1 mM 4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS) partially inhibits luminal alkalinization caused by apical SCFA. DIDS has no effect on luminal alkalinization caused by transepithelial CO2 gradients. Probenecid (1 mM), alpha-cyano-4-hydroxycinnamic acid (4 mM) or basolateral DIDS (1 mM) do not affect pHo regulation. Results suggest that DIDS-sensitive, SCFA-dependent transport in the colonocyte apical membrane contributes to pHo regulation.

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

PubMed1991

Short chain fatty acids in the terminal ileum accelerate stomach to caecum transit time in the rat.

We have previously shown that infusion of triglycerides and long chain fatty acids into the ileum of humans and rats delays small bowel transit time. The present studies have investigated the effect on the stomach to caecum transit time of a baked bean meal of the ileal infusion of 20 mM, 50 mM, and 100 mM acetic, butyric, hexenoic, and caprylic acids in rats. After an 18 hour fast either a control or a short chain fatty acid (SCFA) solution (pH 6.5) was infused into the ileum for 30 minutes (0.3 ml/hour). A test meal was given by gavage and the infusion continued for a further 150 minutes. The arrival of the meal in the colon was signalled by a rise in the exhaled hydrogen concentration. Acetic acid (20 mM, 50 mM, 100 mM), butyric acid (100 mM), and caprylic acid (100 mM) produced a significant acceleration of transit which was inversely proportional to SCFA chain length. In a separate experiment, infusion of 100 mM acetic acid, the most potent SCFA, into an isolated ileal Thirty-Vella loop failed to accelerate transit of the test meal. Our results suggest that SCFAs accelerate transit via a local enteric reflex.

Acetates↗

PubMed1993

Colonic fermentation of complex carbohydrates in patients with familial adenomatous polyposis.

Decreased production of butyric acid by colonic carbohydrate fermentation may predispose to colonic carcinogenesis, with the implicit assumption that the decrease in faecal butyrate found predates the development of the tumour. The influence of the genetic predisposition to colonic tumours and the presence of colonic polyps on in vitro fermentation of carbohydrates was examined. Stool samples from 11 normal controls and 20 patients with familial adenomatous polyposis (FAP) were incubated anaerobically with a range of carbohydrates. Fermentation patterns were similar for glucose and raffinose. These sugars produced different short chain fatty acid (SCFA) patterns from the two polysaccharides, starch and arabinogalactan, which differed one from the other. The FAP gene carriers with polyps produced less butyrate than normal controls (p < 0.005) and gene carriers without polyps (p < 0.05). There were corresponding decreases in the molar ratios of butyrate. Gene carriers without polyps produced less absolute amounts of acetate than normal controls (p < 0.05) and slightly less total SCFAs (p < 0.05) but were otherwise not significantly different. The decreased production of butyrate noted by other workers may be secondary to the tumours rather than a contributory cause.

Adenomatous Polyposis Coli↗