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PubMed2003

Short-chain fatty acids stimulate colonic transit via intraluminal 5-HT release in rats.

We studied whether physiological concentration of short-chain fatty acids (SCFAs) affects colonic transit and colonic motility in conscious rats. Intraluminal administration of SCFAs (100-200 mM) into the proximal colon significantly accelerated colonic transit. The stimulatory effect of SCFAs on colonic transit was abolished by perivagal capsaicin treatment, atropine, hexamethonium, and vagotomy, but not by guanethidine. The stimulatory effect of SCFAs on colonic transit was also abolished by intraluminal pretreatment with lidocaine and a 5-hydroxytryptamine (HT)(3) receptor antagonist. Intraluminal administration of SCFAs provoked contractions at the proximal colon, which migrated to the mid- and distal colon. SCFAs caused a significant increase in the luminal concentration of 5-HT of the vascularly isolated and luminally perfused rat colon ex vivo. It is suggested that the release of 5-HT from enterochromaffin cells in response to SCFAs stimulates 5-HT(3) receptors located on the vagal sensory fibers. The sensory information is transferred to the vagal efferent and stimulates the release of acetylcholine from the colonic myenteric plexus, resulting in muscle contraction.

Animals↗

PubMed2004

Short-chain fatty acids induce colonic mucosal injury in rats with various postnatal ages.

Short chain fatty acids (SCFAs) may play a role in the pathogenesis of neonatal necrotizing enterocolitis. To evaluate the injurious effect of SCFAs on the colonic mucosa of rats at various postnatal developmental stages, we studied a total of 170 newborn Sprague-Dawley rats at postnatal ages days 3, 9, and 23. A 1.8-F silastic catheter or umbilical catheter was inserted rectally deep into the proximal colon of the rats. Rats from each of the three postnatal age groups were randomly divided to receive one of the following distinct SCFA solutions: acetic acid, butyric acid, propionic acid, or a mixture of above SCFAs solutions. An additional subgroup of rats from each of the age groups received normal saline as a control. The concentration of each SCFA solution was 300 mM, and the pH of all solutions was adjusted to 4.0. The volume of administered solution was 0.1 mL/10 g of body weight. After 24 h, all rats were killed and the daily weight change was recorded and proximal colon was collected for histologic examination. A histologic injury score was used to quantify the severity of mucosal injury. The severity of mucosal injury induced by luminal SCFAs administration decreased as the rats matured; by postnatal day 23, the injury caused by SCFAs was minimal. Thus, the severity of the colonic mucosal injury induced by luminal SCFAs is maturation dependent; the immature state of the mucosal defense in early postnatal age in newborn rat may explain its greater vulnerability to luminal SCFAs.

Acetic Acid↗

PubMed2004

Short-chain fatty acids decrease the frequency of spontaneous contractions of longitudinal muscle via enteric nerves in rat distal colon.

Short-chain fatty acids (SCFAs) produced by the bacterial fermentation of carbohydrates in the cecum and proximal colon are reported to modify colonic motility as a luminal factor. Besides the physical stimuli in the distal colon, SCFAs in the intestinal lumen also seem to affect colonic motility under physiological concentrations. This study therefore used fasted rats to investigate the effect of SCFAs on the spontaneous contractions of longitudinal muscle (LM) in rat distal colon, including mucosa in vitro. The frequency of spontaneous contractions of LM strips from the distal colon was 9.4 +/- 0.5 contractions/20 min. The exogenous addition of >5 mM SCFAs decreased the frequency of spontaneous contractions of the LM to 6.1 +/- 0.8 contractions/20 min. Among SCFAs, only acetate elicited this inhibitory response. TTX and the combination of hexamethonium and granisetron abolished SCFA-induced inhibitory response, suggesting that this inhibitory response is mediated via the ENS, including nicotinic and 5-HT(3) receptors. In conclusion, it is suggested that SCFAs in rat distal colon decrease the frequency of spontaneous contractions of the LM and that SCFAs may contribute to colonic motility, including the peristaltic reflex, by regulating the frequency of spontaneous contractions of the LM through the enteric nervous system (ENS).

Animals↗

PubMed1996

Short-chain fatty acids in the non-adapted and adapted pelvic ileal pouch.

BACKGROUND: Adaptation to colonic conditions occurs in the bacterial flora and faecal short-chain fatty acids (SCFAs) of the pelvic ileal pouch. METHODS: Faecal SCFAs were studied in 14 J-pouch patients within 10 days after closure of the ileostomy (non-adapted pouch) and more than 6 months after ileostomy closure (adapted pouch). RESULTS: Concentrations of faecal SCFAs were low in non-adapted pouches (mean +/- SE, 20.3 +/- 3.4 mmol/l), increasing to intermediate levels, 53.3 +/- 8.4 mmol/l, between 6 months and a year after ileostomy closure, and to 96.3 +/- 7.9 mmol/l, after more than a year of adaptation. Production of SCFAs in faecal homogenates was correspondingly low in non-adapted (6.3 +/- 2.0 mmol/l) compared with adapted pouches (32.0 +/- 3.6 mmol/l; p = 0.001) and could not be overcome by the addition of fermentable carbohydrates. Percentages of the predominant SCFAs (acetate, propionate, butyrate) were not affected by adaptation, nor were production and concentration of lactate. Stool volume decreased from 1019 +/- 134 to 603 +/- 77 ml/24 h (p = 0.02) during adaptation, sodium excretion decreased from 132 +/- 19 to 67 +/- 11 mmol/24 h (p = 0.02), and osmolality increased from 316 +/- 6 to 398 +/- 13 (p = 0.001). Excretions of carbohydrates, nitrogen, and potassium were not altered. CONCLUSIONS: The bacterial production of SCFAs is low in non-adapted pouches, resulting in low concentrations of SCFAs comparable to concentrations found in conventional ileostomies. Pouch adaptation gradually increases SCFA production and concentration severalfold and reaches concentrations normally found in non-colectomized individuals after approximately 1 year.

Adaptation, Physiological↗

PubMed1996

Short-chain fatty acid (SCFA) volume regulation in proximal and distal rabbit colon is different.

SCFAs increase the volume of many different cell types rarely exposed to significant concentrations of these weak electrolytes. SCFAs swell isolated cells from colonic carcinoma cell lines, but the-mechanism(s) of volume regulation in normal colonocytes, which are generally exposed to > 100 mM SCFAs, has not been well characterized. AIMS. To determine the effect of SCFAs on volume regulation in proximal and distal rabbit colonocytes. METHODS. Isolated colonocytes were plated on coverslips and placed in a perfusion apparatus that permitted fluid changes. Cells were continuously monitored by video-microscopy; volume was estimated by measured changes in the radius of individual cells. RESULTS. Distal colonocytes (DC) consistently had a slightly greater basal volume than proximal colonocytes (PC): [14.2 pl/fl:9.8 pl/fl] In HEPES-buffered solutions, an isotonic change to a 90 mM NaCl/50 mM Na propionate solution elicited a significant increase in cell volume within 10 min, but no noticeable regulatory volume decrease over 30 min: V/Vo in DC: 1.29 +/- .09; in PC: 1.25 +/- .05. In HCO3-buffered solutions, 50 mM PROP caused significantly greater cell swelling; in DC: 1.74 +/- .21; in PC: 1.52 +/- .08. In DC both amiloride and EIPA blocked the SCFA-induced increase in cell volume. A hypotonic challenge confirmed that these cells were capable of swelling. In contrast, amiloride did not significantly inhibit SCFA-induced swelling in PC: control, 1.25 +/- .05; amiloride, 1.36 +/- .10. Cell volume increased in PC perfused with an isosmotic 50 mM propionate, Na-free solution: 1.22 +/- .04. CONCLUSIONS. (i) SCFAs induce significant cell swelling, but no regulatory volume decrease, in isolated colonocytes; (ii) HCO3 augments SCFA-induced cell swelling; (iii) volume increase in DC is dependent on Na-H exchange, but in PC appears to be Na-independent. SIGNIFICANCE. There are fundamental differences in how proximal and distal colon respond to isosmotic volume challenge of SCFAs.

Animals↗

PubMedDate not supplied

Identification and comparative analysis of human colonocyte short-chain fatty acid response genes.

Short-chain fatty acids (SCFAs) butyrate, propionate, and acetate produced during fiber fermentation promote colonic differentiation and can reverse or suppress neoplastic progression. We sought to identify candidate genes responsible for SCFA activity on colonocytes and to compare the relative activities of independent SCFAs. cDNA was generated from polyA+ mRNA isolated from control Caco-2 cells and cells treated with equimolar butyrate, propionate, and acetate. GeneCalling, a restriction-based differential RNA expression platform linked to a DNA sequence database lookup, was applied. A total of 30,000 individual genetic sequences were analyzed for differential expression among the three SCFAs. Differentially expressed peaks corresponding to cancer-related genes were isolated, sequenced, and cross-referenced to the GenBank human database. Gene identities were independently confirmed by oligonucleotide poisoning. More than 1000 gene fragments were identified as being substantially modulated in expression by butyrate. Butyrate tended to have the most pronounced effects and acetate the least. Five fragments selected for further study were fully sequenced and proved 100% homologous with human sequences for clusterin, amyloid precursor-like protein 2, and caudal homeobox 2 protein, not previously known to be modulated by SCFAs. In each case, a similar order of potency for the three SCFAs studied was observed. The common SCFAs appear to exert different effects. This study suggests the diversity of the SCFA response at the molecular level and facilitates identifying genes important in the biologic activity of dietary fiber.

Alzheimer Disease↗

PubMed2000

Short chain fatty acids but not lactate or succinate stimulate mucus release in the rat colon.

BACKGROUND: Short chain fatty acids (SCFAs) affect various intestinal functions. Mucus is an important physiological component of the intestinal mucosal barrier. However, the effect of SCFAs or other organic acids on the intestinal mucus release is poorly understood. The aim of this study was to investigate whether lumen SCFA stimulates mucus release into the rat colon. METHODS: A solution of SCFA, lactate or succinate was infused into the colon of anesthetized rats, and we then measured the hexose content of the effluent. We also examined the influence of cholinergic antagonists on the effects of SCFA. RESULTS: A SCFA mixture (75 mM acetate, 35 mM propionate and 20 mM butyrate) or individual SCFAs (130 mM) increased the mucus release into the colon in a similar manner. The individual SCFAs, but not lactate or succinate, stimulated colonic mucus secretion in similar concentration-dependent manners. Butyrate stimulated colonic mucus secretion at 20 mM, but acetate, propionate, lactate and succinate at this concentration did not. Pretreatment with an anti-cholinergic agent diminished the stimulatory effects of SCFAs on mucus secretion. CONCLUSIONS: Lumen SCFAs, but not lactate or succinate, stimulate mucus release from the rat colon via a cholinergic nerve mechanism.

Animals↗

PubMed1998

Review article: short chain fatty acids in health and disease.

Short chain fatty acids (SCFAs) have been the subject of much research over the past few decades. They play a vital role in maintenance of colonic integrity and metabolism. They are produced when dietary fibre is fermented by colonic bacteria. SCFAs are avidly absorbed in the colon, at the same time as sodium and water absorption and bicarbonate secretion. Once absorbed, SCFAs are used preferentially as fuel for colonic epithelial cells and have trophic effects on the epithelium. Clinically, SCFAs have been studied as possible therapeutic agents in diversion colitis, ulcerative colitis, radiation proctitis, pouchitis and antibiotic-associated diarrhoea. Although some promising effects have been observed in uncontrolled studies, a specific therapeutic role for SCFAs remains to be defined. SCFAs may be the effector of the beneficial role of fibre in prevention of colon cancer.

Animals↗

PubMed2001

In vivo absorption of medium-chain fatty acids by the rat colon exceeds that of short-chain fatty acids.

BACKGROUND AND AIMS: Short-chain fatty acids (SCFAs) are main fuels of the colonic epithelium, and are avidly absorbed by the colon of animal and man. The current knowledge on colonic metabolism and absorption of medium-chain fatty acids (MCFAs) is limited. In some clinical situations, colonic absorption of high-energy substances could compensate for reduced absorptive capacity because of a shortened or malfunctioning small bowel. We evaluated and compared colonic absorption and metabolism of MCFAs (octanoate, decanoate, and dodecanoate), SCFAs (acetate and butyrate), and long-chain fatty acids (LCFAs) (oleate). METHODS: Rats were surgically operated on to cannulate a 7-cm segment of proximal colon, isolate the vasculature, and cannulate the right colic vein draining this segment. The lumen was perfused with (14)C-labeled substrates for 100 minutes. Right colic vein blood was analyzed for total (14)C, (14)CO(2), and metabolites by scintillation counting and high-performance liquid chromatography. RESULTS: The transport from the colonic lumen to mesenteric blood of substrate carbon from MCFAs exceeded by 2-13-fold that of SCFAs and LCFAs. The CO(2) production from the oxidation of MCFAs was as high as or higher than that from SCFAs. CO(2) produced from the LCFA, oleate, was lower than from SCFAs or MCFAs. In addition to CO(2), ketone bodies were major metabolites of SCFAs and MCFAs. Ketogenesis from butyrate and the MCFAs was significantly higher than from acetate and oleate. A substantial proportion (50%-90%) of all substrates was absorbed without being metabolized. CONCLUSIONS: The colonic epithelium serves to absorb and partially metabolize MCFAs. For patients with a compromised small-bowel function, colonic absorption of MCFAs could represent an important way of receiving calories.

Animals↗

PubMed1990

Parenteral nutrition supplemented with short-chain fatty acids: effect on the small-bowel mucosa in normal rats.

When enteral nutrition is excluded from animals maintained solely with total parenteral nutrition (TPN), atrophy of the intestinal mucosa is observed. Short-chain fatty acids (SCFAs) are produced in the colon by the fermentation of dietary carbohydrates and fiber polysaccharides and have been shown to stimulate mucosal-cell mitotic activity in the intestine. This study compared the effects of an intravenous and an intracecal infusion of SCFAs on the small-bowel mucosa. Rats received standard TPN, TPN with SCFAs (sodium acetate, propionate, and butyrate), TPN with an intracecal infusion of SCFAs, or rat food. After 7 d jejunal and ileal mucosal weights, DNA, RNA, and protein were determined. Standard TPN produced significant atrophy of the jejunal and ileal mucosa. Both the intracecal and intravenous infusion of SCFAs significantly reduced the mucosal atrophy associated with TPN. The intravenous and intracolonic infusion of SCFAs were equally effective in inhibiting small-bowel mucosal atrophy.

Animals↗

PubMed1992

Production of short chain fatty acids by the intestinal microflora during the first 2 years of human life.

We have followed the establishment of one group of intestinal microflora-associated characteristics, namely, the production of short chain fatty acids (SCFAs), in 30 healthy children, by gas chromatography analysis of fecal samples taken at 0, 1, 3, 6, 9, 12, 15, 18, 21, and 24 months of age. Acetic and propionic acids were the principal SCFAs at 1 and 3 months. Successively, the production of iso- and n-butyric, valeric, and caproic acids was established. At 2 years, the absolute amounts of all SCFAs with the exception of n-valeric acid had reached adult values. However, not all children had achieved a typically adult range of stool SCFAs by the end of the study. Both absolute and relative amounts of SCFAs were influenced by exposure to foods other than breast milk and exposure to antibiotic therapy. After standardization for exposure to foods other than breast milk, a positive age factor could be seen between 0 and 1 month of age for total amounts produced of SCFAs, acetic, propionic, and n-butyric acids. After this time, however, no clear age factor could be distinguished.

Age Factors↗

PubMed2007

The relationship between the effects of short-chain fatty acids on intestinal motility in vitro and GPR43 receptor activation.

The G protein-coupled receptors, GPR41 and GPR43, are activated by short-chain fatty acids (SCFAs), with distinct rank order potencies. This study investigated the possibility that SCFAs modulate intestinal motility via these receptors. Luminal SCFA concentrations within the rat intestine were greatest in the caecum (c. 115 mmol L(-1)) and proximal colon. Using similar concentrations (0.1-100 mmol L(-1)), SCFAs were found to inhibit electrically evoked, neuronally mediated contractions of rat distal colon, possibly via a prejunctional site of action; this activity was independent of the presence or absence of the mucosa. By contrast, SCFAs reduced the amplitude but also reduced the threshold and increased the frequency of peristaltic contractions in guinea-pig terminal ileum. In each model, the rank-order of activity was acetate (C2) approximately propionate (C3) approximately butyrate (C4) > pentanoate (C5) approximately formate (C1), consistent with activity at the GPR43 receptor. GPR43 mRNA was expressed throughout the rat gut, with highest levels in the colon. However, the ability of SCFAs to inhibit neuronally mediated contractions of the colon was similar in tissues from wild-type and GPR43 gene knockout mice, with identical rank-orders of potency. In conclusion, SCFAs can modulate intestinal motility, but these effects can be independent of the GPR43 receptor.

Animals↗

PubMed2003

Induction of an embryonic globin gene promoter by short-chain fatty acids.

Short-chain fatty acids (SCFAs) and dimethyl sulfoxide (DMSO) induce adult erythroid differentiation in murine erythroleukemia (MEL) cells, but only SCFAs concurrently up-regulate expression from the endogenous embryonic globin gene epsilony. The epsilony promoter, linked to a reporter gene and stably transfected into MEL cells, was tested during adult erythroid differentiation. Both the epsilony-CACCC site at -114 bp and enhancer sequences (hypersensitive site 2 [HS2]) from the beta-globin locus control region (LCR) were essential to maximal SCFA-mediated induction of expression from these constructs in MEL cells. Gel-shift analyses of binding activity from SCFA-induced MEL cell nuclear extracts showed in vitro binding by specificity proteins 1 and 3 (SP1, SP3) and basic or erythroid Krüppel-like factors (BKLF, EKLF) at the epsilony-CACCC site. In a functional analysis, transient cotransfections in nonerythroid NIH/3T3 cells of SP1, SP3, BKLF, or EKLF and HS2 epsilony promoter-luciferase constructs, with or without coactivators (p300, CREB-binding protein [CBP], or p300/CBP-associated factor [PCAF]) and SCFAs, were performed. SP1, SP3, and EKLF further increased expression from HS2 epsilony promoter constructs following exposure to SCFAs. This effect was variably augmented by coactivators and was diminished in EKLF mutants that were unable to undergo histone/factor-acetyl transferase (H/FAT)-mediated acetylation. In addition, acetylation of SP1 was detectable in NIH/3T3 cells following exposure to SCFAs. In sum, LCR sequence and an embryonic globin gene promoter CACCC site were essential to that promoter's up-regulation during SCFA-mediated induction of adult erythroid differentiation in vitro. Of factors that interact at the CACCC site, SCFA-mediated acetylation is implicated in SP1 and EKLF, and may be a mechanism through which SCFAs induce embryonic/fetal globin gene promoters during adult erythroid differentiation.

Acetylation↗

PubMed1986

Influence of ampicillin, clindamycin, and metronidazole on faecal excretion of short-chain fatty acids in healthy subjects.

The faecal excretion of short-chain fatty acids (SCFAs) has been measured in groups of six healthy subjects before, during, and after they received the antibiotics clindamycin, ampicillin, or metronidazole perorally for 6 days. Intake of clindamycin reduced the median total concentration of SCFAs from 62.9 mmol/kg faeces (wet weight) to 7.3 mmol/kg (p less than 0.05). During therapy the relative amounts of acetic acid increased from 50% to 90% of the total concentration (p less than 0.05). Ampicillin reduced the median SCFAs concentration from 62.4 mmol/kg to 47.8 mmol/kg (p less than 0.05), whereas metronidazole did not change the SCFAs concentrations significantly. The SCFAs concentrations returned to normal within 5 weeks after the treatment in all subjects. Clindamycin was detected in high concentrations in faeces during therapy. Ampicillin was detected in only one faecal sample, which was from the only subject in the ampicillin group without detectable beta-lactamase activity in faeces. Metronidazole could not be detected in faeces from any subjects receiving this drug. Clindamycin and ampicillin, but not metronidazole, induce pronounced changes in faecal SCFAs, most likely reflecting severe changes in the colonic ecosystem. An antibiotic's influence on the colonic microflora may in part depend on its antimicrobial spectrum and the concentration of antimicrobially active drug in the gut.

Administration, Oral↗

PubMed1995

Colonic fermentation of complex dietary carbohydrates in short-bowel patients. No association with hydrogen excretion and fecal and plasma short-chain fatty acids.

BACKGROUND: The colonic degradation of carbohydrates (fermentation) to short-chain fatty acids (SCFAs) appears to have major impacts on colonocyte function, sodium and water absorption, and large-bowel energy salvation, but how to quantify the in vivo fermentation in man is still debatable. METHODS: Indicators of colonic fermentation, fecal and plasma SCFAs and breath hydrogen (H2), were measured in 10 short-bowel patients (mean +/- SE; 106 +/- 21 cm) with totally preserved large bowels who were on a 60% high-carbohydrate, 20% low-fat diet, compared with the reversed isocaloric 20% low-carbohydrate, 60% high-fat diet. This human model showed large differences in large-bowel fermentation, as excretions of calories were reduced (40%; 485 +/- 151 kcal/day) and excretions of carbohydrates were unchanged and low with the high-carbohydrate diet as compared with the low-carbohydrate diet, in contrast to unchanged calorie excretion in short-bowel patients with no colonic function. RESULTS: Fecal concentrations of SCFAs did not change when the diet was changed from the high content to the low content of carbohydrates (82 +/- 11 mmol/l and 79 +/- 9 mmol/l, respectively). The ratio of acetate in feces increased (from 48 +/- 4% to 54 +/- 3%; p = 0.01) on the high-carbohydrate diet, whereas the percentage of the other SCFAs decreased proportionally. Plasma SCFAs 2 h and 6 h after breakfast were also identical when comparing the two dietary regimens. Nor were the peak H2 breath excretion and the area under the H2 excretion-versus-time curve increased by the threefold increase in the intake of dietary carbohydrates. CONCLUSIONS: Fecal and plasma SCFAs and breath H2 excretion are of limited value in the evaluation of even large differences in colonic fermentation of complex dietary carbohydrates.

Adult↗

PubMed1996

Antibiotic-associated diarrhoea, Clostridium difficile, and short-chain fatty acids.

BACKGROUND: It has been hypothesized that Clostridium difficile and decreased colonic production of short-chain fatty acids (SCFAs) cause the development of antibiotic-associated diarrhoea. We therefore wanted to investigate the effects of an intensive and uniform antibiotic therapy on faecal SCFAs concentrations. C. difficile, and extent of diarrhoea. METHODS: Fifteen liver-transplanted patients who received oral bowel flora suppression therapy (6.3 g cefuroxime, 0.6 g tobramycin, and 0.5 g nystatin three times daily) were studied for 12 days before and 12 days after discontinuation of therapy. RESULTS: Thirteen of the 15 patients (87%) developed diarrhoea. Colonic fermentation was negligible in all patients, judged by very low levels of faecal SCFAs (< 10 mmol/l). Diarrhoea lessened as suppression therapy proceeded despite continuous low levels of SCFAs. Initial stool frequency of 4.1 +/- 0.6 and viscosity of 2.5 +/- 0.2 per day (on a scale of 1-3; mean +/- SE) decreased to 2.2 +/- 0.5 (p = 0.0009) and 1.6 +/- 0.2 (p = 0.003) per day, respectively, just before cessation of suppression therapy. Both SCFAs and stool habits normalized within days after discontinuation of antibiotics. Only a few samples from 2 patients were culture-positive for C. difficile during therapy, whereas 9 of the 15 patients (60%) became culture-positive (6 cytotoxin-positive) after cessation of suppression therapy at a time when none had diarrhoea. CONCLUSIONS: Intensive treatment with antibiotics directed against the colonic flora resulted in diarrhoea in the vast majority of patients, but the diarrhoea was self-limiting despite continual antibiotic treatment and very low faecal concentrations of SCFAs. C. difficile was not associated with antibiotic-associated diarrhoea but was a common finding after treatment with antibiotics was stopped at the time when diarrhoea had ceased.

Adult↗

PubMed1984

Short-chain fatty acids in the normal human feces.

The short-chain fatty acids ( SCFAs ) have been studied in the feces of 20 healthy subjects--10 methane excretors and 10 non-methane excretors. The analytical procedure included homogenization of fecal samples followed by vacuum distillation and subsequent gas chromatography. This method for analysis of fecal SCFAs showed recoveries of the individual acids from 90% to 109% and coefficients of variation for the inter-assay reproducibility from 6.0% to 19.7%, highest for those acids present in the smallest concentrations. There was no difference in the concentrations or relative compositions of SCFAs between methane-excreting subjects and non-methane-excreting subjects. The concentrations of SCFAs , given as mmol/kg feces (wet weight), were (median and range): total, 76.8 (27.9-187.7); acetic acid, 37.4 (12.8-103.4); propionic acid, 12.5 (4.5-27.8); i-butyric acid, 2.2 (0.7-3.8); n-butyric acid, 12.4 (4.0-53.0); i-valeric acid, 3.2 (0.8-5.9); n-valeric acid, 2.4 (0.6-3.8) and n-caproic acid, 0.5 (0.0-3.6). The study shows that the SCFAs are quantitatively the most important anions in the feces of healthy subjects. The pronounced individual variations in the concentrations of SCFAs are real biological variations and cannot be explained by methodological variations.

Adult↗

PubMed1990

The starved colon--diminished mucosal nutrition, diminished absorption, and colitis.

Nutrition of colonic epithelial cells is mainly from short chain fatty acids (SCFAs) produced by bacterial fermentation in the colonic lumen. n-Butyrate contributes more carbon of oxidation to epithelial cells than glucose or glutamine from the vasculature. Incomplete starvation of colonic epithelial cells through lack of luminal SCFAs leads, in the short term, to mucosal hypoplasia with either diminished absorption or diarrhea. A chronic lack of SCFAs or complete organ starvation in conjunction with other factors leads to nutritional colitis, either "diversion colitis" or "starvation colitis." Whether predominantly diarrhea or colitis develops in mucosal malnutrition appears to depend upon the severity and duration of starvation. Ulcerative colitis may be classified as a nutritional colitis in that colonic epithelial cells are unable to utilize SCFAs reflecting epithelial starvation despite abundant SCFAs.

Animals↗