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Human Nutrition and Metabolism
Research Communication

Fecal Acetate Is Inversely Related to Acetate Absorption from the Human Rectum and Distal Colon^1,2

Janet A. Vogt^* and Thomas M. S. Wolever^*,,3

^* Department of Nutritional Sciences, University of Toronto, and St. Michael’s Hospital, Toronto, Canada

³To whom correspondence should be addressed. E-mail: zemailthomas.wolever{at}utoronto.ca.

	ABSTRACT

TOP ABSTRACT SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
In humans, colonic bacteria ferment unabsorbed carbohydrates, producing the SCFA acetic, propionic and n-butyric acids. To test for interactions among the SCFA that may affect their absorption, healthy subjects (n = 10) were given 300-mL rectal infusions containing acetate (60 mmol/L), propionate (20 mmol/L) and butyrate (20 mmol/L), alone or in combinations of two or three. The solutions were retained for 30 min, and then subjects voided a sample for SCFA measurement. To examine the relationship between absorption and fecal SCFA concentrations, a fecal sample was collected at the end of the study. The mean percentage of butyrate absorption (30.2 ± 4.6%) exceeded that of acetate (24.1 ± 3.7%) (P < 0.05). Absorption tended to be less (P = 0.12) when a SCFA was infused alone (26.7 ± 4.0%) than when all three were infused (32.0 ± 5.7%). Bicarbonate concentration was higher after butyrate-containing infusions than after saline. The fecal molar acetate percentage was inversely correlated with the percentage of acetate absorption from the infusion of three SCFA (r = -0.834, P < 0.005). We conclude that there was no combination effect on SCFA absorption, and the chain-length effect suggests passive diffusion as a likely mechanism of absorption. Furthermore, fecal acetate may reflect absorption, rather than production of colonic acetate.

KEY WORDS: • acetate • propionate • SCFA • absorption • colon.

SCFA are produced by bacterial fermentation of unabsorbed carbohydrates in the human colon. The three main SCFA, acetic (AC),³ propionic (PR) and n-butyric (BU) acids, occur in a molar ratio of 60:20:20 in the colon (1). AC is a substrate for cholesterol synthesis (2), whereas PR is a gluconeogenic (3) substrate, and BU is both an energy substrate for colonocytes (4) and a differentiation-inducing antineoplastic agent (5). SCFA also function as systemic energy substrates (6–8).

SCFA absorption from the colonic lumen has been studied using both animal and human models (9,10). In one study, rectal infusion of AC and PR in a 3:1 mol/L ratio enhanced AC absorption, but did not affect PR absorption (11). In another study, when AC, PR and BU were infused together, a longer-chain length was related to increased absorption (12). This result is compatible with both the passive diffusion model and the carrier-mediated bicarbonate exchange model (13,14). However, AC, PR and BU were present in equimolar concentrations rather than a 60:20:20 ratio in the infusate, and bicarbonate was not measured.

It has also been suggested that SCFA absorption may differ between methane (CH₄) producers and nonproducers (15), but this has not been tested using a SCFA absorption model. Furthermore, the relationship between fecal SCFA concentrations and SCFA absorption from the human colon is unclear. The primary objectives of this study were to determine whether interactions occur among AC, PR and BU that affect their absorption, and to examine the relationship between SCFA absorption from the colon and fecal SCFA concentrations. Secondary objectives were to measure bicarbonate levels during SCFA absorption and the CH₄-producing status of subjects.

	SUBJECTS AND METHODS

TOP ABSTRACT SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Healthy adults (8 women, 2 men; 30.9 ± 2.9 y old; BMI, 22.1 ± 1.5 kg/m²) participated. Anyone with endocrine or gastrointestinal disorders, or who had taken antibiotics within the previous 3 mo was excluded. Subjects signed a consent form approved by the Human Subjects Review Committee at the University of Toronto.

Each subject was studied 10 times, at intervals of at least 3 d. They were told to eat a low fiber dinner the day before, and were provided with lists of high fiber foods to be avoided and low fiber foods to select from. After a 12-h overnight fast, subjects put 2 cm of the end of a piece of Tygon flexible plastic tubing (Norton Performance Plastics, Akron, OH; o.d., 4 mm) into their rectum, infused 500 mL of doubly distilled water, and emptied their colon; 15 min later, they replaced the tubing to infuse 300 mL of test solution. A sample of infused solution (15 mL) was withdrawn and infused again two times, followed by removal of a 20-mL baseline sample. The solution was held for 30 min, then voided into a collection bag.

Seven SCFA solutions were given in random order: each SCFA alone, the three pairs, and all three SCFA together (APB). Three saline infusions were given: at the start, middle, and end of the study.⁴ Baseline samples were collected in airtight 20-mL syringes and end-point samples were collected in plastic bags, and kept on ice until the pH was measured with a 32 pH meter (Beckman Instruments, Fullerton, CA). Samples were centrifuged and divided into four aliquots. The aliquot for bicarbonate analysis was stored at -20°C until analysis.

Samples for SCFA analysis were centrifuged at 9000 x g for 10 min. The supernatant (90 µL) was acidified to pH 3, using 180 µL of 0.04 mol/L sulfuric acid (95.0–98.0% pure, British Drug House, Toronto, Canada) to ensure complete SCFA recovery, and 30 µL of 2-methylbutyric acid (#M 0516, Sigma Chemical) added as an internal standard. Triplicate samples were distilled cryogenically (16), then analyzed by HPLC as described previously (17). Polyethylene glycol 4000 (PEG) was analyzed in triplicate, following the method of Malawer et al. (18), on an UltrospecII Spectrophotometer (LKB Biochrom, Cambridge, UK). Bicarbonate was analyzed on a Nova 4 electrolyte analyzer (Nova Biomedical, Waltham, MA) at the Main Biochemistry Laboratory of St. Michael’s Hospital in Toronto.

Fecal samples were collected at least 1 wk after the infusion protocol and were analyzed following the method of Zijlstra et al. (19). Aliquots were centrifuged at 9000 x g for 10 min and the supernatant frozen at -20°C. HPLC analysis was the same as for the rectal infusion samples, both with and without the internal standard.

At least five fasting breath samples were taken on three separate days from each subject using a modified Haldane-Priestley tube (20), and room air was sampled each time. Smokers (n = 3) refrained for 30 min or more before giving samples (21). Samples were stored in syringes at -20°C, then analyzed for CH₄ within 5.5 ± 0.6 h, on a Microlyzer (Model DP; Quintron Instruments, Milwaukee, WI). CH₄ producers were subjects with mean breath CH₄ concentrations 1 ppm (0.045 µmol/L) above room air.

The saline solutions did not contain SCFA. For each subject, the SCFA concentrations of the three saline end-point samples were plotted as AC vs. PR, AC vs. BU, PR vs. AC, PR vs. BU, BU vs. AC, and BU vs. PR. Individual regression equations were calculated for each subject and used to determine how much of an infused SCFA in a baseline or end-point SCFA infusion sample was due to fecal contamination, based on the amount of another SCFA present that had not been infused. Contamination of baseline samples from SCFA infusions, expressed as the percentage of the amount of that SCFA present in the infusion, never exceeded 1% for AC and PR, and 0.5% for BU. The mean level of contamination of end-point samples was 2% for all three SCFA.

To assess the effect of SCFA combination on SCFA absorption, the mean percentage of absorption was pooled for all infusions of one SCFA, a SCFA plus the shorter of the others, a SCFA plus the longer of the others, and the infusion containing all three SCFA (APB). The percentage of SCFA absorption is the absolute value of that calculated as the mmol of SCFA absorbed, divided by the mmol of SCFA present at baseline, and multiplied by 100.

The amount of SCFA absorbed is the mmol of SCFA in the end-point sample less the mmol in the baseline sample. The mmol of SCFA in each sample is calculated as the SCFA/PEG ratio multiplied by the amount of PEG infused (750 mg), minus the amount of PEG withdrawn in the 20-mL baseline sample.

All statistical procedures were performed using SAS 8.01 (SAS Institute, Cary, NC). To examine the effects of combination and SCFA chain length on the percentage of SCFA absorption, a two-factor ANOVA with repeated measures on both factors was used. The error term to test a main effect in this model was specified as the effect x subject interaction (22). A one-factor ANOVA with repeated measures was used to examine the effect of treatment on end-point bicarbonate concentration. Tukey’s post-hoc test was used to adjust for multiple comparisons when comparing individual means. To assess the effects of SCFA chain length, combination and CH₄-producing status in the same model, a three-factor ANOVA with repeated measures on two factors (combination and SCFA) was used. The subjects were nested within CH₄-producing status. The error term to test a main effect in this model was specified as the effect x [subject(CH₄)] interaction (23). Differences were considered significant at P < 0.05.

	RESULTS

TOP ABSTRACT SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
The effect of the combination on the percentage of SCFA absorption was not significant (P = 0.12) with or without the inclusion of CH₄-producing status in the model. There was a significant effect of chain length (P < 0.05). The percentage absorption of BU (30.2 ± 4.6%) was greater than that of AC (24.1 ± 3.7%), but not that of PR (27.9 ± 4.1%). There were no interactions between SCFA chain length, combination or CH₄-producing status. Five subjects were classified as CH₄-producers, and their overall breath CH₄ concentration was 1.4 ± 0.5 µmol/L. The fecal molar percentages of AC, PR and BU were 59.7 ± 0.9, 20.2 ± 1.5 and 20.1 ± 1.4, respectively.

The pooled SCFA absorption in mmol, for all the SCFA infusions except APB, was correlated with the total SCFA concentration infused (r = 0.999, P < 0.0001, Fig. 1). The percentage of AC absorption from the APB solution was negatively correlated with the fecal molar percentage of AC (r = -0.834, P < 0.005, Fig. 2). Neither PR nor BU showed any correlation between their absorption from the APB solution and their respective fecal molar percentages. End-point bicarbonate concentration was higher (P < 0.02) after the BU and APB infusions than after saline (Table 1).

View larger version (23K): [in this window] [in a new window]   FIGURE 1 Total SCFA absorption as a function of total SCFA concentration in healthy subjects given 300 mL rectal infusions containing acetate (60 mmol/L), propionate (20 mmol/L) and butyrate (20 mmol/L), alone or in combinations. Values are means ± SEM, n = 10. Regression line is shown. AB, acetate + butyrate; AC, acetate; AP, acetate + propionate; APB, acetate + propionate + butyrate; BU, butyrate; PB, propionate + butyrate; PR, propionate; SAL, saline.

View larger version (16K): [in this window] [in a new window]   FIGURE 2 Relationship between the percentage absorption of acetate from the APB solution and fecal acetate in healthy subjects given 300 mL rectal infusions containing acetate (60 mmol/L), propionate (20 mmol/L) and butyrate (20 mmol/L), alone or in combinations. Regression line is shown. Each point represents one individual, n = 10. APB, acetate + propionate + butyrate.

	DISCUSSION

TOP ABSTRACT SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

There was a significant effect of chain length in this study; the mean percentage of absorption of BU was significantly greater than that of AC. This was also shown in a study using a rectal infusion with 40 mmol/L each of AC, PR, and BU (12). One study suggested that the permeability coefficient of intestinal cell membranes for SCFA increases by a factor of 1.58 with each methyl group (24). This chain length effect supports passive diffusion as the primary mechanism of SCFA absorption (9,10,25).

The correlation between total SCFA absorption and SCFA concentration, when the APB solution is excluded (Fig. 1), lends further support to passive diffusion. The large SCFA concentration gradient between the colonic lumen and the blood favors this mechanism, and other studies have shown that SCFA absorption is concentration dependent (9,26). However, the mean total absorption of SCFA from the APB solution was greater than that predicted by the regression line (Fig. 1). Although not significantly different due to larger variation, the position of the mean for the APB solution, relative to the regression line, suggests that another mechanism, in addition to passive diffusion, might play a role in SCFA absorption when all three SCFA are present at physiological levels.

In this study, bicarbonate concentration was significantly higher after infusions of either BU alone or all three SCFA, compared with infusions of saline. Bicarbonate may be secreted into the colonic lumen when SCFA are absorbed. There is evidence of a BU-bicarbonate exchange mechanism in the distal colon of rats (13). In mammals, a carrier-mediated mechanism such as the SCFA-bicarbonate exchange may enhance transmural SCFA transport at high SCFA concentrations, with passive diffusion as the primary mechanism (27). On the other hand, bicarbonate in the colonic lumen can also be generated by luminal CO₂ hydration (28). BU is a primary fuel for human colonocytes (4) which, when oxidized, yields CO₂. Because BU is preferentially metabolized over AC and PR (29), an infusion containing BU would yield more CO₂ than one containing AC or PR. The SCFA-bicarbonate exchange raises both the pH and partial pressure CO₂ (pCO₂), whereas luminal CO₂ hydration lowers the pCO₂. In humans, colonic pCO₂ has been shown to decrease when SCFA are absorbed (25). Assuming that some CO₂ diffuses into the lumen of the colon, this would make luminal hydration of CO₂ the more plausible mechanism for the increase in bicarbonate.

In this study, AC absorption from the APB infusion was inversely related to the fecal molar percentage of AC. That is, subjects with low fecal AC tended to have high AC absorption from an APB infusion and presumably, high absorption of colonically produced AC. The correlation coefficient of -0.834, one could argue, indicates that 70% of the variation in fecal AC concentration is explained by its absorption from the colon. Because fecal AC concentration reflects a balance between colonic production and absorption of AC, the present data suggest that fecal SCFA concentrations may better reflect SCFA absorption than production. Variation in fecal SCFA concentrations among individuals has been observed previously, and it was speculated that the individuals might have differed in their ability to absorb SCFA from the intestinal tract (30). However, SCFA absorption was not measured in that study.

Assuming that passive diffusion is the predominant mechanism of SCFA absorption from the colon, two factors that would influence the degree of absorption are the resident time of the digesta (31) and the surface area of the mucosa. No attempt was made in this study to determine the resident time of the digesta, and information on subjects’ bowel habits was not collected. However, an attempt was made to determine the site of absorption. Twelve months after completion of this study, we infused 6 of the 10 subjects with 300 mL of a technetium-labeled saline infusion. Subjects followed the same protocol as in the present study. During the retention period, anterior scans of the abdomen were acquired at intervals of 1 min (unpublished data). In two subjects, with overall percentage of SCFA absorptions of 49.5 ± 14.1 and 24.7 ± 7.3%, the solution stayed in the sigmoidal colon. In three subjects, with absorption values of 26.4 ± 5.8, 17.7 ± 5.4, and 17.5 ± 6.6%, the solution was in the sigmoidal colon at the time of the baseline sample, but had reached the splenic flexure by the end of the retention period. In the remaining subject, who had an overall percentage of SCFA absorption of 50.3 ± 8.6%, the solution had reached the splenic flexure at the time of the baseline sample and had crossed the transverse colon by the end of the retention period. A nonparametric ANOVA on the overall percentage of SCFA absorption for each subject, with the technetium data grouped into three categories (as described above) was not significant. Therefore, we assume that the differences in the overall percentage of absorption among subjects are not due to differences in the amount of colonic mucosa exposed to the infusion.

Flick and Perman suggested a link between CH₄-producing status and SCFA absorption (15). They studied the effect of malabsorbed carbohydrate on fecal pH in CH₄-producers and nonproducers and found that in spite of similar in vitro acid production from fecal samples, the nonproducers had significantly lower fecal pH. This prompted them to suggest that SCFA absorption was higher in CH₄-producers. We found that CH₄-producing status had no main effect on, nor any interaction with SCFA absorption. However, human in vitro studies have shown that CH₄ production is maximal at neutral pH (32). Because the pH in the distal colon is 7.0, this is the primary site of CH₄ production in humans (33,34). Therefore, it is possible that the cleansing enema given to our subjects 15–30 min before breath sampling may have affected the determination of CH₄-producing status by washing out the methanogenic bacteria.

In conclusion, we did not find a significant combination effect on SCFA absorption from the human distal colon. The observed effects of both chain length and concentration support passive diffusion as the predominant mechanism of absorption up to a luminal concentration of 80 mmol/L. Another mechanism, such as the BU-bicarbonate exchange, may be important at higher concentrations. Furthermore, the present data suggest that fecal AC concentration should be viewed as an indicator of the rate of AC absorption from the colon, rather than the rate of its production.

	FOOTNOTES

 
¹ Presented in part at Experimental Biology 96, April, 1996, Washington, D.C. [Vogt, J. A. & Wolever, T.M.S. (1995) Absorption of short chain fatty acids from the human rectum and distal colon. FASEB J. 9(3): A440] and the Canadian Federation of Biological Sciences, June, 1996, London, Canada [Vogt, J. & Wolever, T.M.S. (1996) Absorption of Short Chain Fatty Acids from the Human Rectum and Distal Colon].

² Supported by the Natural Sciences and Engineering Research Council of Canada.

⁴ Abbreviations used: AC, acetate; APB, acetate + propionate + butyrate; BU, butyrate; pCO₂, partial pressure CO₂; PEG, polyethylene glycol 4000; PR, propionate.

⁵ All solutions were made up in doubly distilled water with 0.188 mmol/300 mL polyethylene glycol 4000 (PEG) (Mallinckrodt Canada, Pointe-Claire, Canada) as an unabsorbable marker. The SCFA solutions contained 60 mmol/L sodium acetate (99.0% pure, #S-8750, Sigma Chemical, St. Louis, MO), 20 mmol/L sodium propionate (Food Grade; Van Waters and Rogers, Toronto, Canada), and 20 mmol/L sodium butyrate (98.0% pure, Aldrich Chemical, Milwaukee, WI), either alone or in combination. The sodium concentration was kept at 150 mmol/L by adding sodium chloride (Analytical Grade, British Drug House, Darmstadt, Germany) and the osmolality was 300 mOsm/L. Each solution was titrated to pH 7 with either hydrochloric acid or sodium hydroxide (36.5–38% or 97.0% pure, respectively, Fisher Chemical, Fair Lawn, NJ).

Manuscript received 16 April 2003. Initial review completed 27 May 2003. Revision accepted 23 July 2003.

	LITERATURE CITED

TOP ABSTRACT SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 

1. Cummings, J. H., Pomare, E. W., Branch, W. J., Naylor, C. P. & Macfarlane, G. T. (1987) Short chain fatty acids in human large intestine, portal, hepatic and venous blood. Gut 28:1221-1227.[Abstract/Free Full Text]

2. Wolever, T. M., Brighenti, F., Royall, D., Jenkins, A. L. & Jenkins, D. J. (1989) Effect of rectal infusion of short chain fatty acids in human subjects. Am. J. Gastroenterol. 84:1027-1033.[Medline]

3. Wolever, T. M., Spadafora, P. & Eshuis, H. (1991) Interaction between colonic acetate and propionate in humans. Am. J. Clin. Nutr. 53:681-687.[Abstract/Free Full Text]

4. Roediger, W. E. (1980) Role of anaerobic bacteria in the metabolic welfare of the colonic mucosa in man. Gut 21:793-798.[Abstract/Free Full Text]

5. Kim, Y. S., Gum, J. R. & Ho, S. B. (1994) Colonocyte differentiation and proliferation: overview and the butyrate-induced transcriptional regulation of oncodevelopmental placental-like alkaline phosphatase gene in colon cancer cells. Binder, H. J. Cummings, J. H. Soergel, K. H. eds. Falk Symposium 73: Short Chain Fatty Acids 1994:119-134 Kluwer Academic Publishers London, UK. .

6. McNeil, N. I. (1984) The contribution of the large intestine to energy supplies in man. Am. J. Clin. Nutr. 39:338-342.[Abstract/Free Full Text]

7. Grossklaus, R. (1983) Energy gap?. Nutr. Res. 3:595-604.

8. Wisker, E. & Feldheim, W. (1994) Energy value of fermentation. Binder, H. J. Cummings, J. H. Soergel, K. H. eds. Falk Symposium 73: Short Chain Fatty Acids 1994:20-28 Kluwer Academic Publishers London, UK. .

9. Engelhardt, W. v., Busche, R. & Gros, G. (1991) Absorption of short-chain fatty acids: mechanisms and regional differences in the large intestine. Roche, A. F. eds. Short-Chain Fatty Acids: Metabolism and Clinical Importance, Report of the Tenth Ross Conference on Medical Research 1991:60-62 Ross Laboratories Columbus, OH. .

10. Bugaut, M. (1987) Occurrence, absorption and metabolism of short chain fatty acids in the digestive tract of mammals. Comp. Biochem. Physiol. B 86:439-472.[Medline]

11. Wolever, T. M., Trinidad, T. P. & Thompson, L. U. (1995) Short chain fatty acid absorption from the human distal colon: interactions between acetate, propionate and calcium. J. Am. Coll. Nutr. 14:393-398.[Abstract]

12. Saunders, D. (1991) Absorption of short chain fatty acids in human stomach and rectum. Nutr. Res. 11:841-847.

13. Rajendran, V. M. & Binder, H. J. (1994) Short chain fatty acid stimulation of electroneutral NaCl absorption: role of apical SCFA-HCO₃ and SCFA-Cl Exchanges. Binder, H. J. Cummings, J. H. Soergel, K. H. eds. Falk Symposium 73: Short Chain Fatty Acids 1994:104-116 Kluwer Academic Publishers London, UK. .

14. Harig, J. M., Knaup, S. M. & Shoshara, J. (1990) Transport of n-butyrate into human colonic luminal membrane vesicles. Gastroenterology 98:A543 (abs.).

15. Flick, J. A. & Perman, J. A. (1989) Nonabsorbed carbohydrate: effect on fecal pH in methane-excreting and nonexcreting individuals. Am. J. Clin. Nutr. 49:1252-1257.[Abstract/Free Full Text]

16. Tollinger, C. D., Vreman, H. J. & Weiner, M. W. (1979) Measurement of acetate in human blood by gas chromatography: effects of sample preparation, feeding, and various diseases. Clin. Chem. 25:1787-1790.[Abstract/Free Full Text]

17. Fernandes, J., Rao, A. V. & Wolever, T. M. (2000) Different substrates and methane producing status affect short-chain fatty acid profiles produced by In vitro fermentation of human feces. J. Nutr. 130:1932-1936.[Abstract/Free Full Text]

18. Malawer, S. J. & Powell, D. W. (1967) An improved turbidimetric analysis of polyethylene glycol utilizing an emulsifier. Gastroenterology 53:250-256.

19. Zijlstra, J. B., Beukema, J., Wolthers, B. G., Byrne, B. M., Groen, A. & Dankert, J. (1977) Pretreatment methods prior to gas chromatographic analysis of volatile fatty acids from faecal samples. Clin. Chim. Acta 78:243-250.[Medline]

20. Metz, G., Gassull, M. A., Leeds, A. R., Blendis, L. M. & Jenkins, D. J. (1976) A simple method of measuring breath hydrogen in carbohydrate malabsorption by end-expiratory sampling. Clin. Sci. Mol. Med. 50:237-240.[Medline]

21. Tadesse, K. & Eastwood, M. (1977) Breath-hydrogen test and smoking. Lancet 2:91.

22. Cody, R. P. & Smith, J. K. (1991) Applied Statistics and the SAS Programming Language 3rd ed. 1991 North-Holland New York, NY.

23. Winer, B. J., Brown, D. R. & Michels, K. M. (1991) Statistical Principles in Experimental Design 3rd ed. 1991 McGraw-Hill New York, NY.

24. Thomson, A. & Dietschy, J. (1981) Intestinal lipid absorption: major extracellular and intracellular events. Johnson, L. eds. Physiology of the Gastrointestinal Tract 1981:1147-1220 Raven Press New York, NY. .

25. Ruppin, H., Bar-Meir, S., Soergel, K. H., Wood, C. M. & Schmitt, M. G., Jr (1980) Absorption of short-chain fatty acids by the colon. Gastroenterology 78:1500-1507.[Medline]

26. Schmitt, M. G., Jr, Soergel, K. H. & Wood, C. M. (1976) Absorption of short chain fatty acids from the human jejunum. Gastroenterology 70:211-215.[Medline]

27. Titus, E. & Ahearn, G. A. (1992) Vertebrate gastrointestinal fermentation: transport mechanisms for volatile fatty acids. Am. J. Physiol. 262:R547-R553.

28. Watson, A. J., Elliott, E. J., Rolston, D. D., Borodo, M. M., Farthing, M. J. & Fairclough, P. D. (1990) Acetate absorption in the normal and secreting rat jejunum. Gut 31:170-174.[Abstract/Free Full Text]

29. Roediger, W.E.W. (1995) The place of short-chain fatty acids in colonocyte metabolism in health and ulcerative colitis: the impaired colonocyte barrier. Cummings, J. H. Rombeau, J. L. Sakata, T. eds. Physiological and Clinical Aspects of Short-Chain Fatty Acids 1995:337-351 Cambridge University Press Cambridge, UK. .

30. Fleming, S. E. & Rodriguez, M. A. (1983) Influence of dietary fiber on fecal excretion of volatile fatty acids by human adults. J. Nutr. 113:1613-1625.

31. Lewis, S. J. & Heaton, K. W. (1997) Increasing butyrate concentration in the distal colon by accelerating intestinal transit. Gut 41:245-251.[Abstract/Free Full Text]

32. Gibson, G. R., Cummings, J. H., Macfarlane, G. T., Allison, C., Segal, I., Vorster, H. H. & Walker, A. R. (1990) Alternative pathways for hydrogen disposal during fermentation in the human colon. Gut 31:679-683.[Abstract/Free Full Text]

33. Levitt, M. D. & Ingelfinger, F. J. (1968) Hydrogen and methane production in man. Ann. N.Y. Acad. Sci. 150:75-81.[Medline]

34. Flourie, B., Pellier, P., Florent, C., Marteau, P., Pochart, P. & Rambaud, J. C. (1991) Site and substrates for methane production in human colon. Am. J. Physiol. 260:G752-G757.[Medline]

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