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PubMedDate not supplied

Colonic digestion and absorption of energy from carbohydrates and medium-chain fat in small bowel failure.

Gut function and the degree of intestinal insufficiency or failure in short bowel patients can be quantified with respect to wet weight and energy absorption by the use of balance studies. This enables the physician to distinguish patients with extreme intestinal failure inconsistent with the restoration of intestinal autonomy by dietary manipulation from short bowel patients with borderline gut failure in whom dietary manipulations may result in the weaning from parenteral support. A high-carbohydrate, low long-chain fat diet and a diet where long-chain fat has been replaced by medium-chain triglycerides increase absorption of energy in patients with small bowel failure, provided that they have a preserved colon in continuity. This is due to the ability of the colonic flora to ferment carbohydrates malabsorbed in the small bowel to the short-chain fatty acids (SCFAs). These SCFAs are easily absorbed across the colonic mucosa resulting in a salvage of carbohydrate energy that otherwise would have been lost in feces. In contrast, long-chain fatty acids are not absorbed by the colon, and long-chain fat malabsorbed in the small bowel of short bowel patients are not retained in the large bowel. Recent work has indicated that the water soluble medium-chain fatty acids are effectively absorbed in the large bowel similar to the SCFAs. This may explain an almost complete absorption of medium-chain triglycerides in short bowel patients, even in patients with virtually no absorption of long-chain fat, and why this only occurs in patients with a colon in continuity. Manipulation of the dietary fat:carbohydrate ratio is much less efficacious in short bowel patients with no colonic function, and the use of medium-chain triglycerides has no proven effect on overall energy absorption from short bowel patients without a large bowel in continuity. Hence, the colon has increasingly important digestive functions as small bowel failure proceeds, not only when it comes to absorption of water and sodium, but also of energy from carbohydrates and medium-chain fat.

Dietary Carbohydrates↗

PubMedDate not supplied

The interactions of diet and colonic microflora in regulating colonic mucosal growth.

The colonic mucosa can adapt its growth to alterations in diet. Metabolites from colonic microflora are frequently implicated as the primary factor in mediating the colonic mucosal response to diet; however, there is also evidence indicating that diet may have a direct effect in mediating this response. The aim of this study was to determine the role of diet, microflora, and microflora metabolites in altering the growth of the colonic mucosa. Two 28-day feeding studies were conducted using Sprague-Dawley rats. The first study compared the growth of the colonic mucosa in germ-free and conventional rats fed 6 different diets. The second study compared the growth of the colonic mucosa to the concentration of bacterial-derived short-chain fatty acids (SCFs), bile acids, and ammonia. The diets that were fed consisted of (1) AIN-76a diet without dietary fiber; (2) standard AIN-76a diet, which contained 5% cellulose; (3) AIN-76a diet with 5% guar gum; (4) a "Western" human diet with 20% fat and 10% cellulose; (5) AIN-76a diet formulated to mimic Diet 4 in fat content but with 2.5% cellulose; and (6) Purina Rodent Chow. Quantitative volumetric and stereologic analysis was used to assess changes in total colonic mucosal volume as a measure of mucosal growth. In germ-free rats, Diets 2-4 and 6 induced a significant increase (18-38%) in mucosal volume compared to Diet 1. In conventional animals, only Diets 4 and 6 induced a significant increase (up to 63%) in mucosal volume compared to Diet 1. Relative to the germ-free animals, only conventional animals on Diets 4 and 6 had an increase in mucosal volume. The increases in mucosal volume in Diets 4 and 6 were not consistently associated with increased SCFAs, ammonia, or bile acids. There was a wide range in the colonic concentrations of SCFAs (2-fold), ammonia (6-fold), and bile acids (10-fold). The presence of colonic microflora in and of itself does not lead to enhanced colonic mucosal growth. Rather, there are unique interactions between specific types of diet and microflora that lead to a growth-promoting effect. This effect could not be explained by alterations in the concentration of SCFAs, ammonia, or bile acids in colonic contents.

Ammonia↗

PubMed2003

The long-term oral administration of a product derived from a probiotic, Clostridium butyricum induced no pathological effects in rats.

Recent studies have suggested that short chain fatty acids (SCFAs) exert a therapeutic effect on some human and experimental animal diseases. In our previous study, we showed that Clostridium butyricum produces high levels of SCFAs in the culture system used. In addition, an additive based on yogurt was effective in eliminating and masking the odor derived from these SCFAs in the product. Recently, we reported that the oral administration of a high concentration (50% w/w) of this product derived from Clostridium butyricum for 17 days caused no pathological abnormalities in rats. The aim of the present study was to investigate the effects of the prolonged oral administration of this product in rats. Male and female Wistar Hannover GALAS rats, 5 weeks old, were given a mixture of a standard diet plus the product derived from Clostridium butyricum (5% w/w) with 0.1% additive for 16 months (n=6). The control rats were allowed the same standard diet plus tap water (5% w/w) with 0.1% additive (n=6). After 16 months, a laparotomy was performed. A hemocyte count, and biochemical and electrolyte analyses were subsequently carried out. The esophagus, stomach, small intestine, large intestine and pancreas were investigated macroscopically and microscopically. The results showed that the rats grew normally for the duration of the experimental period. The body weights of the product-fed rats were comparable with those of the control-fed rats. There were no significant differences in the organ weight between the product- and control-fed rats, except for a significantly increased weight of the large intestine in the product-fed male rats. No pathological abnormalities were found in the hemocyte count, the biochemical and electrolyte analyses, or the macroscopic and microscopic findings.

Administration, Oral↗

PubMed2004

Clostridium butyricum, a probiotic derivative, suppresses dextran sulfate sodium-induced experimental colitis in rats.

Recent studies have suggested that probiotics or short chain fatty acids (SCFAs) exert a therapeutic effect on inflammatory bowel disease (IBD) patients. In a previous study, we demonstrated that Clostridium butyricum produces high levels of SCFAs in culture. In addition, a yogurt-based additive effectively masked, completely eliminating the unpleasant odor derived from the SCFAs. We recently reported that the oral administration of both high and low dose diets (50% w/w for 17 days and 5% w/w for 16 months, respectively) of the Clostridium butyricum derivative did not cause pathological abnormalities in rats. In the present study, we evaluated the effects of this product against dextran sulfate sodium (DSS)-induced experimental colitis in rats. Five-week-old male Wistar Hannover GALAS rats were given a mixture of a standard diet containing 3% (w/w) of DSS for 8 days. In the derivative-fed group, Clostridium butyricum derivative (20% w/w) with 0.1% (w/w) additive was also added to their diet. The control-fed group was given tap water (20% w/w) with 0.1% (w/w) additive. After 8 days, a laparotomy was performed, and macroscopic and microscopic inflammation scoring was determined. The Clostridium butyricum derivative effectively prevented bloody diarrhea. In addition, mucosal damage to the derivative-fed group was significantly reduced macroscopically compared to that of the control-fed group. The potential clinical efficacy of the Clostridium butyricum derivative in IBD patients is also discussed.

Administration, Oral↗

PubMedDate not supplied

Physiological functions of resistant proteins: proteins and peptides regulating large bowel fermentation of indigestible polysaccharide.

Animal studies have shown conclusively that feeding of resistant starch (RS) increases production of large bowel total short-chain fatty acids (SCFAs). However, fermentation products of RS may be affected considerably by other dietary ingredients. In rats fed a 20% high-amylose cornstarch (HAS) with casein as the sole protein source, greater cecal SCFAs production was observed compared with that in rats fed a regular cornstarch diet. However, with this diet, the cecal succinate production was also very high. In contrast, when rice or potato protein with lower digestibility was used in place of casein, cecal succinate production decreased with a concomitant increase in butyrate. These observations suggest that nondigested protein, namely resistant protein, might play a role in correcting an imbalance in the ratio of carbohydrate and nitrogen as fermentative substrates for cecal bacteria and in promoting butyrate production. Epidemiological and biochemical data indicate a possible linkage between the fermentation products of starch (butyrate in particular) and the prevention of colorectal cancer as well as ulcerative colits. Accordingly, a fermentation strategy of RS favoring SCFA production should be established to elucidate the potentially beneficial effects of SCFAs on large bowel physiology.

Amylose↗

PubMed2006

[The role of short chain fatty acids and lactate in regulation of the gastric secretion].

The investigation was carried out in acute experiments by means of isolated stomach perfusion by Ghosh and Shild and in chronic experiments in dogs with fistula of the stomach and duodenum. In rats with intact nervous system lactulose as the source of short chain fatty acids (SCFAs) diminished basal and stimulated by insulin, pentagastrin and histamine gastric acid secretion. By contrast it did not influence carbachol gastric acid secretion. In dogs with intact nervous system lactulose also suppressed the intensity, debit of acid and pepsin of gastric juice stimulated by insulin and histamine. It suggests that the effect of lactulose does not dependent on kinds of animals. Truncal vagotomy removed the inhibitory action of lactulose on pentagastrin and histamine gastric acid secretion in rats. SCFAs and lactic acid suppressed pentagastrin gastric acid secretion in rats. Lactulose, propionate potassium, lactate potassium enhanced the blood glucose level. Truncal vagotomy did not influence the increase of the blood glucose level evoked by lactulose. It is concluded that SCFAs decreases gastric secretion in the third intestinal phase through central inhibition. The mechanism of inhibitory action of lactic and propionic acids depends on their role in the liver gluconeogenesis which leads to increase of the blood glucose level. Hyperglycemia as it is known suppress gastric secretion through diminishing of neural cholinergic activity of nerves vagus.

Animals↗

PubMed1984

Short-chain fatty acids in the proximal gastrointestinal tract of healthy subjects.

The total concentration of short-chain fatty acids (SCFAs) in healthy subjects, measured by gas chromatography, was in saliva and jejunal aspirates (n = 6) (median (range] 4480 (2780-9940) mumol/l and 265 (185-1470) mumol/l and in gastric and duodenal aspirates (n = 7) 719 (425-1770) mumol/l and 480 (137-778) mumol/l, respectively. Acetic and propionic acid accounted for 85% and 11%, respectively, and i-butyric, n-butyric, and i-valeric for less than 2% each in jejunal aspirates. A very similar relative distribution was present also in saliva and gastric and duodenal aspirates, essentially different from that of feces. Through anaerobic culturing from jejunum, 10(3) to 10(8) bacteria/ml was obtained; there was no correlation between the log number of bacteria and the SCFAs concentration before and after ingestion of sucrose. Swallowed exogenous radiolabeled propionate was partly recovered in the jejunum. The findings indicate that the SCFAs recovered from the jejunum in healthy subjects are mainly produced in the mouth and swallowed with the saliva.

Adult↗

PubMed1996

Regulation of alpha 2A-adrenergic receptor expression in the human colon carcinoma cell line HT29: SCFA-induced enterocytic differentiation results in an inhibition of alpha 2C10 gene transcription.

Previous studies on the intestinal epithelium from various species have shown that the number of alpha 2-adrenergic receptors in immature cells from the crypts is several-fold higher than in mature cells from the villi, thus suggesting an inverse relationship between enterocytic differentiation and the expression of this inhibitory receptor. The receptor density along the surface-crypt axis of the human colonic mucosa is correlated with the amount of alpha 2C10 mRNA; however, the mechanisms underlying this regulation remain unknown. The human colonic adenocarcinoma cell line HT29, which expresses the alpha 2A-adrenergic receptor and is able to undergo enterocytic differentiation, is a suitable model with which to investigate this question in vitro. In this study, we explored the effects of short chain fatty acids (SCFAs), differentiating agents normally present in the colon lumen, on alpha 2-adrenergic receptor expression. Exposure of HT29 cells to butyrate and propionate, but not acetate, resulted in a large diminution of [3H]RX821002 binding sites. The reduction of alpha 2-adrenergic receptor number induced by butyrate or propionate was due to decreased amounts of alpha 2C10 mRNA and was associated with an increase of alkaline phosphatase activity, which reflected the emergence of a more differentiated phenotype. The changes in alpha 2C10 mRNA level induced by both SCFAs were dose-dependent, rapid, and reversible and resulted from a diminution in the transcription rate of the alpha 2C10 gene. Finally, these effects were mimicked by trichostatin A, indicating that they are triggered primarily through inhibition of histone deacetylases. The present findings demonstrate that decrease of alpha 2-adrenergic receptor expression is a very early event of the HT29 cell differentiation process. They also suggest that SCFAs, which originate from bacterial fermentation of dietary fibers, may play a role in the regulation of the alpha 2-adrenergic receptivity of colonic mucosa in vivo.

Acetates↗

PubMed2000

Downregulation of p53 by sustained JNK activation during apoptosis.

In a previous study, we prepared short-chain fatty acid (SCFA) mixtures mimicking the composition of the digested fibers from wheat bran, oat bran, pectin, and cellulose and tested the products on U4 cells, a cell-line model for normal colonocytes. These SCFA mixes induced the cyclin-dependent kinase (cdk) inhibitors p21 and p27, which bound to cdk2/cyclin E and cdk4/cyclin D1 complexes, blocking their kinase activity and arresting cell growth. SCFAs from digested fiber may control intestinal crypt height in vivo by inducing apoptosis in growth-arrested cells at the top of the crypt. In the present study, we report that SCFA mixes induced apoptosis of U4 cells and unexpectedly caused both a sustained activation of the stress-activated protein kinase c-jun N-terminal kinase 1 (JNK1) and downregulation of the tumor suppressor protein p53. JNK1 bound to p53, and the amount of JNK1-bound p53 accurately reflected the amount of total cellular p53. After activation by SCFAs, JNK1 phosphorylated its bound p53. This phosphorylation is likely to have converted p53 into an apoptotic target because p53 breakdown correlated with caspase-3 activity, was inhibited by a caspase-3 inhibitor in a dose-dependent manner, and was inhibited by transfection of dominant-negative JNK1. Because JNK1 activation was sustained in SCFA-treated U4 cells, JNK1 can bind, phosphorylate, and release p53 for proteolysis and then continue this cycle until many p53 molecules have been phosphorylated. Loss of p53 protein was likely due to proteolysis and not to transcriptional changes because a sixfold decrease in p53 protein occurred within 3-24 h of SCFA treatment, whereas p53 mRNA levels were downregulated as much only after 2-3 d. SCFA mixes targeted p53 and possibly other cellular proteins for degradation during apoptosis by causing a sustained activation of JNKs.

Apoptosis↗

PubMed2004

Novel physiological function of fructooligosaccharides.

Two key properties of short chain fructooligosaccharides (sc-FOS) which lead to physiological functions are indigestibility in the small intestine and fermentability in the colon. Sc-FOS is converted into short chain fatty acids (SCFAs) by intestinal bacteria in the colon and absorbed. Through the metabolic pathway, sc-FOS improves gastrointestinal (GI) condition such as relief from constipation, formation of preferable intestinal microflora and intestinal immunomodulation those are known as prebiotics' function. Besides improvement of GI condition, dietary sc-FOS influences on calcium and magnesium absorption in the colon. A major mineral absorption site is the small intestine, but the colon also works as a Ca and Mg absorption site with an aid of SCFAs made from sc-FOS. Furthermore dietary sc-FOS influences on bioavailability of soy-isoflavones. Plasma and urinal concentration of Genistein and Daidzein, aglycones of Daidzin and Genistin, are higher in the rat fed with sc-FOS than the control rat. An additive effect of dietary isoflavone and sc-FOS was observed on the bone mineral density in OVX mice and moreover sc-FOS increased ceacal beta-glycosidase activity and equol production. These results suggest that FOS increase the bioavailability of isoflavones.

Animals↗

PubMed2026

Mechanistic Insights Into the Association Between Gut Microbiota Diversity and Atherosclerosis, Acute Coronary Syndrome, and Peripheral Arterial Disease Progression.

BACKGROUND: The gut microbiome has emerged as a potential contributor to cardiovascular diseases (CVDs), including atherosclerosis, acute coronary syndrome (ACS), and peripheral arterial disease (PAD). While observational studies link dysbiosis to CVD, causal relationships remain uncertain. METHODS: This narrative review synthesizes evidence from human observational studies, clinical interventions, and experimental models to distinguish association from mechanistic plausibility and clinical causality. Literature was searched through July 2026 in PubMed/MEDLINE, Web of Science, and Scopus. RESULTS: Microbial metabolites-including trimethylamine N-oxide (TMAO), short-chain fatty acids (SCFAs), bile acids, and lipopolysaccharide (LPS)-modulate endothelial function, immune cell programming, platelet activity, and plaque stability through receptor-mediated signaling and epigenetic regulation. SCFAs demonstrate potentially protective effects via GPCR and HDAC pathways, while TMAO is associated with atherothrombotic risk. However, much mechanistic evidence derives from preclinical studies. Heterogeneity from diet, geography, host characteristics, renal function, and medications substantially influences microbiota-CVD associations. CONCLUSION: The gut-vascular connection is biologically plausible, but definitive clinical causality remains unproven. Microbiome-directed therapies (dietary modulation, pre/pro/synbiotics, targeted metabolite inhibition) are investigational. Prospective, standardized, adequately powered human studies with clinically meaningful outcomes are essential before routine cardiovascular application.

Gastrointestinal Microbiome↗

PubMed2005

Effects of the nematode Gyrinicola batrachiensis on development, gut morphology, and fermentation in bullfrog tadpoles (Rana catesbeiana): a novel mutualism.

We describe a novel mutualism between bullfrog tadpoles (Rana catesbeiana) and a tadpole-specific gastrointestinal nematode (Gyrinicola batrachiensis). Groups of tadpoles were inoculated with viable or nonviable nematode eggs, and development, morphology, and gut fermentation activity were compared between nematode-infected and uninfected tadpoles. Nematode infection accelerated tadpole development; the mean time to metamorphosis was 16 d shorter and the range of times to metamorphosis was narrower in nematode-infected tadpoles than in uninfected tadpoles. At metamorphosis, infected and uninfected bullfrogs did not differ in body size or condition. Colon width, wet mass of colon contents, and concentrations of most fermentation byproducts (short-chain fatty acids: SCFAs) in the hindgut were greater in infected tadpoles. Furthermore, in vitro fermentation yields for all SCFAs combined were over twice as high in infected tadpoles than in uninfected tadpoles. One explanation for accelerated development in infected tadpoles is the altered hindgut fermentation associated with the nematodes. Energetic contributions of fermentation were estimated to be 20% and 9% of the total daily energy requirement for infected and uninfected tadpoles, respectively. Infection by G. batrachiensis nematodes potentially confers major ecological and evolutionary advantages to R. catesbeiana tadpoles. The mutualism between these species broadens our understanding of the taxonomic diversity and physiological contributions of fermentative gut symbionts and suggests that nematodes inhabiting the gut regions of other ectothermic herbivores might have beneficial effects in those hosts.

Animals↗

PubMed1999

In vitro studies on active calcium absorption from ovine rumen.

From various in vivo and in vitro studies it has been shown that the rumen represents a significant site of Ca2+ absorption in sheep and goats. It was the aim of the present study to further characterize the underlying mechanisms. Unidirectional flux rates of Ca2+ across rumen wall epithelia of sheep were measured in vitro by applying the Ussing-chamber technique in the absence of electrochemical gradients. Under these conditions, significant Ca2+ net flux rates (Jnet) clearly indicate the presence of active mechanisms for Ca2+ transport. Short chain fatty acids (SCFAs) caused highest stimulation of Ca2+ Jnet (6.3 +/- 1.9 nmol.cm-2.h-1) when used as a mixture of acetate, proprionate and butyrate in physiological proportions (36, 15, 9 mmol.l-1, respectively). The effect of 30 mmol.l-1 butyrate (3.2 +/- 0.6 nmol.cm-2.h-1) was higher than respective amounts of propionate and acetate (0.6 +/- 0.8 nmol.cm-2.h-1 and 0.9 +/- 0.8 nmol.cm-2.h-1, respectively). Eliminating SCFAs resulted in Ca2+ Jnet of 0.4 +/- 1.1 nmol.cm-2.h-1. Addition of Ca channel blocker verapamil (mucosal 1 mmol.l-1) had no significant effect on SCFA-stimulated Jnet of Ca2+, whereas application of Na+/H- inhibitor amiloride (mucosal 1 mmol.l-1) further enhanced the Ca2+ Jnet by > 65%. The Ca(2+)-pump inhibitor vanadate had no significant effect on Jnet of Ca2+. Dietary Ca depletion enhanced calcitriol plasma concentrations but had no effect on active Ca2+ absorption across the rumen wall of sheep. In addition, no effect on active Ca2+ absorption could be observed during early lactation. In conclusion, there is clear evidence for the rumen as a main site for active Ca2+ absorption in sheep. Our results suggest the presence of a Ca2+/H+ exchange mechanism in the apical membrane of rumen epithelial cells which depends on SCFA absorption and which does not seem to be under the control of calcitriol. Basolateral Ca2+ extrusion occurs independently from Ca(2+)-pump activity and may be accomplished via Na+/Ca2+ exchange.

Absorption↗

PubMed2000

Total artificial nutrition is associated with major changes in the fecal flora.

BACKGROUND: Animal studies have demonstrated dramatic changes in the intestinal flora during total enteral (TEN) or parenteral (TPN) nutrition. AIM OF THE STUDY: To assess the impact of TEN and TPN on human intestinal microflora. METHODS: Eight patients on fiber-free TEN, five patients on TPN, and ten controls were studied. Fecal bacteria were identified and numbered (logCFU/g feces), and fecal short-chain fatty acids (SCFAs) were measured in stool samples, by gas-liquid chromatography. RESULTS: In TEN patients, compared to controls (P < 0.01), aerobes were increased (8.46 +/- 0.24) while anaerobes were decreased (5.79 +/- 0.84). In TPN patients, both aerobes and anaerobes were decreased compared to controls (5.64 +/- 0.27 and 5.31 +/- 1.09 respectively, P < 0.01). Total SCFAs were lower in TPN patients than in TEN patients (48.3 +/- 16.6 vs 118.6 +/- 24.1 mmol/kg, P < 0.05). CONCLUSIONS: Both TPN and TEN induce modifications in the intestinal microflora. During TPN, a homogeneous decrease occurs in both aerobic and anaerobic bacteria. TEN decreases only anaerobic bacteria, while aerobic bacteria are increased. This imbalance may play a role in the pathophysiology of TEN-induced diarrhea.

Bacteria, Aerobic↗

PubMed1994

Inhibition of short-chain fatty acid absorption and Na+ absorption during acute colitis in the rabbit.

BACKGROUND/AIMS: Short-chain fatty acids (SCFAs) provide energy for colonocytes and stimulate colonic fluid and electrolyte absorption. The impact of acute colitis on SCFA-stimulated Na+ absorption and SCFA absorption was examined. METHODS: Proximal colon from rabbits infected with Yersinia entercolitica, a pair-fed group, and controls was mounted in Ussing chambers, and Na+ transport, short-circuit current, and tissue conductance were examined during a basal period and after stimulation with the SCFAs, butyrate, or propionate. Propionate transport and luminal SCFA concentration were evaluated. RESULTS: Butyrate and propionate stimulated electroneutral Na+ absorption above basal levels in the control and pair-fed groups, as evidenced by significant increases in mucosal-to-serosal and net Na+ fluxes with no change in serosal-to-mucosal flux, short-circuit current, or conductance. Butyrate-stimulated Na+ absorption and propionate absorption were blocked by amiloride, an inhibitor of Na(+)-H+ exchange. In the infected group, both butyrate and propionate failed to stimulate colonic Na+ absorption above basal levels. Propionate absorption was inhibited, and epinephrine failed to stimulate Na+ or propionate absorption. Luminal SCFA concentrations were increased in acute colitis. CONCLUSIONS: Inhibition of SCFA-stimulated Na(+)-H+ exchange and SCFA absorption contribute to the diarrheal fluid loses observed in acute colitis and may reduce colonocyte energy supply.

Acute Disease↗

PubMed1990

Enteral nutrition and the function of the intestinal microflora in healthy adults.

An oral feeding formula was given to 5 healthy volunteers for 8 days. Faecal samples were collected before, during and after the feeding period. The effect of enteral nutrition (EN) on the following seven intestinal microflora-associated characteristics (MACs) was studied: formation of urobilinogen, coprostanol and deoxycholic acid, degradation of mucin and beta-aspartylglycine, faecal tryptic activity, and production of short-chain fatty acids (SCFAs). None of the microbial functions studied were lost during the study. The urobilinogen level increased during EN (P < 0.05) but it seems reasonable to assume that this was a concentration effect due to a decrease in stool mass. The concentration of SCFAs decreased during EN (P < 0.05) and this reflects the absence of dietary fibre in the feed used.

Journal Article↗

PubMed1994

Fibre utilization by Kalahari dwelling subterranean Damara mole-rats (Cryptomys damarensis) when fed their natural diet of gemsbok cucumber tubers (Acanthosicyos naudinianus).

Kalahari dwelling Damara mole-rats (Cryptomys damarensis) naturally feed on a high fibre diet of underground gemsbok cucumber tubers, Acanthosicyos naudinianus. We investigated the degree of fibre utilization and fermentation on this diet by measuring caecal characteristics (namely temperature, pH and weight) and in vitro rates of gas and short chain fatty acid (SCFA) production in these underground dwelling hind-gut fermentors. Rectal temperatures (33.8 +/- 0.6 degrees C) were consistently higher than caecal temperatures (33.3 +/- 0.6 degrees C). Furthermore, a 0.8 degrees C gradient of temperatures existed within the caecum, with the lowest temperature occurring in the corpus caeci. Both rates of gas production (4.74 +/- 0.6 ml/g dry matter/hr) and SCFA production (266.80 +/- 9.251 mumol/caecum per hr) were high, with proportionately more acetic acid produced than any other SCFA. Nevertheless, the initial concentrations of SCFAs present in the caecum were low (52 +/- 17 mM) implying a rapid rate of absorption of these SCFAs. The high rates of fermentation provide a considerable amount of energy that would otherwise be trapped in fibre and thus unavailable to the animal. This highly efficient caecal fermentation enables the Damara mole-rat to maximally exploit the underground food resources in the arid-zone ecotope.

Animals↗

PubMed1989

Oxidative metabolism of rabbit and rat intestine with short chain fatty acids and glucose: an evaluation of data analysis.

1. Glucose sustained VO2 of rabbit ileum, caecum, and distal colon better than SCFAs. 2. In rabbit proximal colon, while VO2 was stimulated in the presence of butyrate it was not sustained. 3. Rat caecum utilized glucose but it was not necessarily the best substrate for either the ileum or colon of this species and SCFAs appeared to stimulate VO2 of rat ileum and inhibit VO2 in rat caecum and colon. 4. It was concluded from the comparison of the two methods of data analyses that curve-fitting the data by a negative exponential equation provides for a more clear and in depth interpretation of such studies.

Animals↗