Dietary fiber defined as nonstarch polysaccharides (NSP) has been added to liquid formula diets in order to approach a more physiological state of nutrition. There are interesting experimental data supporting a role for fiber in artificial enteral feeding: NSP components have been shown to increase fecal bacterial mass, to favor colonic sodium and water absorption, to stimulate colonic crypt proliferation and to delay small intestinal glucose absorption. The number of controlled studies testing the effects of fiber added to liquid formulas is, however, small. Thus, there is no firm basis for the routine use of fiber-enriched formulas although these products are commercially available and in widespread clinical use. Research in this important field of digestive physiology is encouraged as many experimental data are in favor of supplementing formula diets with fiber.

Dietary Fiber↗

PubMedDate not supplied

Effect of short-chain fatty acids on the human colonic mucosa in vitro.

Fermentable dietary fiber components are known to stimulate colonic crypt proliferation. As these compounds are rapidly degraded to short-chain fatty acids (SCFAs) by the anaerobic microflora, the hypothesis was tested that this trophic effect of fiber may be mediated by SCFAs. Biopsies were taken from normal cecal mucosa of 45 individuals during routine colonoscopy. They were incubated for 3 hours with sodium salts of SCFAs at physiological concentrations (three SCFAs = acetate 60 mmol/L + propionate 25 mmol/L + butyrate 10 mmol/L; acetate 60 mmol/L; propionate 25 mmol/L; butyrate 10 mmol/L) or equimolar NaCl (control). Cell proliferation was measured autoradiographically by subsequent pulse labeling with [3H]thymidine (1 hour). The labeling index (number of labeled cells divided by the total number of cells) was computed for the crypt as a whole and for five equal crypt compartments (compartment 1 = crypt base, compartment 5 = crypt surface). Cecal crypt proliferation was raised significantly in all incubation experiments with SCFAs. Butyrate (10 mmol/L, increase + 89%) and propionate (25 mmol/L, + 70%) were as effective in stimulating proliferation as the combination of three SCFAs (+103%), although the effect of acetate (+31%) was minor. Increasing the butyrate concentration to 25 mmol/L or 60 mmol/L did not result in a further increase of cell labeling. SCFAs stimulated proliferation in the basal three crypt compartments only. An expansion of the proliferative zone to compartments 4 and 5 was not observed. SCFAs, especially butyrate and propionate, are luminal trophic factors for the cecal epithelium.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗

PubMedDate not supplied

Effect of a single oat bran cereal breakfast on serum cholesterol, lipoproteins, and apolipoproteins in patients with hyperlipoproteinemia type IIa.

Serum cholesterol-lowering effects of oat bran-enriched diets have been indicated in several studies in which oat bran was given several times a day. Concomitant changes in the daily diet, ie, a diminished energy intake or changes in the composition of fats in the diet, also have been reported and used to explain the hypocholesterolemic effect of oats. The present study was designed to replace only the conventional continental breakfast by a single oat bran cereal muesli containing 60 g of oat bran and to measure the effects of this dietetic modification on serum lipids in 13 patients with hypercholesterolemia type IIa. Compared with a 3-week baseline period, total serum cholesterol (7.38 +/- 0.35 mmol/L, mean +/- SEM) was reduced by 10.9, 8.4, and 9.7% in the first, second, and third week of oat bran ingestion (p < .01). High-density lipoprotein and low-density lipoprotein cholesterol as well as apolipoprotein A1 decreased to the same extent (8 to 11%; p < .05) during the oat bran period, whereas a pronounced reduction of 25.8% was seen for apolipoprotein B100 (p < .01), which is a major component of low-density lipoprotein. Dietary data obtained by 3-day food records at baseline, oat bran, and follow-up period did not show any differences between the study periods except for dietary fiber, which was increased from 21.9 g/day to 42.4 g/day (p < .002) during the test period because of the daily oat bran intake.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMedDate not supplied

Effects of deoxycholic acid and butyrate on mucosal prostaglandin E2 release and cell proliferation in the human sigmoid colon.

BACKGROUND: A high-fat, low-fiber diet resulting in increased excretion of fecal secondary bile acids is regarded as a major risk factor for colon cancer. Incubation of human colonic biopsies with the secondary bile acid deoxycholic acid (DCA) leads to hyperproliferation with expansion of the proliferative zone, ie, a biomarker of increased cancer risk. Antiproliferative effects on various colon cancer cell lines, however, were reported for butyrate (BUT), a fermentation product of dietary fiber. METHODS: In the following in vitro study we incubated biopsies from the normal sigmoid colon of 12 patients (age 55.8 +/- 3.6 years) with 5 microM DCA or a combination of 5 microM DCA plus 10 mM BUT (DCA/BUT) and determined epithelial proliferation by bromodeoxyuridine immunohistochemistry. As a possible mediator for the DCA effects on colonic cell proliferation, mucosal prostaglandin E2 (PGE2) release into the incubation medium was measured by 125I-PGE2 radioimmunoassay. RESULTS: Incubation with DCA alone revealed a significantly higher labeling index for the whole crypt (.17 vs .11, p < .01) and for the upper 40% of the crypt (.05 vs .01, p < .01) compared with DCA/BUT. Mucosal PGE2 release during DCA/BUT incubation showed a trend toward lower values compared with DCA incubation (357.07 vs 434.29 pg/mg per hour; p = .07). CONCLUSION: The results indicate a normalization of DCA-induced hyperproliferation of colonic epithelium by butyrate that is not clearly mediated by PGE2. Considering that nutrition affects the luminal concentrations of DCA and butyrate, our findings may have implications for colonic carcinogenesis.

Bromodeoxyuridine↗

PubMedDate not supplied

In vitro fermentation of high-amylose cornstarch by a mixed population of colonic bacteria.

BACKGROUND: Malabsorbed starch is probably the most important substrate for bacterial fermentation in the human large intestine. Fermentability of starch may depend on the composition of the colonic flora and its adaptation to the substrate supply. METHODS: Ten healthy volunteers were fed a controlled diet containing either 7.0 to 8.3 or 50.7 to 59.7 g/d of resistant starch (Hylon VII) for 4 weeks. At the end of each diet period, fecal starch concentrations were measured. Fecal samples were incubated in 48-hour batch cultures containing 10 g/L Hylon VII or digestible Lintner's starch. Bacterial breakdown of starch and short-chain fatty acid concentrations were measured at 0, 3, 6, 12, 24, and 48 hours. RESULTS: Fecal starch concentrations were higher during the Hylon VII period (35.7 +/- 16 vs 8.9 +/- 3.3 mg/g). Starch was fermented rapidly and completely in vitro in all but two subjects. Fermentability of resistant starch was comparable to that of digestible starch. No differences were found between the dietary periods. Fermentation of resistant starch produced higher rates of n-butyrate. Two subjects had substantially higher fecal starch concentrations. In vitro starch breakdown in these subjects was slow and incomplete. CONCLUSIONS: Fermentation of resistant starch by the colonic microflora was rapid and complete in 8 of 10 subjects. No adaptation of the fermentation capacity was observed after 4 weeks of dietary resistant starch supplementation. Fermentation of resistant starch increased the proportion of n-butyrate in vitro. In two subjects, fecal starch concentrations were substantially higher than in the other subjects and in vitro starch fermentation was slow and incomplete.

Adult↗

PubMedDate not supplied

[Studies on the amount of roughage consumption by healthy subjects and in gastrointestinal diseases].

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Adolescent↗

PubMedDate not supplied

Amylase activity of parotid saliva in acute and chronic pancreatitis.

The activity of the alpha-amylase was estimated in the parotid resting saliva of 17 subjects without evidence of pancreatic disease, 17 patients with chronic relapsing pancreatitis in the intervals between acute attacks, and also in 4 patients with acute pancreatitis and 3 patients with an acute attack of chronic relapsing pancreatitis. In the patients with chronic relapsing pancreatitis between attacks the concentration, output and specific activity of the salivary amylase were significantly lowered. The patients with acute pancreatitis exhibited salivary amylase concentrations in the uppper normal to grossly supranormal range, whereas those of the patients with acute attacks of chronic relapsing pancreatitis were distinctly reduced. Unlike the amylase output, the amylase concentration was independent of the rate of salivary flow. Simultaneous infusion of secretin and pancreozymin produced a significant increase in the parotid salivary amylase levels in both the patients without pancreatic disease and in those with chronic relapsing pancreatitis between acute attacks.

Acute Disease↗