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Biomedical subjects

W Scheppach

Publications and source records attributed to W Scheppach.

At least 55 records · Page 3Linked to original sources
PubMed1996

Treatment of distal ulcerative colitis with short-chain fatty acid enemas. A placebo-controlled trial. German-Austrian SCFA Study Group.

Rectal enemas containing a short-chain fatty acid mixture, butyrate alone, or saline placebo were administered to 47 patients with active distal ulcerative colitis. Enemas were instilled twice daily and the patients' condition was evaluated at entry and after four and eight weeks of local therapy. A disease activity index, chosen as the major end point, decreased significantly after all three modes of treatment with no difference among groups. The endoscopic appearance of the mucosa and the histologic degree of inflammation was not different among groups. After eight weeks, fewer colonic segments were affected endoscopically following butyrate than placebo treatment. This study showed trends towards a beneficial effect of topical short-chain fatty acids in active ulcerative colitis, but more patients are needed to demonstrate this effect with sufficient statistical power.

Adult↗
PubMed1996

Antagonistic effects of sulfide and butyrate on proliferation of colonic mucosa: a potential role for these agents in the pathogenesis of ulcerative colitis.

It has been shown that feces of patients with ulcerative colitis uniformly contain sulfate reducing bacteria. Sulfide produced by these bacteria interferes with butyrate-dependent energy metabolism of cultured colonocytes and may be involved in the pathogenesis of ulcerative colitis. Mucosal biopsies from the sigmoid rectum of 10 patients (no caner, polyps, inflammatory bowel disease) were incubated with either NaCl, sodium hydrogen sulfide (1 mmol/L), a combination of both sodium hydrogen sulfide and butyrate (10 mmol/L), or butyrate. Mucosal proliferation was assessed by bromodeoxyuridine labeling of cells in S-phase. Compared to NaCl, sulfide increased the labeling of the entire crypt significantly, by 19% (p < 0.05). This effect was due to an expansion of the proliferative zone to the upper crypt (compartments 3-5), where the increase in proliferation was 54%. Sulfide-induced hyperproliferation was reversed when samples were coincubated with sulfide and butyrate. The study shows that sodium hydrogen sulfide induces mucosal hyperproliferation. Our data support a possible role of sulfide in the pathogenesis of UC and confirm the role of butyrate in the regulation of colonic proliferation and in the treatment of UC.

Biopsy↗
PubMed1996

Effects of fish oil on fecal bacterial enzymes and steroid excretion in healthy volunteers: implications for colon cancer prevention.

Diet-induced changes in fecal excretion of secondary bile acids, certain neutral sterols, and bacterial enzyme activities are known to play a role in colon cancer development. Dietary fish oil (FO) has been implicated as a protective agent in colon carcinogenesis. In the present study, the effects of FO and corn oil (CO) on these fecal parameters were investigated in 24 healthy volunteers consuming a low- or a high-fat diet (30% or 50% of energy derived from fat). After four weeks of FO or CO supplementation (4.4 g of n-3 fatty acids/day), no significant differences were noted for fecal activities of beta-glucuronidase, beta-glucosidase, and sulfatase, nor was fecal bile acid excretion significantly affected by FO or CO consumption. However, daily excretion of the putative colon carcinogen 4-cholesten-3-one was significantly lower in the FO than in the CO period during low- and high-fat experiments. This may be another biochemical mechanism by which FO exerts its protective effect on colon cancer development.

Adult↗
PubMed1996

Effect of L-glutamine and n-butyrate on the restitution of rat colonic mucosa after acid induced injury.

BACKGROUND: L-glutamine and n-butyrate are important nutrients for colonocytes affecting both their structure and function. The effect of these epithelial substrates on resealing of rat distal colon after acid induced injury was studied. METHODS: Isolated colonic mucosa of 32 rats was mounted in Ussing chambers and exposed to Krebs-Ringer solution for four hours. Epithelial injury was induced by short-term exposure to luminal hydrochloric acid and resealing was studied with or without added glutamine or butyrate. RESULTS: Glutamine (luminal and serosal) reduced tissue conductance, mannitol and lactulose permeability, and permeation of enteropathogenic Escherichia coli. Glutamine (serosal) diminished conductance and mannitol permeability. Both interventions stimulated bromodeoxyuridine incorporation in nuclei of colonocytes. Luminal butyrate had no measurable effect on these parameters. CONCLUSIONS: These data suggest that L-glutamine stimulates repair mechanisms of rat colonic mucosa after acid injury. This effect on the gut barrier is associated with a stimulation of crypt cell proliferation. The addition of glutamine to parenteral solutions may be beneficial for patients under intensive care whose intestinal barrier is weakened in the course of sepsis and trauma.

Animals↗
PubMed1995

[Modification of fecal bile acid excretion by fish oil in healthy probands].

Several studies indicated a protective effect of fish oil on colon carcinogenesis which might be due to alterations in prostaglandin E2 synthesis of the colonic mucosa. Additional effects on fecal bile acid excretion may also play a role since especially secondary bile acids are known to act as promoters in colon cancer development. In the present study possible influences on bile acid excretion were investigated in 12 healthy volunteers whose daily diet was supplemented for 4 weeks with 11 g of fish oil (FO) and corn oil (CO) per day, respectively. Fecal bile acids were analyzed by gas-liquid-chromatography. Fecal excretion of total bile acids was not different during the periods of FO and CO-supplementation (301.9 vs. 320.3 mg/day). However, a non-significant trend to a lower daily excretion of the secondary bile acid lithocholic acid was found after FO compared to CO-ingestion (99.6 vs. 109.4 mg/day; p = 0.22). Since secondary bile acids are known promoters of colon carcinogenesis, these findings may implicate a favorable situation with respect to colon cancer prevention.

Adult↗
PubMed1995

Influence of starch fermentation on bile acid metabolism by colonic bacteria.

Secondary bile acids (BA) may be involved in the pathogenesis of colorectal cancer. In vivo, starch malabsorption has been shown to reduce fecal excretion of secondary BA. The present in vitro study was performed to investigate the effect of starch fermentation on BA metabolism by colonic bacteria. Fecal samples of healthy volunteers were incubated in anaerobic batch cultures for 48 hours with the primary bile acids cholic (0.6 g/l) and chenodeoxycholic acid (0.4 g/l). Media were starch free or enriched with starch (10 g/l). The pH was controlled and held at 6 or 7. In the starch-free incubations, secondary BA were rapidly formed, and degradation of primary to secondary BA was complete within 24 hours. The formation of secondary BA was partially inhibited by the addition of starch to the media. This effect was stronger at pH 6 than at pH 7. Starch was rapidly and completely fermented. In conclusion, this study showed that formation of secondary BA by fecal bacteria is inhibited when starch is simultaneously fermented, an effect that is mainly, but not completely, explained by reduction of pH.

Bacteria, Anaerobic↗
PubMed1995

Missing anti-proliferative effect of fish oil on rectal epithelium in healthy volunteers consuming a high-fat diet: potential role of the n-3:n-6 fatty acid ratio.

Several studies have indicated dietary fish oil (FO) as a protective agent in colon carcinogenesis. Rectal cell proliferation as an intermediate biomarker of cancer risk was shown to be reduced by dietary FO in patients with adenomatous polyps and healthy subjects consuming a low-fat diet. Because the synthesis of prostaglandins (PG) which seem to be involved in this process is dependent on the ratio of n-3:n-6 fatty acids in the diet, the present study was designed to investigate whether this FO effect is also detectable in volunteers eating a high-fat diet (50% of energy) with a low n-3:n-6 ratio of 0.25. Twelve healthy volunteers received in addition to a controlled basal diet either FO (4.4 g n-3 fatty acids/day) or corn oil supplements (double-blind, crossover) for two 4-week periods. No significant differences between the two study periods were found for rectal cell proliferation as assessed by bromodeoxyuridine immunohistochemistry and ornithine decarboxylase activity, as well as for mucosal PGE2 release and mucosal membrane fatty acid composition. The results emphasize the importance of dietary n-3:n-6 ratio in determining the effects of FO on rectal cell proliferation.

Administration, Oral↗
PubMed1995

[Hydrogen metabolism in the large intestine--physiology and clinical implications].

During the anaerobic metabolism of the colonic bacterial flora short chain fatty acids and the gases hydrogen (H2) and carbon dioxyde (CO2) are produced. In about 50% of a European and North-American population and in 90% of rural black Africans, methane is generated from H2 and CO2. In methane-negative individuals, sulfate reducing bacteria utilize H2 to reduce sulfate to sulfide. Methanogenesis and sulfate reduction are usually mutually exclusive. A competition exists for the common substrate hydrogen which is potentially regulated by the availability of sulfate in the colonic lumen. Other bacteria can use H2 to reduce CO2 to acetate (homoacetogenesis). Methane is an inert gas and has probably no direct effect in man. The metabolites of sulfate reduction (mercaptides, hydrogen sulfide) are toxic and hydrogen sulfide is supposed to play a role in the pathogenesis of ulcerative colitis. All H2-utilizing metabolisms reduce the gaseous volume in the colon and thus prevent flatulence. In patients with pneumatosis cystoides intestinalis methanogenesis is absent and sulfate reduction is insignificant. This deficiency provides an explanation for the massive H2-excretion in those patients and their symptoms.

Colitis, Ulcerative↗
PubMed1995

[Nonobstructive mesenteric ischemia--a diagnostic problem in internal intensive care].

Four cases of acute gut ischemia in elderly patients due to non-occlusive disease (NOD) are presented. Bowel necrosis occurred after episodes of hypotension in the course of myocardial infarction, arrhythmias and sepsis. Symptoms and clinical findings were blurred by the underlying extraintestinal disease. Angiography showed coexistent atherosclerosis but no occlusion of the major celiac and mesenteric vessels. At laparotomy (three cases) or autopsy (one case) extensive small and large bowel necroses were detected. Early laparotomy (possibly preceded by laparoscopy) is recommended for patients with suspected acute gut ischemia even if angiography fails to reveal occlusion of the large splanchnic arteries.

Aged↗
PubMed1994

Effect of free glutamine and alanyl-glutamine dipeptide on mucosal proliferation of the human ileum and colon.

BACKGROUND/AIMS: Glutamine (Gln) is considered a trophic factor for small intestinal epithelia, which is important during severe illness. Its use in parenteral nutrition is precluded by its instability, a problem that may be overcome by use of the stable dipeptide L-alanyl-L-glutamine (Ala-Gln). The hypothesis was tested that Gln or Ala-Gln may stimulate cell proliferation not only in the ileum but also in the proximal and distal colon and, thus, may contribute to the gut barrier function. METHODS: Biopsy samples from the normal human ileum, proximal colon, and rectosigmoid were incubated for 4 hours with Gln (2 mmol/L), Ala-Gln (2 mmol/L), and saline (control). Cells in S phase were labeled with bromodeoxyuridine. In longitudinal crypt sections labeled and quiescent cells were counted. RESULTS: Gln as well as Ala-Gln stimulated crypt cell proliferation in the ileum, proximal colon, and rectosigmoid colon. In ileal specimens, labeling was greater in the entire crypt, whereas in both colonic regions, the trophic effect was confined to the basal crypt compartments. CONCLUSIONS: Gln and Ala-Gln have trophic effects not only in the ileum, but also in the proximal and distal colon. This could be important during parenteral nutrition when mucosal atrophy may weaken the gut barrier.

Adult↗
PubMed1994

Does yogurt enriched with Bifidobacterium longum affect colonic microbiology and fecal metabolites in health subjects?

Diet-induced changes in the colonic microflora seem to play a role in colon carcinogenesis. In this study the effects of a yogurt (500 mL/d for 3 wk) enriched with Bifidobacterium longum and 5 g lactulose/L (A) on the fecal bacterial flora and various risk indexes for colon carcinogenesis were tested in 12 healthy volunteers and compared with a conventional yogurt (B). Increased excretion of bifidobacteria (P < 0.017) was found after consumption of both yogurts compared with the prestudy periods, whereas cultural counts of aerobes and anaerobes were not different. Breath-hydrogen exhalation was elevated and mouth-to-cecum transit time was accelerated in the period of yogurt A ingestion (P < 0.05) whereas no differences were found for oral-anal mean transit time, stool weight and pH, and fecal concentrations of short-chain fatty acids, bile acids, and neutral sterols. The results generally indicate great stability of the human fecal flora to this kind of dietary intervention.

Adult↗
PubMed1994

Effects of short chain fatty acids on gut morphology and function.

Short chain fatty acids (SCFAs) are the products of colonic bacterial degradation of unabsorbed starch and non-starch polysaccharide (fibre). They are important anions in the colonic lumen, affecting both colonocyte morphology and function. The three main acids (acetate, propionate, and butyrate) stimulate colonic sodium and fluid absorption and exert proliferative effects on the colonocyte. Experimental animal studies have shown that they promote adaptive responses to small intestinal resection and colonic anastomosis. Acetate increases colonic blood flow and enhances ileal motility. Butyrate has been shown to be the preferred energy substrate for the colonocyte and to be a potent differentiating agent in cell culture. Butyrate may also have a role in preventing certain types of colitis. A diet low in resistant starch and fibre, which will result in a low production of SCFAs in the colon, may explain the high occurrence of colonic disorders seen in the Western civilization.

Cell Differentiation↗
PubMed1994

Antagonistic effects of deoxycholic acid and butyrate on epithelial cell proliferation in the proximal and distal human colon.

Colon cancer is a major malignant disease in Western countries where--for unknown reasons--it occurs predominantly in the distal colon. Fecal secondary bile acids are an important risk factor whereas butyrate may be a protective agent. In this in-vitro study biopsies from the normal ascending and sigmoid colon of 24 subjects were incubated with 5 microM DCA (proximal vs. sigmoid colon) or DCA and DCA plus 10 mM butyrate (DCA vs. DCA/BUT, only sigmoid colon) and cell proliferation measured by bromodeoxyuridine immunohistochemistry. Whole crypt labeling index (LI) after DCA-incubation was similar in the ascending (15.4%) and sigmoid colon (15.4%) indicating an equal mucosal response of the two colonic subsites to DCA. Compared to DCA/BUT, incubation with DCA alone resulted in a significantly higher LI for the whole crypt (16.8 vs. 11.4%, p < 0.01) and for the upper 40% of the crypt (4.5 vs. 0.8%, p < 0.01). This may indicate a butyrate-related decrease in the susceptibility for colon cancer. Since luminal concentrations of DCA and butyrate are influenced by dietary interventions the findings of this study may be of particular interest with regard to colon cancer development and prevention.

Butyrates↗
PubMed1993

Proliferation of human colonic mucosa as an intermediate biomarker of carcinogenesis: effects of butyrate, deoxycholate, calcium, ammonia, and pH.

A high-fat/high-protein diet has been reported to promote colon cancer by increasing luminal bile acid and ammonia concentrations, whereas butyrate, calcium, and low colonic pH may have protective effects. In this study, bromodeoxyuridine labeling of colonic epithelium was investigated after incubating biopsies from the ascending colon of 70 patients with HCl (20 mM, pH 6.0), butyric acid (H-BUT, 20 mM, pH 6.0), sodium butyrate (Na-BUT, 10 mM, pH 8.0), CaCl2 (10 mM), calcium butyrate (Ca-BUT, 10 mM), ammonium butyrate (NH4-BUT, 10 mM), deoxycholic acid (DCA, 5 microM), and a combination of DCA and Na-BUT (DCA/Na-BUT, 5 microM/10 mM). Compared to NaCl, H-BUT and Na-BUT increased the whole crypt-labeling index significantly, whereas HCl and CaCl2 had no effect. Reduced labeling, however, occurred with Ca-BUT in comparison to equimolar Na-BUT. No differences in the labeling indexes were found for NH4-BUT compared to Na-BUT, but increased labeling with expansion of the proliferative zone to the upper 40% of the crypt was seen with DCA compared to NaCl. DCA-induced hyperproliferation was abolished by coincubation with DCA/Na-BUT. These data suggest that butyrate, calcium, and DCA have complex influences on mucosal proliferation. Since luminal concentrations of these compounds are influenced by dietary interventions, the findings of this study may be of particular interest with regard to colon cancer development and prevention.

Adult↗
PubMed1993

[Acute pancreatitis and stomach wall necrosis caused by cholesterol embolisms].

A 60-year-old man was hospitalized because of a sudden onset of severe pain in the epigastrium and haematemesis. Acute pancreatitis was diagnosed on the basis of an increased serum amylase concentration (642 U/l). Abdominal ultrasound and computed tomography demonstrated a necrotic zone with central liquefaction in the tail of the pancreas adjoining the stomach wall. Gastroscopy revealed as source of the bleeding an extensive mucosal necrosis at the greater curvature of the stomach. At laparotomy, partial resection of the pancreas, gastrectomy and splenectomy were performed. Histological examination of the resected specimens showed multiple cholesterol emboli in the small arteries of the pancreas and the gastric submucosa.

Acute Disease↗
PubMed1993

Effects of fish oil on rectal cell proliferation, mucosal fatty acids, and prostaglandin E2 release in healthy subjects.

BACKGROUND: Experimental studies have indicated dietary fish oil as a protective agent in colon carcinogenesis. Prostaglandins have been suggested to be involved in this process. In the present study, the effects of fish oil on rectal cell proliferation (i.e., intermediate biomarker of cancer risk), mucosal membrane fatty acids, and prostaglandin E2 (PGE2) release were investigated in 12 healthy volunteers. METHODS: In addition to a controlled basal diet, the test subjects received either fish oil (4.4 g omega-3 fatty acids/day) or corn oil supplements for two 4-week periods in a double-blind, crossover trial. Rectal cell proliferation was determined by bromodeoxyuridine immunohistochemistry and ornithine decarboxylase activity. After 2-hour incubation with bromodeoxyuridine, PGE2 concentration in the incubation medium was measured by radioimmunoassay. Mucosal membrane fatty acids were analyzed by gas chromatography. RESULTS: Bromodeoxyuridine labeling index (9.2% vs. 10.9%; P < 0.05), ornithine decarboxylase activity (19.7 vs. 36.4 pmol.mg protein-1.h-1; P < 0.005), and PGE2 release from rectal biopsy specimens (435.5 vs. 671.5 pg/mg wet tissue; P < 0.05) were significantly lower during the fish oil than the corn oil period, whereas membrane fatty acids were not statistically different. CONCLUSIONS: The results support the hypothesis that dietary fish oil may protect against colon cancer.

Adult↗
PubMed1993

Impaired hydrogen metabolism in pneumatosis cystoides intestinalis.

BACKGROUND: Pneumatosis cystoides intestinalis (PCI) is characterized by high levels of breath hydrogen. Clinical features of PCI may be due to abnormal H2 metabolism. METHODS: Breath levels of H2 and CH4 were measured in 3 patients and total gas in 2 patients with PCI on a polysaccharide-free (basal) diet and after administration of 15 g of lactulose. Metabolic activities and counts of methanogenic (MB) and sulfate-reducing (SRB) bacteria were measured in feces. Ten volunteers were also studied. RESULTS: Total H2 levels in patients were 383-420 mL/day on the basal diet and 1430-1730 mL/day after lactulose administration compared with 35 +/- 6 mL/day and 262 +/- 65 mL/day, respectively, in controls. Basal breath H2 levels in controls were 27 +/- 6 vs. 214 +/- 27 mL/day in patients and after lactulose ingestion, 115 +/- 18 vs. 370 +/- 72 mL/day. Four controls were methanogenic and had high fecal MB counts. The other controls had high SRB counts and sulfate reduction rates. All patients were nonmethanogenic and had low sulfate reduction rates. CONCLUSIONS: Patients with PCI excrete more H2 than controls. In normal subjects, H2 is consumed by MB or SRB; the activity of these bacteria is virtually absent in PCI. This may explain the gas accumulation in these patients.

Adult↗