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Biomedical subjects

T Menzel

Publications and source records attributed to T Menzel.

At least 19 recordsLinked to original sources
PubMed2006

Effect of isomalt consumption on faecal microflora and colonic metabolism in healthy volunteers.

Due to its low digestibility in the small intestine, a major fraction of the polyol isomalt reaches the colon. However, little is known about effects on the intestinal microflora. During two 4-week periods in a double-blind, placebo-controlled, cross-over design, nineteen healthy volunteers consumed a controlled basal diet enriched with either 30 g isomalt or 30 g sucrose daily. Stools were collected at the end of each test phase and various microbiological and luminal markers were analysed. Fermentation characteristics of isomalt were also investigated in vitro. Microbiological analyses of faecal samples indicated a shift of the gut flora towards an increase of bifidobacteria following consumption of the isomalt diet compared with the sucrose diet (P<0.05). During the isomalt phase, the activity of bacterial beta-glucosidase decreased (P<0.05) whereas beta-glucuronidase, sulfatase, nitroreductase and urease remained unchanged. Faecal polyamines were not different between test periods with the exception of cadaverine, which showed a trend towards a lower concentration following isomalt (P=0.055). Faecal SCFA, lactate, bile acids, neutral sterols, N, NH3, phenol and p-cresol were not affected by isomalt consumption. In vitro, isomalt was metabolized in several bifidobacteria strains and yielded high butyrate concentrations. Isomalt, which is used widely as a low-glycaemic and low-energy sweetener, has to be considered a prebiotic carbohydrate that might contribute to a healthy luminal environment of the colonic mucosa.

Adult↗
PubMed2005

Effects of isomalt consumption on gastrointestinal and metabolic parameters in healthy volunteers.

The polyol isomalt (Palatinit) is a well established sugar replacer. The impact of regular isomalt consumption on metabolism and parameters of gut function in nineteen healthy volunteers was examined in a randomised, double-blind, cross-over trial with two 4-week test periods. Volunteers received 30 g isomalt or 30 g sucrose daily as part of a controlled diet. In addition to clinical standard diagnostics, biomarkers and parameters currently discussed as risk factors for CHD, diabetes or obesity were analysed. Urine and stool Ca and phosphate excretions were measured. In addition, mean transit time, defecation frequency, stool consistency and weight were determined. Consumption of test products was affirmed by the urinary excretion of mannitol. Blood lipids were comparable in both phases, especially in volunteers with hyperlipidaemia, apart from lower apo A-1 (P=0.03) for all subjects. Remnant-like particles, oxidised LDL, NEFA, fructosamine and leptin were comparable and not influenced by isomalt. Ca and phosphate homeostasis was not affected. Stool frequency was moderately increased in the isomalt phase (P=0.006) without changes in stool consistency and stool water. This suggests that isomalt is well tolerated and that consumption of isomalt does not impair metabolic function or induce hypercalciuria. In addition, the study data indicate that isomalt could be useful in improving bowel function.

Adult↗
PubMed2003

Expression of the cathelicidin LL-37 is modulated by short chain fatty acids in colonocytes: relevance of signalling pathways.

BACKGROUND AND AIMS: Short chain fatty acids (SCFA) exert profound effects on the colonic mucosa. In particular, SCFA modulate mucosal immune functions. The antimicrobial cathelicidin LL-37 is expressed by colon epithelial cells. In the present study the effect of SCFA on LL-37 expression was investigated. METHODS: LL-37 expression in vivo was assessed by immunohistochemistry. Real time quantitative reverse transcription-polymerase chain reaction was employed to determine LL-37 expression in colonocytes in vitro after treatment with various cytokines, SCFA, or flavone. LL-37 levels were correlated to cell differentiation which was determined by alkaline phosphatase (AP) activity. In addition, intracellular signalling pathways such as MEK-ERK (mitogen/extracellular signal protein kinase (MEK)/extracellular signal regulated protein kinase (ERK)) and p38/mitogen activated protein (MAP) kinase were explored. RESULTS: In vivo, LL-37 expression in healthy mucosa was restricted to differentiated epithelial cells in human colon and ileum. In colonocytes, increased LL-37 expression associated with cell differentiation was detected in vitro following treatment with butyrate, isobutyrate, propionate, and trichostatin A. Flavone induced LL-37 transcription but did not affect AP activity while cytokines had no effect. To dissect pathways mediating differentiation and LL-37 expression, specific inhibitors were applied. Inhibition of the protein kinase MEK enhanced butyrate induced AP activity while LL-37 expression in colon epithelial cells was blocked. In contrast, inhibition of p38/MAP kinase blocked cell differentiation without inhibiting LL-37 expression. CONCLUSIONS: Expression of the cathelicidin LL-37 in colonocytes and cellular differentiation are separately modulated by SCFA via distinct signalling pathways. These data may provide a rationale for dietary modulation of mucosal defence mechanisms.

Adult↗
PubMed2002

[Quantitative analysis of the left main coronary artery by 3D echocardiography. Role, possibilities and limitations of noninvasive imaging of the left coronary artery].

The left main coronary artery was investigated in 30 patients using a transesophageal approach, and a 3D reconstruction of the 2D databases was performed. Two groups of patients were analyzed. First, patients with calcified aortic stenosis were investigated and the reconstructed data obtained were compared to the left ventricular angiogram of the left coronary artery. Second, the 2D databases of patients with non-calcified aortic valve and aortic anulus were reconstructed using the 3D technique. In group 1 the estimate in size of the left ventricular coronary artery was closely related to the diameter of the left coronary artery as obtained by the coronary angiogram (mean difference 0.08 mm, interval of confidence at 95%, -0.48 and +0.32 mm). In both groups a substantial increase in imaging of the left coronary artery was obtained compared to the standard 2D echocardiographic view (% in group 1, and % in group 2, respectively). Independent of the 3D reconstruction of the left coronary artery in the any-plane mode, an orthogonal imaging of the artery could be obtained in only 15% of patients in group 1 but in 40% of patients in group 2. We conclude that 3D reconstruction of the left coronary artery (LAD) is superior to 2D echocardiography in echo-imaging of the proximal part of the LAD and correlates strongly to the diameters measured in the left coronary angiogram. In patients with major calcification of the aortic anulus and/or a calcified native aortic valve this approach is associated with multiple artifacts in imaging. The rapid technical evolution in this technique including improvement in computer technology and appropriate software may ensure a further important role of 3D echo imaging in noninvasive visualization of the normal and diseased left main coronary artery.

Adult↗
PubMed2002

Quantitative assessment of right ventricular volumes in severe chronic thromboembolic pulmonary hypertension using transthoracic three-dimensional echocardiography: changes due to pulmonary thromboendarterectomy.

AIMS: Evaluation of a three-dimensional reconstruction method to show the changes of right ventricular volume and systolic function when patients undergo pulmonary thromboendarterectomy for chronic thromboembolic pulmonary hypertension. METHODS AND RESULTS: In the examination of 11 patients (four female, seven male; age 56+/-10 years) before and after pulmonary thromboendarterectomy, end-diastolic and end-systolic right ventricular volumes were determined as a sum total of the calculated volumes of derived parallel slices of the right ventricle. Using a Tomtec workstation and a Vingmed CFM 800 echocardiography device, the acquired data were ECG-and respiration-triggered in the course of transthoracic examination, using step intervals of 5 degrees. The ventricular outline was traced manually on 5mm slices from longitudinal cut planes. For subsequent correction, their area measurements were displayed and the volume cross-checked against the volume from orthogonal cut planes. End-diastolic and end-systolic volumes could be quantified in 11/11 cases before surgery, but data could only be attained for 9/11 patients after surgery, because a limited apical window rendered the postoperative three-dimensional reconstruction impossible in two cases. Before surgery, right ventricular size was larger than normal and systolic function was clearly impaired in all of the patients (end-diastolic volume: 121+/-37 ml; end-systolic volume 91+/-30 ml; ejection fraction 25+/-8%). The decrease in mean pulmonary artery pressure after surgery was significant (47+/-8 vs 26+/-8 mmHg; P<0.05). End-diastolic and end-systolic right ventricular volumes had been reduced (80+/-33 ml and 54+/-31 ml respectively), and the ejection fraction had increased (36+/-9%). CONCLUSIONS: Successfully performed pulmonary thromboendarterectomy leads to a significant reduction of right ventricular chamber size and improvement of systolic function, which can be determined with great precision and quite easily, using transthoracic three-dimensional echocardiography. Published by Elsevier Science Ltd. All rights reserved.

Adult↗
PubMed2002

Butyrate inhibits NF-kappaB activation in lamina propria macrophages of patients with ulcerative colitis.

BACKGROUND: In ulcerative colitis (UC) the activation (i.e. nuclear translocation) of nuclear factor kappa B (NF-kappaB) is an important step in the regulation of cytokines secreted by lamina propria macrophages. Clinical trials suggest anti-inflammatory effects of locally administered butyrate in UC. The potential effects of butyrate on NF-kappaB activation in lamina propria macrophages of UC patients were investigated. METHODS: Eleven patients with distal UC were treated for up to 8 weeks with butyrate at 100 mM (n = 6) or placebo (n = 5) enemas. At entry and after 4 and 8 weeks, clinical status was noted and intestinal inflammation was graded endoscopically and histologically. Double-staining with antibodies against NF-kappaB (p65) and CD68 was employed to detect NF-kappaB and macrophages, respectively. RESULTS: In untreated patients, nuclear translocation of NF-kappaB was detectable in virtually all macrophages. Butyrate treatment for 4 and 8 weeks resulted in a significant reduction in the number of macrophages being positive for nuclear translocated NF-kappaB. In addition, butyrate significantly reduced both the number of neutrophils in crypt and surface epithelia and of the lamina propria lymphocytes/plasma cells. These findings correlated with a significant decrease in the Disease Activity Index (DAI). CONCLUSIONS: The decrease in DAI and mucosal inflammation in butyrate-treated patients is associated with a reduction of NF-kappaB translocation in lamina propria macrophages. Since the inflammatory process in UC is mainly sustained by macrophage-derived cytokines, the known anti-inflammatory effects of butyrate may in part be mediated by an inhibition of NF-kappaB activation in these macrophages.

Adult↗
PubMed2002

Butyrate and aspirin in combination have an enhanced effect on apoptosis in human colorectal cancer cells.

Laboratory and epidemiological studies suggest that butyrate, a metabolic product of microbial fermentation of dietary fibre, and aspirin, a non-steroidal antiphlogistic drug, both reduce the risk of developing colon cancer. Notably, few data exist on potential interactions of these two substances. In this study, the effects of a butyrate-aspirin combination on human colon cancer cells were compared with treatment with aspirin or butyrate alone. Both substances decreased proliferation and induced differentiation and apoptosis. Butyrate reduced mutant p53 expression, whereas aspirin did not affect p53 expression. Butyrate-induced apoptosis correlated with an increase in Bak expression and a decrease in the expression of Bcl-XL. Aspirin had no effect on the investigated apoptosis-controlling factors. The antiproliferative and pro-apoptotic effects of the butyrate-aspirin combination were markedly enhanced. The combination resulted in a stronger decrease in the expression of PCNA and cdk2. Our data suggest that the anticarcinogenic effect of aspirin might effectively be augmented by combination with the short-chain fatty acid butyrate.

Apoptosis↗
PubMed2002

Spectral karyotype analysis of colon cancer cell lines of the tumor suppressor and mutator pathway.

BACKGROUND AND AIMS: Microsatellite instability (MSI) is characterized by the size variation of microsatellites in tumor DNA as compared to matching normal DNA due to defects in the mismatch repair system. To examine the chromosomal differences in microsatellite-stable (MSS) and -unstable (MSI) tumors in detail, we analyzed MSS (Caco-2, Colo-205, SW948) and MSI (HCT-15, HCT-116, LoVo) cell lines by spectral karyotyping (SKY). METHODS: SKY is a sensitive method to detect chromosome aberrations by visualizing each chromosome in a different color. Metaphases were hybridized with a SKY probe mixture. Images were visualized with the SpectraCube system and analyzed with the SKYview imaging software. RESULTS: The average number of chromosomes was 49 in LoVo, 45 in HCT-116, 46 in HCT-15, 71 in Colo-205, 89 in Caco-2 and 66 in SW-948. Three aberrant chromosomes were detected in LoVo, three in HCT-116, two in HCT-15, seventeen in Colo-205, fourteen in Caco-2 and nine in SW948. CONCLUSION: The karyotypes of MSS colon cancer cells displayed complex numerical and structural aberrations. In contrast the chromosomes of MSI colon cancer cells were mostly unaltered but displayed a few isolated numerical and structural aberrations. We speculate that these isolated aberrations may be specifically involved in the pathogenesis of MSI tumors.

Chromosome Banding↗
PubMed2001

Cytokine-activated degradation of inhibitory kappaB protein alpha is inhibited by the short-chain fatty acid butyrate.

Butyrate, a short-chain fatty acid, is generated by anaerobic fermentation within the colon. Clinical trials suggest that short-chain fatty acids ameliorate inflammation in ulcerative colitis. Nuclear factor (NF) kappaB, an inducible transcription factor that is activated in inflamed colonic tissue, is sequestered to the cytoplasm by its inhibitory IkappaB proteins. The anti-inflammatory effects of butyrate are associated with an inhibition of NF-kappaB nuclear translocation. To investigate the mechanism of NF-kappaB inhibition we examined the effects of butyrate on IkappaBalpha. Human adenocarcinoma cells (SW480, SW620, and HeLa229) were treated with butyrate for up to 48 h followed by tumor necrosis factor (TNF) alpha stimulation. NF-kappaB was detected by immunofluorescence staining with an antibody against its p65 subunit. Levels of IkappBalpha and phosphorylated IkappaBalpha were determined by western blot. Stimulation with TNFalpha resulted in rapid phosphorylation and degradation of IkappaBalpha followed by NF-kappaB nuclear translocation. Butyrate pretreatment successfully inhibited NF-kappaB activation. Pretreatment of adenocarcinoma cells with butyrate is associated with inhibition of TNFalpha-mediated phosphorylation and degradation of IkappaBalpha and effective blocking of NF-kappaB nuclear translocation. The anti-inflammatory effects of butyrate may at least in part be mediated by an inhibition of IkappaBalpha mediated activation of NF-kappaB.

Adenocarcinoma↗
PubMed2001

Butyrate inhibits interleukin-1-mediated nuclear factor-kappa B activation in human epithelial cells.

Nuclear factor-kappa B (NF-kappaB) is a critical transcription factor for the inducible expression of multiple genes involved in inflammation. NF-kappaB is sequestered in the cytoplasm by inhibitory IkappaB proteins. Extracellular stimuli, notably interleukin-1beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha) activate NF-kappaB nuclear translocation via IkappaB phosphorylation and degradation. Since previous reports suggest that the short chain fatty acid butyrate has antiinflammatory properties, the effects of butyrate on NF-kappaB nuclear translocation in human epithelial cells (HeLa229) were tested. In cells pretreated with butyrate, a time- and dose-dependent inhibition of IL-1beta-mediated NF-kappaB nuclear translocation was observed. However, IkappaB alpha phosphorylation and degradation occurred rapidly in both butyrate pretreated and nonpretreated cells, respectively. These data indicate that inhibition of IL-1beta-induced NF-kappaB activation by butyrate does not require an intact IkappaB alpha protein.

Butyrates↗
PubMed2001

[Tumor cell embolism to pulmonary arteries].

A 69-year-old male presented with symptoms of fulminant lung embolism and, despite immediate therapy with plasminogen activator, died of acute right heart failure. At autopsy multiple tumor cell emboli were detected in small pulmonary vessels in addition to widespread liver metastases from an urothelial carcinoma. - In a 23-year-old female a malignant gastric ulcer and multiple liver metastases were diagnosed at initial presentation. She too died from pulmonary hypertension due to a series of lung embolisms which occurred despite heparin therapy. At autopsy, many small pulmonary arteries were filled with adenocarcinoma cells; the primary gastric tumor and liver metastases were confirmed. These cases demonstrate that the shedding of tumor cells from hepatic metastases can obstruct the pulmonary vessels and lead to acute cor pulmonale. Tumor cell emboli should be considered in the differential diagnosis of acute pulmonary hypertension, especially in patients with a known tumor. They may, however, also represent the first clinical signs of previously unrecognized malignancy.

Adenocarcinoma↗
PubMed2001

Beneficial health effects of low-digestible carbohydrate consumption.

Low-digestible carbohydrates represent a class of enzyme-resistant saccharides that have specific effects on the human gastrointestinal tract. in the small bowel, they affect nutrient digestion and absorption, glucose and lipid metabolism and protect against known risk factors of cardiovascular disease. In the colon they are mainly degraded by anaerobic bacteria in a process called fermentation. As a consequence, faecal nitrogen excretion is enhanced, which is used clinically to prevent or treat hepatic encephalopathy. Low-digestible carbohydrates are trophic to the epithelia of the ileum and colon, which helps to avoid bacterial translocation. Short-chain fatty acids are important fermentation products and are evaluated as new therapeutics in acute colitis. They are considered in the primary prevention of colorectal cancer. The bifidogenic effect of fructo-oligosaccharides merits further attention, Unfermented carbohydrates increase faecal bulk and play a role in the treatment of chronic functional constipation, symptomatic diverticulosis and, possibly, the irritable bowel syndrome. In conclusion, low-digestible carbohydrates may play a role in the maintenance of human digestive health. However, the strength of evidence differs between disease entities.

Cardiovascular Diseases↗
PubMed2001

Butyrate and propionate downregulate ERK phosphorylation in HT-29 colon carcinoma cells prior to differentiation.

We have characterized the effects of different short-chain fatty acids (SCFAs) on cell growth and differentiation as well as the phosphorylation state of ERK1 and 2 in the human colon adenocarcinoma cell line HT-29. Of the five SCFAs tested, only butyrate and propionate impaired cellular proliferation. Moreover, butyrate and propionate specifically resulted in a decrease in ERK1 and 2 phosphorylation at 3 and 6 hours post-treatment, suggesting a correlation between the ability of these SCFAs to inhibit cellular proliferation and decrease ERK phosphorylation. Notably, the decrease in ERK phosphorylation was observed prior to the induction of the differentiation markers alkaline phosphatase (AP) and carcinoembryonic antigen (CEA) by butyrate and propionate from days 6 to 18 post-treatment. In the case of butyrate- and propionate-induced differentiation, ERK phosphorylation is a marker and may play a role in the proliferation and/or differentiation states of this cell line.

Alkaline Phosphatase↗
PubMed2000

CXC chemokines Gro(alpha)/IL-8 and IP-10/MIG in Helicobacter pylori gastritis.

Infection with Helicobacter pylori causes chronic active gastritis, which is characterized by neutrophils infiltrating the gastric epithelial layer and the underlying lamina propria as well as by T, B lymphocytes and macrophages accumulating in the lamina propria. In this study, the chemokine profile responsible for the recruitment of these inflammatory cells is investigated. Using both RNA/RNA in situ hybridization and immunohistochemistry, the expression of the neutrophil and/or lymphocyte-attractant CXC chemokines growth-related oncogene alpha (Gro(alpha)), IL-8, interferon-gamma (IFN-gamma)-inducible protein-10 (IP-10), monokine induced by IFN-gamma (MIG) and the CC chemokines macrophage inflammatory protein-1alpha (MIP-1alpha), -1beta, regulated on activation normal T cell expressed and secreted (RANTES) and monocyte chemoattractant protein-1 (MCP-1) is studied and microanatomically localized in the gastric mucosa. Macrophages in the lamina propria at sites with neutrophil infiltration and gastric epithelium infiltrated by neutrophils highly expressed the neutrophil-attractant chemokines Gro(alpha) and IL-8. Additionally, Gro(alpha) and IL-8 were expressed by neutrophils themselves localized within gastric epithelium, in the foveolar lumen and in the cellular debris overlying mucosal erosion. IP-10 and to a lower extent MIG, both selectively chemotactic for inflammatory T cells, were expressed by endothelial cells of gastric mucosal vessels and by mononuclear cells at sites with T cell infiltration. Expression of all other CC chemokines tested was significantly lower. These in vivo data indicate that a set of predominantly CXC chemokines modulates the inflammation in H. pylori gastritis. Gro(alpha) and IL-8 may play an important role in neutrophil trafficking from the mucosal vessel into the gastric epithelium, whereas IP-10 and MIG contribute to the recruitment of inflammatory T cells into the mucosa.

Chemokine CCL2↗
PubMed2000

Spectral karyotyping of the human colon cancer cell lines SW480 and SW620.

The cell lines SW480 and SW620, derived from different stages of colon carcinoma in the same patient, have been used for a number of biochemical, immunological, and genetic studies on colon cancer. A comparative analysis of their karyotypes may identify chromosomal aberrations that might represent markers for metastatic spread. In the present study spectral karyotyping (SKY) was applied to these two colon cancer cell lines. Compared to previously reported G-banded karyotypes, 9 (SW480) and 7 (SW620) markers were identical, 3 (SW480) and 3 (SW620) markers could be redefined, 5 (SW480) and 8 (SW620) markers were newly identified, and 4 (SW480) and 5 (SW620) of the previous described markers could not be confirmed. The redefined aberrations include very complex rearrangements, such as a der(16) t(3;16;1;16;8;16; 1;16;10) and a der(18)t(18;15;17)(q12; p11p13;??) in SW620 and a der(19)t(19;8;19;5) in SW480, that have not been identified by conventional banding techniques. The resulting chromosome gains (5q11-->5q15, 7pter-->q22, 11, 13q14-->qter, 20pter-->p12, X) and losses (8pter-->p2, 18q12-->qter, Y) found in both SW480 and SW620 were in good agreement with those frequently described in colorectal tumors as primary changes in the stem cell. Abnormalities found exclusively in SW620 cells only (gains of 5pter-->5q11, 12q12-->q23, 15p13-->p11, and 16q21-->q24 and losses of 2pter-->2p24, 4q28-->qter, and 6q25-->qter) can be viewed as changes that occurred in a putative metastatic founder cell.

Abdominal Neoplasms↗
PubMed2000

Pathophysiology of impaired right and left ventricular function in chronic embolic pulmonary hypertension: changes after pulmonary thromboendarterectomy.

STUDY OBJECTIVES: This study sought to evaluate the pathophysiology of left and right heart failure in patients with chronic thromboembolic pulmonary hypertension (CTEPH) who were hospitalized to undergo pulmonary thromboendarterectomy (PTE). DESIGN: Thirty-nine patients (16 women and 23 men; mean +/- SD age, 55+/-12 years) with severe CTEPH were examined before and 13+/-8 days after PTE by way of transthoracic echocardiography and right heart catheterization. MEASUREMENTS AND RESULTS: Examination results confirmed in all cases that before surgery the right ventricles were enlarged and systolic function was impaired. Moderate to severe tricuspid valve regurgitation was observed. Left ventricular eccentricity indexes reflected a leftward displacement of the interventricular septum. End-diastolic left ventricular size and systolic function had decreased, and the left ventricular filling pattern showed impaired diastolic function. After surgery, mean pulmonary artery pressure was significantly lower (48+/- 10 mm Hg vs. 25+/-7 mm Hg; p<0.05). The calculated end-diastolic and end-systolic right ventricular areas had decreased: 30+/-7 cm(2) vs 21 +/-5 cm(2) (p<0.05) and 24+/-6 cm(2) vs. 14+/-4 cm(2) (p<0.05), respectively. Right ventricular fractional area change had increased (20+/-7% vs. 33+/-8%; p<0.05). Most of the patients exhibited a marked decrease in the severity of tricuspid regurgitation. Septal motion, left ventricular systolic function, and diastolic filling pattern returned to normal values (early to late diastolic left ventricular inflow ratio, 0.70+/-0.33 vs. 1.35+/-0.51; p<0.05). The mean cardiac index also improved (2.7+/-0.6 L/min/m(2) vs. 3.7+/-0.8 L/min/m(2)). CONCLUSIONS: In CTEPH, functions are impaired in the right as well as the left ventricles of the heart. Improved lung perfusion and the reduction of right ventricular pressure overload are direct results of PTE, which in turn bring a profound reduction of right ventricular size and a recovery of systolic function. Normalization of interventricular septal motion as well as improved venous return to the left atrium lead to a normalization of left ventricular diastolic and systolic function, and the cardiac index improves.

Adult↗
PubMed2000

[Effect of nutrition factors on the pathogenesis of colorectal carcinoma].

There is convincing evidence that nutrition affects colorectal carcinogenesis in a complex fashion. Dietary components either promote or inhibit the carcinogenic process. The composition of dietary fats seems to be less important as a promoting factor than a positive energy balance, especially in combination with low physical activity. Excessive consumption of red meat is associated with increased risk, which may be due to the heme contained in myoglobin. Alcohol stimulates cell proliferation in the rectum and may thus increase cancer risk. Complex carbohydrates (e.g., dietary fiber) are degraded in the colon to short-chain fatty acids which exhibit protective effects in experimental models of carcinogenesis. The putative protection from vitamins and trace elements merits further attention.

Animals↗