A very low intake of fat is required to decrease fecal bile acid concentrations in rats (original) (raw)
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Journal of Nutrition
The mechanism by which calcium may protect against colon carcinogenesis was studied in rats fed three levels of calcium (0.5, 1.0 and 1.5 g/100 g diet) and a high butter diet (20 g/100 g). Results were compared with values obtained using a low butter diet (5 g/100 g) supplemented with 0.5 g à ‡a/100 g diet. Con centration and relative proportions of individual fecal bile acids were determined by gas chromatography, and in vivo colonie cell proliferation was assessed using [3H]thymidine. Total fecal output and total fecal lipids increased as dietary calcium increased. When calcium supplementation remained at 0.5%, raising the level of fat in the diet increased the fecal concentrations of deoxycholate, U-muricholate and total bile acids. However, when the level of fat supplementation re mained constant at 20 g/100 g diet, but dietary calcium was 1.0 or 1.5 g/100 g, the concentration of these bile acids returned to the level found in feces of rats fed the low fat diet. Despite the significant decrease in the con centrations of certain fecal bile acids with increasing calcium supplementation, these differences were not reflected in substantive changes in epithelial cytokinetics. These data show that in rats fed high butter diets, 1.0% calcium is sufficient to lower total bile acid concentration and the concentrations of certain in dividual bile acids to those found in feces of rats fed low fat diets. Despite the significant effects of calcium on bile acid concentrations, minimal effects were observed on indices of colonie cell proliferation. J. Nutr. 124: 188-195, 1994.
The American Journal of Clinical Nutrition, 2004
Background: Dietary fat content influences bile salt metabolism, but quantitative data from controlled studies in humans are scarce. Objective: The objective of the study was to establish the effect of dietary fat content on the metabolism of primary bile salts. Design: The effects of eucaloric extremely low-fat (0%), intermediatefat (41%; control diet), and extremely high-fat (83%) diets on kinetic values of cholate and chenodeoxycholate metabolism were determined after 11 d by using stable isotope dilution in 6 healthy men. All diets contained identical amounts of cholesterol. Results: The total primary bile salt pool size was not significantly affected by dietary fat content, although the chenodeoxycholate pool was significantly higher during the low-fat diet. Fractional turnover rates of both primary bile salts were 30-50% lower during the lowand high-fat diets than during the control diet. Total hepatic bile salt synthesis was Ȃ30% lower during both the high-and low-fat diets, but synthesis rates of the 2 primary bile salts were differentially affected. The molar ratio of cholate to total bile salt synthesis increased from 0.50 Ȁ 0.05 (x Ȁ SD) to 0.59 Ȁ 0.05 and 0.66 Ȁ 0.04 with increasing fat intake, whereas the molar ratio of chenodeoxycholate to total bile salt synthesis decreased from 0.50 Ȁ 0.05 to 0.41 Ȁ 0.05 and 0.34 Ȁ 0.04. The relative concentration of deoxycholate in plasma increased during the low-fat period, which indicated increased absorption from the colon. Conclusions: Both low-and high-fat diets reduce the synthesis and turnover rates of primary bile salts in humans, although probably through different mechanisms, and consequently they affect the removal of cholesterol from the body.
Journal of Clinical Investigation, 1978
A B S T R A C T Epidemiological observations and animal experiments suggest that large bowel cancer is related to several factors. Among them, high dietary intakes of animal fat, the presence in the colon of relatively high levels of bile acids, specific patterns of intestinal microflora, slow transit through the gut, and low stool weights. Under metabolic conditions we have observed the effect on these variables of diets containing 62 or 152 g/day of fat mainly of animal origin in six healthy young men over 4-wk periods. No change attributable to the diet was observed in the subjects' bowel habit, fecal weight, mean transit time through the gut, or in the excretion of dry matter. Total fecal bile acid excretion was significantly higher on the high fat diet (320±+120 mg/day) than on the low fat diet (139.7 +63 mg/day) t test = 7.78 P < 0.001 as also was the total fecal fatty acid excretion, 3.1+0.71 and 1.14±0.35 g/day, respectively t test = 11.4 P < 0.001). The fecal microflora including the nuclear dehydrogenating clostridia were unaltered by the dietary changes as was fecal /3-glucuronidase activity. Dietary changes which increase animal fat intake clearly influence fecal bile acid excretion in a way that would favor the development of large bowel cancer if current theories prove to be true. Dietary fat however has no effect on overall colonic function so other components of the diet must be responsible for the observed associations of bowel cancer with slow transit and reduced fecal bulk.
Background: Dietary fat content influences bile salt metabolism, but quantitative data from controlled studies in humans are scarce. Objective: The objective of the study was to establish the effect of dietary fat content on the metabolism of primary bile salts. Design: The effects of eucaloric extremely low-fat (0%), intermediate- fat (41%; control diet), and extremely high-fat (83%) diets on kinetic values of cholate and chenodeoxycholate metabolism were determined after 11 d by using stable isotope dilution in 6 healthy men. All diets contained identical amounts of cholesterol. Results: The total primary bile salt pool size was not significantly affected by dietary fat content, although the chenodeoxycholate pool was significantly higher during the low-fat diet. Fractional turnover rates of both primary bile salts were 30 -50% lower during the low- and high-fat diets than during the control diet. Total hepatic bile salt synthesis was 30% lower during both the high- and low-fat di...
Ultrastructural Modifications of Intestinal and Colonic Mucosa Induced by Free or Bound Bile Acids
Cancer Research, 1981
There is substantial evidence that bile acids may enhance the colon tumorigenesis induced by chemical carcinogens and that agents stimulating increased bile acid excretion may show similar promoting or enhancing activity. To test the premise that these agents might modify topographical ultrastructure of the small intestine and colon in the absence of carcinogens, rats were fed for 6 weeks on chemically defined diets contain ing 2% levels of three commercial bile acid sequestrants or 15% levels of wheat bran, cellulose, pectin, or alfalfa. Major qualitative and quantitative deviations from normal morphology were observed with each of the three sequestrants. Similar but less dramatic modifications occurred with diets containing al falfa or pectin, both of which either â€b ind' â€b ile acids in vitro or result in increased bile acid excretion. Bran and cellulose, which neither â€ẫ€˜bind' â€b ile acids nor increase their fecal excre tion, were without significant effects on intestinal or colonic morphology. The morphological deviations observed with bile acid sequestrants were shown to be a direct response to free or bound bile acids by comparing the morphological modifica tions resulting from daily intracolonic infusions of free bile acids, sequestrant-bound bile acids, or the sequestrant alone.
Effects of caloric restriction and dietary fat on epithelial cell proliferation in rat colon
Cancer research, 1993
Epidemiological studies indicate that caloric intake and dietary fat content influence colonic carcinogenesis. In rodents, caloric restriction reduces, and some fats increase, carcinogen-induced colon cancer incidence. The present study was designed to investigate the effects of caloric restriction on colonic cell proliferation (CCP) in carcinogen-treated or control rats fed low- or high-fat diets. F344 rats were treated with azoxymethane (15 mg/kg x2) and then fed an isocaloric AIN 76A diet containing either 5 or 23% corn oil, ad libitum or calorie-restricted to 70 or 80% of the kilocalories consumed by ad libitum rats. Biopsies of the distal colon were taken at 10 and 20 weeks, and rats were sacrificed at 21 or 34 weeks on the experimental diets. Distal CCP was determined by microautoradiography after [3H]thymidine labeling in vitro or presacrifice administration in vivo. The labeling index and number of labeled cells per crypt column were significantly reduced by caloric restrict...
The relationship between faecal bile acids and the development of experimental colon cancer
British journal of experimental pathology, 1988
Human metabolic studies have suggested a positive association between dietary intake, faecal bile acid excretion and the development of colon cancer. Similar investigations in experimental models of this disease have also implicated faecal bile acids but in both animals and man the results remain equivocal. This study sequentially examines the outputs and concentrations of faecal bile acids in dimethylhydrazine (DMH) treated groups of rats (n = 10), killed at 5-weekly intervals from the 10th to 40th week following the first injection. The sequential results showed that both the output and concentration of faecal bile acids decreased with time and accompanied an increase in both the incidence and numbers of colonic neoplasms over the 40 weeks of the study. When the animals were grouped according to the histological classification of their tumours, the faecal bile acids did not differ between animals with and without tumours. Further, when the latter group were sub-divided into those ...
Bile acid metabolism by fresh human colonic contents: a comparison of caecal versus faecal samples
Gut, 2001
Background-Deoxycholic acid (DCA), implicated in the pathogenesis of gall stones and colorectal cancer, is mainly formed by bacterial deconjugation (cholylglycine hydrolase (CGH)) and 7dehydroxylation (7-dehydroxylase (7-DH)) of conjugated cholic acid (CA) in the caecum/proximal colon. Despite this, most previous studies of CGH and 7-DH have been in faeces rather than in caecal contents. In bacteria, CA increases 7-DH activity by substrate-enzyme induction but little is known about CA concentrations or CA/7-DH induction in the human colon. Aims and methods-Therefore, in fresh "faeces", and in caecal aspirates obtained during colonoscopy from 20 patients, we: (i) compared the activities of CGH and 7-DH, (ii) measured 7-DH in patients with "low" and "high" percentages of DCA in fasting serum (less than and greater than the median), (iii) studied CA concentrations in the right and left halves of the colon, and examined the relationships between (iv) 7-DH activity and CA concentration in caecal samples (evidence of substrate-enzyme induction), and (v) 7-DH and per cent DCA in serum. Results-Although mean CGH activity in the proximal colon (18.3 (SEM 4.40) ×10 −2 U/mg protein) was comparable with that in "faeces" (16.0 (4.10) ×10 − 2 U/mg protein) , mean 7-DH in the caecum (8.54 (1.08) ×10-4 U/mg protein) was higher (p<0.05) than that in the left colon (5.72 (0.85) ×10-4 U/mg protein). At both sites, 7-DH was significantly greater in the "high" than in the "low" serum DCA subgroups. CA concentrations in the right colon (0.94 (0.08) µmol/ml) were higher than those in the left (0.09 (0.03) µmol/ml; p<0.001) while in the caecum (but not in the faeces) there was a weak (r=0.58) but significant (p<0.005) linear relationship between 7-DH and CA concentration. At both sites, 7-DH was linearly related (p<0.005) to per cent DCA in serum. Interpretation/summary-These results: (i) confirm that there are marked regional diVerences in bile acid metabolism between the right and left halves of the colon, (ii) suggest that caecal and faecal 7-DH influence per cent DCA in serum (and, by inference, in bile), and (iii) show that the substrate CA induces the enzyme 7-DH in the caecum.
Morphological disruption of colonic mucosa by free or cholestyramine-bound bile acids
Digestive Diseases and Sciences, 1984
In order to assess the effects offree or resin-bound bile acids on colonic topography, adult rats were surgically provided with an indwelling infusion catheter in the proximal cecum, which exited at the neck behind the head. Conscious, unrestrained rats were allowed chow ad libitum and were administered 1 ml of a n infusion mixture twice daily for five days. The infusion mixtures included either carrier saline, 100 mg cholestyramine, 165 txmol mixed bile acids, or the bile acids bound to cholestyramine. Additional groups of rats were fed defined diets with and without 2% cholestyramine, Compared to fed controls, colonic infusions of saline had little effect on colon topography. Infusions of 100 mg of cholestyramine in saline twice each day did cause some apparent damage to surface morphology of the colon, but not to the extent observed during feeding of the resin as 2% of the diet. In contrast, extensive surface damage of the colon was observed by twice daily infusions of either 165 txmoI of an equimolar mixture of cho!ic, deoxycholic, and chenodeoxycholic acids, or by the bile acids mired previously with the ion-exchange resin. The data suggest that topographical damage of the colon observed during feeding of bile acid-sequestering resins is in large part due to !ncreased concentrations of either bound or unbound bile acids in the large bowel. Conjugated or unconjugated bile acids have been reported to cause disruptive changes in colonic ultrastructure (1) and to exert a marked influence on electrolyte and water transport in the colon (2, 3).