Showing papers by "Bandaru S. Reddy published in 1979"
TL;DR: The results indicate that the effect of fiber in colon carcinogenesis depends on the type of fiber and, possibly, the fiber's mode of action.
Abstract: The effect of dietary alfalfa, pectin, and wheat bran on colon carcinogenesis was studied in female inbred F344 rats. Weanling rats were fed semipurified diets containing 0 or 15% alfalfa, pectin, or wheat bran. At 7 weeks of age, all animals except controls were given azoxymethane (AOM) sc at a dose rate of 8 mg/kg body weight/week for 10 weeks or methylnitrosourea (MNU) intrarectally at a dose rate of 2 mg/rat twice a week for 3 weeks. The AOM-treated group was autopsied 40 weeks and the MNU-treated group 30 weeks after the first injection of the carcinogen. No tumors were observed in the colon or other organs of untreated rats fed the various diets. The animals fed the alfalfa diet and treated with MNU had a higher incidence of colon tumors than did those fed the control diet or the diets containing pectin or wheat bran. The incidence of MNU-induced colon tumors did not differ between the animals fed the control diet or the diets containing pectin or wheat bran. However, the incidence of AOM-induced colon tumors in rats fed diets containing pectin or wheat bran was lower than that in rats fed the control diet or the alfalfa diet. These results thus indicate that the effect of fiber in colon carcinogenesis depends on the type of fiber and, possibly, the fiber's mode of action.
160 citations
Journal Article•
TL;DR: It is concluded that sodium lithocholate, but not cholesterol, cholesterol epoxide, triol, or their microbial products, had a promoting effect in MNNG-induced colon carcinogenesis in rats.
Abstract: The promoting effect of sodium lithocholate, cholesterol, cholesterol-5α,6α-epoxide (cholesterol epoxide), and cholestane-3β,5α,6β-triol (triol) on colon carcinogenesis was studied in female Fischer (F-344) conventional and germ-free rats. Evaluation of these compounds for their colon tumor-promoting activity in a germ-free animal system would indicate whether further modification of these compounds by gut microflora is required for tumor promotion. At 7 weeks of age, groups of germ-free and conventional rats were given intrarectal instillations of N-methyl-N′-nitro-N-nitrosoguanidine (MNNG) at a dose rate of 2.5 mg/rat, twice a week for 2 weeks, and then were given intrarectal doses of sodium lithocholate, cholesterol, cholesterol epoxide, or triol at a dose rate of 20 mg/rat 3 times a week for 46 weeks; other groups received MNNG for 2 weeks and vehicle thereafter for 46 weeks or lithocholate or cholesterol metabolites alone for 48 weeks. No tumors were detected in rats given sodium lithocholate, cholesterol, cholesterol epoxide, or triol alone, which suggested that these compounds, or their microbially modified metabolites, were not carcinogenic to colon mucosa under our experimental conditions. Sodium lithocholate increased MNNG-induced colon tumor incidence in both germ-free and conventional rats. The colon tumor incidence was similar in the MNNG, MNNG-plus-cholesterol, MNNG-plus-cholesterol epoxide and MNNG-plus-triol groups. The results obtained in germ-free rats also indicate that lithocholate without being further modified by the gut microflora acts as a colon tumor promoter. It is concluded that sodium lithocholate, but not cholesterol, cholesterol epoxide, triol, or their microbial products, had a promoting effect in MNNG-induced colon carcinogenesis in rats.
136 citations
TL;DR: Evidence suggests that, in absence of caloric excess, lowering of serum lipids and increased removal of fecal sterols is possible on a prudent diet without major modification of the customary foods, but that a high P:S ratio is required.
Abstract: In this study, the amount and type of dietary fat were adjusted to determine the effect on cholesterol metabolism in free-living men.
9 citations
01 Jan 1979
TL;DR: Metabolic epidemiology and laboratory studies reveal that diet could be a source of carcinogens and probably contributes to colon cancer development through alteration of luminal constituents that act as tumor promotors.
Abstract: Epidemiologic data on colon cancer incidence suggest a relationship to diet. Metabolic epidemiology and laboratory studies reveal that diet could be a source of carcinogens and probably contributes to colon cancer development through alteration of luminal constituents that act as tumor promotors. The dietary elements involved in the etiology of colon cancer appear to be high protein, high fat and low fiber.