Dietary inulin suppresses azoxymethane-induced aberrant crypt foci and colon tumors at the promotion stage in young Fisher 344 rats

This study was designed to determine the effect of 10% dietary long-chain inulin on the azoxymethane (AOM)-induced colonic preneoplastic aberrant crypt foci (ACF) and small intestinal and colon tumors at the initiation (I), promotion (P) and I + P stages (20 rats per treatment) in Fisher 344 male weanling rats. After an acclimatization period of 1 wk, groups of Fisher 344 male weanling rats were assigned to consume AIN 93G diet (control) or AIN 93G diet containing 10% inulin. All the rats received 16 mg/kg body AOM dissolved in saline subcutaneously at 7 wk of age followed by a second injection at 8 wk of age. An additional group of five rats received only saline and consumed the control diet. The rats received the assigned diets until asphyxiation by CO(2) at 16 wk of age for the ACF experiment and 45 wk for the end-point tumor experiment. Feed intake, weight gain, diarrheal index, cecal weight, cecal pH, ACF and tumors in the colon were determined. Rats fed inulin had diarrhea after 2 wk of feeding and recovered by approximately 4 wk. Cecal weight was greater in rats fed inulin and cecal pH was lower. The inulin group had more than 66% fewer aberrant crypts and 60% fewer ACF compared with the control group. Tumor incidences in the small intestine and colon of rats in the control, I, P and I + P groups were: 78, 31, 0 and 11% and 90, 73, 69 and 50%, respectively. The corresponding values for the distal portion of the colon were 87, 63, 45 and 33%, respectively. Colon tumors per tumor-bearing rat were 4.2, 3.09, 1.36 and 1.2 for the control, I, P and I + P groups, respectively. All groups differed, P < 0.05. The results of this study indicate that dietary long-chain inulin suppresses AOM-induced ACF formation, an early preneoplastic marker of colon tumorigenesis in rats, and colon tumors, particularly at the promotion stage.     

Effect of dietary benzylselenocyanate on azoxymethane-induced colon carcinogenesis in male F344 rats.

The effect of dietary benzylselenocyanate (BSC) and its analogue, benzylthiocyanate (BTC), and sodium selenite during the initiation and postinitiation phases of azoxymethane (AOM)-induced intestinal carcinogenesis was studied in male F344 rats. Animals intended for initiation study were fed the high-fat (23.5% corn oil) diets containing 25, 50, and 100 ppm BSC (10, 20, and 40 ppm selenium, respectively) and 100 ppm BTC and 4 ppm selenium (as sodium selenite in drinking water); those intended for postinitiation study were fed the high-fat control diet. Two weeks later, all animals were injected subcutaneously with AOM (15 mg/kg body wt) once weekly for two weeks. Three days after the last AOM injection, animals in the initiation and postinitiation studies were transferred respectively to the high-fat diet and high-fat diets containing BSC and BTC and sodium selenite in drinking water. This regimen was continued until 36 weeks post-AOM injection. BSC inhibited the small intestinal and colon adenocarcinoma incidence and multiplicity of colon adenocarcinomas when fed during the postinitiation phase. Sodium selenite inhibited the incidence and multiplicity of colon adenocarcinomas only during the postinitiation phase. BTC had no inhibitory effect when fed during the initiation and postinitiation phases. The colonic mucosal ornithine decarboxylase activity was significantly inhibited by the administration of all three compounds, BSC (78%), BTC (62%), and sodium selenite (44%). It is concluded that the BSC has an inhibitory effect on the intestinal carcinogenesis in animals fed the high-fat diet.     

Extract of Kurosu, a vinegar from unpolished rice, inhibits azoxymethane-induced colon carcinogenesis in male F344 rats

The modifying effects of administering an ethyl acetate extract of Kurosu (EK), a vinegar made from unpolished rice, in drinking water on the development of azoxymethane (AOM)-induced colon carcinogenesis were investigated in male F344 rats. Animals were given 2 weekly subcutaneous injections of AOM (20 mg/kg body weight). They also received drinking water containing 0%, 0.05%, or 0.1% EK for 35 wk, starting 1 wk after the last dosing of AOM. EK administration significantly inhibited the incidence and multiplicity of colon adenocarcinoma (P < 0.05), compared with those in the AOM alone group. These findings suggest that EK may be effective for inhibiting colon carcinogenesis.     

Red wine and black tea polyphenols modulate the expression of cycloxygenase-2, inducible nitric oxide synthase and glutathione-related enzymes in azoxymethane-induced f344 rat colon tumors

Polyphenolic compounds extracted from red wine (WE) and black tea (BT), 50 mg/(kg. d), inhibit the promotion phase of the colon carcinogenesis process induced by azoxymethane (AOM) in rodents. To investigate possible mechanisms of this protective activity, we evaluated by RT-PCR the gene expression of cycloxygenase-2 (COX-2), inducible NO synthase (iNOS), gamma-glutamylcysteine synthetase (gamma-GCS) and two isoforms of glutathione S-transferase (GST), GST-P and GST-M2, in 30 AOM-induced tumors and in the corresponding normal colon mucosa. AOM-induced colon tumors had significantly greater GST-P, GST-M2, COX-2 and iNOS gene expression than the corresponding normal mucosa. However, tumors harvested from rats treated with BT (P < 0.05) and WE (P < 0.01) polyphenols had a lower GST-P mRNA level than tumors from controls. Treatment with WE polyphenols induced a similar inhibitory effect on the colon tumor overexpression of GST-M2 (P < 0.01), COX-2 (P < 0.05) and iNOS (P < 0.05). In the normal mucosa, rats treated with BT polyphenols had greater gamma-GCS expression than controls (P < 0.01). Our results provide evidence that WE and BT polyphenols modulate COX-2, iNOS and glutathione-related gene expression in tumors, suggesting that these compounds have possible chemotherapeutic activity.     

Inhibitory effects of nondigestible carbohydrates of different chain lengths on azoxymethane-induced aberrant crypt foci in Fisher 344 rats

Colon cancer is one of the leading causes of cancer morbidity and mortality in Western countries. The objective of this study was to elucidate the effect of prebiotic carbohydrates of different chain lengths on azoxymethane-induced aberrant crypt foci in Fisher 344 male rats. After an acclimatization period of 1 week, 70 male weanling rats were divided into 7 groups and fed AIN-93G (Control) and 6 experimental diets that contained control + (maltodextrin; Raftiline HP, Raftiline ST, Raftilose P95, Raftilose Synergy1, and Mix; ORAFTI, Tienen, Belgium). All the rats received 16 mg/kg body weight of azoxymethane dissolved in saline subcutaneous at 7 and 8 weeks of age. The rats continued to receive the assigned diets until killed by carbon dioxide asphyxiation at 17 weeks of age. There was a significant (P < .05) increase in cecal weight and a decrease in cecal pH in rats fed prebiotic carbohydrates. The highest reduction of colonic aberrant crypt foci, both in total number as well as crypt, multiplicity was seen in the group fed Mix (63.9%). Consumption of diets containing Raftilose Synergy1, Raftiline ST, and Raftiline HP showed a reduction of total colonic crypts by 52.2%, 29.6%, and 46.3%, respectively, as compared with the control diet.     

Phytoene, phytofluene, and lycopene from tomato powder differentially accumulate in tissues of male Fisher 344 rats

Tomato product consumption is inversely related to prostate cancer incidence, and lycopene (LYC) has been implicated in reduced prostate cancer risk. The contribution of other tomato carotenoids, phytoene (PE) and phytofluene (PF), toward prostate cancer risk has not been adequately studied. The relative uptake and tissue distribution of tomato carotenoids are not known. We hypothesize that PE and PF are bioavailable from a tomato powder diet or from a purified source and accumulate in androgen-sensitive tissues. In this study, 4-week-old male Fisher 344 rats (Harlan, Indianapolis, Ind) were prefed an AIN-93G powder diet composed of 10% tomato powder containing PE, PF, and LYC (0.015, 0.012, and 0.011 g/kg diet, respectively). After 30-day tomato powder feeding, hepatic PF concentrations (168 ± 20 nmol/g) were higher than PE or LYC (104 ± 13 and 104 ± 13 nmol/g, respectively). In contrast, LYC, followed by PF, had the highest accumulation of the measured carotenoids in the prostate lobes and seminal vesicles. When tomato powder–fed rats received a single oral dose of either approximately 2.7 mg PE or approximately 2.7 mg PF, an increase in the dosed carotenoid concentration was observed in all measured tissues, except in the adrenal. The percentages of increases of PF were greater than that of PE in liver, serum, and adipose (37%, 287%, and 49% vs 16%, 179%, and 23%, respectively). Results indicate that the relative tomato-carotenoid biodistribution differs in liver and androgen-sensitive tissues, suggesting that minor changes in the number of sequential double bonds in carotenoid structures alter absorption and/or metabolism of tomato carotenoids.     

Consumption of black beans and navy beans (Phaseolus vulgaris) reduced azoxymethane-induced colon cancer in rats

Beans (Phaseolus vulgaris) are an important food staple in many traditional diets. There is limited evidence to suggest an inverse relationship between bean consumption and colon cancer. The objective of this study was to determine whether consumption of black beans and/or navy beans would reduce colon carcinogenesis in rats. Rats were fed a modified AIN-93G diet (control) or diets containing 75% black beans or 75% navy beans for 4 wk, and then colon cancer was initiated by administration of two injections of azoxymethane 1 wk apart. At 31 wk after the second injection, the incidence of colon adenocarcinomas was significantly lower (P < 0.05) in rats fed the black bean (9%) and navy bean (14%) diets than in rats fed the control diet (36%). Total tumor multiplicity was also significantly lower in rats fed the black bean (1.1) and navy bean (1.0) diets than in rats fed the control diet (2.2). The 44-75% reduction in colon carcinogenesis in rats fed beans was attributed to 1) more controlled appetites, leading to significantly less body fat, and 2) much greater concentrations of butyrate in the distal colon. It was concluded that eating black beans and navy beans significantly lowered colon cancer incidence and multiplicity.     

Effect of dietary Laminaria angustata (brown seaweed) on azoxymethane-induced intestinal carcinogenesis in male F344 rats

The effect of dietary Laminaria angustata (brown seaweed) on azoxymethane (AOM)-induced intestinal carcinogenesis was studied in male F344 rats. Five-week old rats were fed semipurified diets containing 0 and 10% seaweed. When the rats were 7 weeks old, all except the vehicle-treated groups received weekly subcutaneous injections of AOM in normal saline for two weeks (20 mg/kg body wt/week). All animals were fed the experimental diets until the termination of the experiment, which was 28 weeks after the last AOM injection. The incidence (percent of animals with tumors) and multiplicity (tumors/animal) of small intestinal tumors did not differ significantly between the control and seaweed groups. The incidence and multiplicity of colon adenomas along with the size of colon tumors were increased in rats fed the seaweed diet compared with those fed the control diet. Dietary seaweed had no major effect on the concentration of fecal bile acids; however, the concentration of fecal cholesterol and total neutral sterols was decreased in the seaweed group. These results suggest that dietary seaweed increases the risk for colon tumors.     

Inhibitory effects of phytic acid and other inositol phosphates on zinc and calcium absorption in suckling rats

While it is known that phytic acid, inositol hexaphosphate, has a negative effect on zinc and calcium absorption, the effects of inositol which is phosphorylated to a lesser extent are less known. We have prepared inositol triphosphate (IP-3), tetraphosphate (IP-4), pentaphosphate (IP-5) and hexaphosphate (IP-6) by hydrolysis of sodium phytate and separation by ion-exchange chromatography and have studied their effect on zinc and calcium absorption. Using a suckling rat pup model, we found that liver uptake of 65Zn after 6 h was 5% of the total dose from solutions of IP-6, 19% from IP-5, 28% from IP-4, 29% from IP-3 and 31% from ZnCl2 (control). Non-absorbed calcium was 17%, 1.4%, 0.5%, 0.5% and 0.5% of the given dose of 45Ca, respectively. Thus, at a high degree of phosphorylation (IP-6, IP-5), zinc and calcium uptake was inhibited, while no effect was observed for the other phosphates. Consequently, total "phytate" analysis, which includes inositol phosphates with varying degrees of phosphorylation, can give misleading information with regard to mineral availability. In addition, even limited dephosphorylation of inositol hexaphosphate can have a positive effect on mineral absorption.     

Effects of dietary phytic acid (phytate) on the incidence and growth rate of tumors promoted in fischer rats by a magnesium supplement

A Fischer rat tumor model was used to examine the effects of (i) dietary magnesium supplementation on tumor incidence, rate of tumor growth and latent periods for tumor appearance and death, and (ii) addition of phytate to the magnesium-supplemented diet on the same evaluation endpoints. Fifty, three-month old female Fischer rats were assigned to each of three isocaloric test diets fed ad libitum. The diets tested were: (i) certified rodent chow 5002 alone, (ii) chow plus 1.4% magnesium oxide (MgO), and (iii) chow plus 1.4% MgO plus 12.6% phytate. After two weeks each rat was injected subcutaneously with a syngeneic, tumorigenic cell line (1×10⁶ cells per animal). Respective test diets were continued for an additional 23 weeks following cell injection. Rats were sacrificed when tumors reached a limit length or width of 4 cm. The effect of magnesium supplementation was evaluated by comparing the chow group to the MgO test group. The effect of phytate addition was evaluated by comparing the chow+MgO group to the chow+MgO+phytate group. Dietary magnesium supplement exhibited a statistically significant tumor-promoting effect by all four evaluation endpoints measured. Dietary phytate, by the same four evaluation endpoints and all statistical parameters, nullifed the tumor-potentiating effects induced by MgO. Phytate addition highly significantly lowered tumor growth rate (p<0.0001) and increased the survival time (p<0.0001). The data indicate that dietary phytic acid has promise as a pharmacological agent in controlling magnesium-ion-mediated tumor promotion.     

Effect of feeding fermented milk on the incidence of chemically induced colon tumors in rats

The effect of feeding skim milk fermented by Streptococcus thermophilus or Lactobacillus bulgaricus on the incidence of chemically induced colon tumors was studied in rats. Weanling Fisher‐344 rats were fed chow plus skim milk (SM), chow plus SM fermented by S. thermophilus, chow plus SM fermented by L. bulgaricus, or chow plus water until sacrifice at 36 weeks, or before if moribund. Colon tumors were induced by s.c. injections of 1,2‐dimethylhydrazine hydrochloride during weeks 3 through 22. The control (chow + water) group received saline injections. The survival rate of the rats fed fermented milks was significantly higher than that of the rats fed nonfermented milk. The latter had a significantly higher incidence of ear‐duct tumors than the rats receiving fermented milk. The percentage of rats showing colon tumors was similar among all three experimental groups. The control group did not have any tumors. The rats receiving fermented milk had a significantly higher incidence of small‐intestine tumors than those receiving nonfermented milk. The rats on S. thermophilus milk had the lowest percentage of malignant colon tumors of the three experimental groups. Results indicated that the feeding of fermented milks altered the metabolism of 1,2‐dimethylhydrazine and shifted the target organ from the ear duct to the small intestine. In addition, the colon tumor distribution for the fermented‐milk groups appeared to shift toward the anus.     

Effects of green tea and high-fat diet on arachidonic acid metabolism and aberrant crypt foci formation in an azoxymethane-induced colon carcinogenesis mouse model

Excessive fat consumption is a risk factor for colon carcinogenesis, and green tea consumption may reduce the risk of colon and other cancers. The current study was designed to investigate the effects of green tea and a high-fat diet on arachidonic acid metabolism and aberrant crypt foci formation in an azoxymethane (AOM)-induced colon carcinogenesis mouse model. We also determined whether green tea consumption altered the size of regional fat pads. CF-1 female mice were maintained on either a high-fat (20% corn oil) or a low-fat (5% corn oil) diet. AOM was given subcutaneous at a dose of 7.5 mg/kg body weight at 6 wk and then a dose of 10 mg/kg at 7 wk of age. Two weeks after the second AOM injection, 0.6% green tea (6 mg tea solids/ml) was given as the drinking fluid and continued for 10 wk until the experiment was terminated. In the AOM-treated mice not receiving green tea, the high-fat diet significantly enhanced colonic levels of 5-lipoxygenase, leukotriene A4 hydrolase, and leukotriene B4, but it did not significantly alter prostaglandin E2 levels and aberrant crypt foci formation. In AOM-treated mice on the high-fat diet, green tea significantly decreased colonic levels of cytosolic phospholipase A2, 5-lipoxygenase, and leukotriene B4; green tea treatment also decreased the number of aberrant crypt foci (P < 0.05). The weights of parametrial and retroperitoneal fat pads were increased by the high-fat diet and decreased by green tea treatment. The current results indicate that green tea consumption and dietary fat modulate 5-lipoxygenase-dependent pathway of arachidonic acid metabolism during AOM-induced colon carcinogenesis. Green tea inhibits ACF formation in mice on a high corn oil diet, suggesting its possible inhibitory effect on colon carcinogenesis in populations such as those in Western countries that consume high amounts of fat.     

Effects of lyophilized black raspberries on azoxymethane-induced colon cancer and 8-hydroxy-2'-deoxyguanosine levels in the Fischer 344 rat

This study examined the effects of lyophilized black raspberries (BRB) on azoxymethane (AOM)-induced aberrant crypt foci (ACF), colon tumors, and urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels in male Fischer 344 rats. AOM was injected (15 mg/kg body wt i.p.) once per week for 2 wk. At 24 h after the final injection, AOM-treated rats began consuming diets containing 0%, 2.5%, 5%, or 10% (wt/wt) BRB. Vehicle controls received 5% BRB or diet only. Rats were sacrificed after 9 and 33 wk of BRB feeding for ACF enumeration and tumor analysis. ACF multiplicity decreased 36%, 24%, and 21% (P < 0.01 for all groups) in the 2.5%, 5%, and 10% BRB groups, respectively, relative to the AOM-only group. Total tumor multiplicity declined 42%, 45%, and 71% (P < 0.05 for all groups). Although not significant, a decrease in tumor burden (28%, 42%, and 75%) was observed in all BRB groups. Adenocarcinoma multiplicity decreased 28%, 35%, and 80% (P < 0.01) in the same treatment groups. Urinary 8-OHdG levels were reduced by 73%, 81%, and 83% (P < 0.01 for all groups). These results indicate that BRB inhibit several measures of AOM-induced colon carcinogenesis and modulate an important marker of oxidative stress in the Fischer 344 rat.     

Influence of dietary cis- and trans-fat on 1,2-dimethylhydrazine-induced colon tumors and fecal steroid excretion in Fischer 344 rats

To investigate the effects of the difference in the geometry of dietary fatty acids on colon tumorigenesis, male rats were fed semipurified diets containing either partially hydrogenated corn oil (trans-monoene fat) or olive oil (cis-monoene fat) at the 10% level and received a single oral dosage of 1,2-dimethylhydrazine (DMH). The difference in the fatty acid composition of dietary fats was confined essentially to the geometrical isomerism of octadecenoate, and the linoleic acid content was made equivalent (2% of total energy). After about 15 mo of feeding, colon tumor incidence in DMH treated rats was nearly the same in both fat groups. Fecal neutral steroid excretion was higher, while the transformation of cholesterol to coprostanol was lower in rats given the trans-fat. There were no marked differences in the excretion and composition of fecal bile acids between two fat groups. Serum cholesterol and tocopherol levels of rats given trans-fat diets tended to be low. The results suggested that the trans-monoene behaves much like the cis-monoene in the incidence of DMH-induced colon tumors, although there were characteristic differences in metabolic events in the intestine.     

Effect of dietary selenium deficiency on incidence and size of 1,2-dimethylhydrazine-induced colon tumors in rats

Torula yeast diets deficient (less than or equal to 0.02 ppm) in selenium (Se) and a control diet supplemented with sodium selenite (0.1 ppm Se), were fed to 52 male Sprague-Dawley rats per diet for 23 wk following weaning. 1,2-dimethylhydrazine (DMH) was administered (20 mg/kg body weight) in 20 weekly i.p. injections after 3 wk of feeding. After 23 wk, 67% of the rats fed the Se-deficient diet had intestinal adenocarcinomas versus 63% on the 0.1 ppm Se diets. Diet also had no effect on the number or size of tumors per tumor-bearing animal or on the location of the tumors within the colon. The effects of Se deficiency on the hematological variables of white blood cell count, hematocrit, serum urea nitrogen and cholesterol concentrations were examined. Serum urea nitrogen levels were lower in Se-deficient DMH-treated rats (9.6 +/- 0.7 vs. 13.7 +/- 0.9 mg/dl, P less than 0.01) and serum cholesterol was higher in Se-deficient DMH-treated animals (69.0 +/- 5.5 vs. 50.7 +/- 3.9 mg/dl, P less than 0.05). Body weights of the Se-depleted group were lower in the DMH-treated animals (P less than 0.01) although food consumption did not differ. Controls without DMH did not show differences due to Se status for any variable examined. Se deficiency appears to affect DMH toxicity but nutritional adequacy (0.1 ppm Se) does not inhibit tumor development. The results of this study do not support the belief that Se deficiency enhances colon carcinogenesis.     

Egg yolk proteins suppress azoxymethane-induced aberrant crypt foci formation and cell proliferation in the colon of rats

Dietary proteins can influence colonic carcinogenesis; some proteins have a promotional effect, whereas others exhibit a preventive effect. Dietary egg yolk proteins have been reported to suppress the expression of colon tumors in rats. In this study, we investigated the effect of consumption egg yolk proteins on cell proliferation in a rat model of azoxymethane (AOM)-induced colon cancer. We hypothesize, based on the literature of egg yolk protein actions, that they protect against colon tumor development. Therefore, male F344 rats were fed a purified AIN-93G diet containing either 20% casein (control) or 20% egg yolk proteins for 5 weeks. After 1 week on the experimental diet, the rats were administered weekly subcutaneous injections of saline or AOM for 2 weeks to induce aberrant crypt foci. Rats were administered an intraperitoneal injection of 5-bromo-2′-deoxyuridine 1 hour before being euthanized for examination of DNA synthesis in the colonic mucosa. The contents of the cecum were analyzed for the presence of short-chain fatty acids (SCFAs). In the AOM-injected rats, the yolk protein diet suppressed aberrant crypt foci formation and reduced the proliferative 5-bromo-2′-deoxyuridine–labeling index in the proximal colon when compared with the control diet. A significant increase in cecal SCFAs was observed in the rats that were fed egg yolk proteins. These results indicate that dietary egg yolk proteins have a preventive effect on AOM-induced large bowel carcinogenesis in rats; it exerts this effect by altering cell proliferation through SCFA production. This study suggests that the consumption of egg yolk proteins might be protective against colon carcinogenesis.     

Effects of nobiletin on PhIP-induced prostate and colon carcinogenesis in F344 rats

The current study was designed to investigate the effects of nobiletin (5,6,7,8,3',4'-hexamethoxy flavone) on 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)-induced prostate and colon carcinogenesis. PhIP was administered to 6-wk-old F344 male rats intragastrically (100 mg/kg) twice a wk for 10 wk. The animals were given 0.05% nobiletin or the basal diet for 50 wk. At the end of the experiment, serum testosterone, estrogen, and leptin did not differ between the 2 groups. The body weights of nobiletin-treated rats were significantly higher than controls (P<0.05), and feeding of nobiletin significantly reduced the relative prostate (P<0.05) and testes (P<0.05) weights as well as the Ki67 labeling index in the normal epithelium in the ventral prostate (P<0.01). The incidence and multiplicity of adenocarcinomas in nobiletin-treated ventral prostate were 50% and 36%, respectively, of controls, but the differences were not statistically significant. However, nobiletin did significantly reduce the total number of colonic aberrant crypt foci (ACF) compared to the control value (P<0.05). Nobiletin, therefore, may have potential for chemoprevention of early changes associated with carcinogenesis in both the prostate and colon.     

Effects of dietary zinc levels, phytic acid and resistant starch on zinc bioavailability in rats

Summary Background Owing to its fermentability, it has been advocated that resistant starch (RS) has a positive effect on the absorption of minerals by increasing their solubility in the hindgut. In marginally zinc–deficient rats, the enhancement of zinc bioavailability by RS occurs mostly when the diet contains phytic acid. Aim of the study This study aims to investigate the effect of dietary zinc level and phytic acid on the cecal zinc pools and zinc bioavailability of rats fed RS. Methods Wistar rats (male, 3wk old) were divided into eight groups (n = 6), and fed diets containing either 5% cellulose (control fiber: insoluble and low fermentable) or 20 % RS (test fiber: soluble and fermentable), with or without the addition of 1% sodium phytate, at the 10 and 30 mg/kg dietary zinc levels, for 21 days. Results At 10 mg Zn/kg, RS increased femur zinc concentration only in the group receiving the phytate–containing diet, while at 30 mg Zn/kg it increased femur zinc concentration in rats fed both phytate–free and phytate–containing diets. The total content of zinc in the cecum was increased by the higher dietary zinc level and tended to be increased by the addition of phytate, which is assumed to impair zinc absorption in the small intestine. Feeding RS lowered cecal pH values, which correlated with increasing values of zinc solubility (r = –0.3471; P < 0.05). The later was, in turn, directly associated with zinc apparent absorption (r = 0.3739; P < 0.05). Conclusions The increase in zinc bioavailability by RS occurs when dietary zinc levels are adequate and/or zinc absorption is impaired in the small intestine, increasing the influx of unabsorbed zinc into the cecum and favoring the increase of zinc bioavailability when RS fermentation lowers the cecal pH.     

Effects of dietary phytic acid on lead and cadmium uptake and depletion in rats

Rats were given a semipurified diet supplemented with phytate (10 g/kg) or calcium (6 g/kg) and lead (200 mg/kg) or cadmium (5 mg/kg) for 4 weeks. Addition of phytate or calcium reduced the accumulation of lead in bone (P less than 0.001) and in blood and liver samples (P greater than 0.05). The greatest inhibition of tissue lead retention was evident when phytate and calcium were fed together. Cadmium accumulation was measured in the liver and kidney and was increased (P less than 0.05) by the addition of calcium. Phytate inhibited the increase in tissue cadmium promoted by calcium supplementation but did not otherwise influence tissue cadmium levels. In a further experiment, weanling rats were given diets supplemented with cadmium (5 mg/kg) or lead (200 mg/kg) for 4 weeks, and the accumulation of these elements in the body tissues was estimated in some animals. A phytate-supplemented (10 g/kg) or phytate-free semipurified diet (free of lead and cadmium) was then given to the remaining rats for 4 weeks. Phytate supplementation was found to have no significant effect on the rate of loss of lead or cadmium from tissues.     

Description of the long-term lipogenic effects of dietary carbohydrates in male Fischer 344 rats

The introduction of high fructose corn syrup as a substitute sweetener for sucrose in the mid-1970s has contributed to a general increase in fructose consumption in the U.S. diet. Although several previous investigations suggested that dietary fructose increases serum triglyceride concentration and body fat, these studies have, in general, evaluated this effect in young rats fed the experimental diets for a relatively short period of the life span of the animals. Moreover, these investigations did not control for the possible effects that increased adiposity due to fructose feeding may have on serum triglyceride concentration. The purpose of the current investigation was to describe the long-term effects of specific dietary carbohydrates on serum lipid concentrations and body composition. To this end, we measured serum triglyceride, total cholesterol and HDL cholesterol concentrations and body composition of rats aged 9, 18 and 26 mo that had free access to or were restricted to 60% of free access intake of one of five diets that varied in carbohydrate source (cornstarch, sucrose, glucose, fructose or equimolar fructose plus glucose) starting at 3 mo of age. Dietary fructose significantly increased serum triglyceride concentration across the life span in rats that had free access to food or were calorie restricted. The source of dietary carbohydrate did not have a significant effect on body composition, total cholesterol or the distribution of the cholesterol fractions. These data suggest that dietary fructose per se and not the interaction between fructose and the energy content of the diet increases serum triglyceride concentration in rats.