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Biomedical subjects

D F Birt

Publications and source records attributed to D F Birt.

At least 91 records · Page 5Linked to original sources
PubMed1983

Enhancement of the repair of carcinogen-induced DNA damage in the hamster pancreas by dietary selenium.

We measured single strand breaks (SSB) in pancreas DNA produced by N-nitrosobis (2-oxopropyl)amine (BOP) in hamster fed purified diets containing added sodium selenite (Se) at 0.0, 0.1 and 5.0 ppm. There were fewer SSB in those given the 5.0 ppm Se diet throughout the experiment. One hour after dosing with BOP (20 mg/kg), there were 2.26 +/- 0.47, 2.83 +/- 0.43 and 1.74 +/- 0.43 SSB per 10(8) daltons (mean +/- S.E.M.) respectively in the three groups. The SSB were repaired faster in the 5.0 ppm Se-fed group. The approximate half-lives of the SSB were 33, 30 and 8 days, respectively. In the hamsters fed 5.0 ppm Se there was a small, statistically significant increase in pancreatic DNA synthesis. Autoradiographic analysis indicated that this was repair synthesis. In a second experiment, hamsters were fed one of the three diets prior to and for 2 days after administration of a single dose of BOP (20 mg/kg). They were then fed the 5.0 ppm Se diet for 5 days. The number of SSB was compared with those in hamsters fed their original diet for 7 days after BOP dosing. There was a statistically significant difference in the number of SSB in the hamsters fed 0.1 ppm Se before and for 2 days after BOP. In these hamsters there were 1.21 +/- 0.24 SSB per 10(8) daltons compared with 3.19 +/- 0.4 (mean +/- S.E.M.). These results suggest high levels of dietary Se stimulate the repair of carcinogen-induced DNA damage

Animals↗
PubMed1983

Effects of dietary protein level on hepatic microsomal mixed-function oxidase systems during aging in two generations of Syrian hamsters.

Syrian hamsters were fed one of three levels of lactalbumin (10, 20, or 40%) from 4 weeks of age. Parents (F0 generation) and their offspring (F1 generation) remained for life on the parental diet. Randomly selected hamsters from both generations were killed at 0, 6, 18, 30, and 60 weeks to evaluate hepatic microsomal drug metabolism systems. Microsomal protein content rose with increased dietary protein in both generations of females at 30 and 60 weeks and in both generations of males at 18 weeks. Microsomal protein rose during life, but the timing and magnitude of the increase varied with sex, diet, and generation. Cytochrome P-450 content increased with elevation in dietary protein at most measurement times in females and at all measurement times in F1 generation males. Hepatic aryl hydrocarbon hydroxylase (AHH) and aniline hydroxylase (ANH) activities were influenced by dietary protein, primarily at 6, 18, and 30 weeks, and these values tended to decline between maturity and senescence. AHH generally increased as dietary protein rose, except at 30 weeks, at which time the group fed the medium protein level usually had the highest activity. ANH activity was either elevated in groups fed the 20 or 40% lactalbumin levels or depressed in these groups at 6 and 18 weeks when these values were influenced by dietary protein. The effects depended upon sex and generation. Age effects on hepatic microsomal metabolism in hamsters varied by sex and dietary protein and were somewhat different than those reported for other rodents.

Aging↗
PubMed1983

Lack of inhibition by retinoids of bis(2-oxopropyl)nitrosamine-induced carcinogenesis in Syrian hamsters.

Syrian hamsters were treated with either a low (10 mg/kg body weight) or high (40 mg/kg body weight) single dose of bis(2-oxopropyl)nitrosamine (BOP) and beginning 1 week later fed either low (0.2 mmol/kg diet) or high (0.4-1.0 mmol/kg diet) levels of one of four retinoids [13 cis retinoic acid (13-cis-RA), N-ethylretinamide (ERA), N-(2-hydroxyethyl)retinamide (OHERA) or N-(phenyl)retinamide (PRA)] for periods of 40 or 50 weeks. The high retinoid levels (0.4-1.0 mmol/kg diet) fed following the highest BOP treatment enhanced pancreatic carcinoma yields (average number/effective animal) in males fed all four retinoids, and in females fed ERA and 13-cis-RA. Enhanced adenoma yields were also seen in all groups when high retinoid levels were fed following 40 mg BOP/kg body weight. However, these retinoid levels caused an increased adenoma yield in male hamsters only and did not modify carcinoma yields when fed following 10 mg BOP/kg body weight. Similarly, tumor yields at extra-pancreatic sites were elevated in retinoid-fed hamsters of both sexes after 40 mg BOP/kg body weight and in males fed ERA and 13-cis-RA after 10 mg BOP/kg body weight when retinoids were given at the high levels (0.4-1.0 mmol/kg diet). Increased incidences of bile duct and liver tumors in particular were found in hamsters given 40 mg BOP/kg body weight. Consumption of retinoid levels of 0.4 mmol/kg diet and above was also associated with a high incidence of liver cell necrosis, ovarian cysts and ovarian hemorrhage. Retinoids (ERA, OHERA, and PRA) fed at the low level (0.2 mmol/kg diet) following the low BOP dose did not enhance carcinogenesis in the pancreas or at other sites and did not cause alterations in morphologic observations.

Animals↗
PubMed1983

Tolerance of diets deficient or excessive in selenium by Syrian hamsters.

Syrian hamsters were fed torula yeast (TY) diets with 8 selenium (Se) supplement levels (0.0-10.0 ppm Se as sodium selenite) or casein (C) diets with 5 supplement levels (0.0-5.0 ppm Se as sodium selenite) for 25 weeks. Whole blood Se, plasma glutathione peroxidase (GSH-Px) activity and erythrocyte GSH-Px activity were measured after 5, 10, 15 and 25 weeks. At 25 weeks hematology was examined and tissue samples analyzed for Se and evaluated for histopathological lesions. While survival was not influenced by dietary Se, food consumption and body weight gain were altered in animals given TY, as those fed 0.0, 0.05 or 10.0 ppm Se consumed less diet. Weight gains at 25 weeks were highest in animals at the 0.1 ppm Se level and reduced in those given unsupplemented TY or 10.0 ppm Se supplements. Hemoglobin, hematocrit and red blood cell counts were reduced in females fed the lowest and highest Se supplements with TY diets. With both C and TY, whole blood Se rose with increasing dietary Se and in the case of TY, Se was elevated with each feeding increment, except between the 0.05 and 0.1 ppm or the 0.25 and 0.5 ppm levels. Plasma GSH-Px increased with rising Se up to 10 ppm, and erythrocyte GSH-Px activity increased up to 5 ppm Se. Erythrocyte GSH-Px values were higher in animals fed C diets. Histopathological observations were normal at all Se levels. Syrian hamsters tolerated dietary Se from 0.05 to 5.0 ppm Se for 25 weeks of observation without detrimental effects.

Animal Feed↗
PubMed1983

Toxic effects of dietary selenium in the Syrian hamster.

Selenium (Se) toxicity and utilization was evaluated in hamsters fed casein- and torula yeast-based diets. 4-week-old hamsters received semipurified diets for 21 days. In experiment I diets were supplemented with either 0.25, 10, 20, 40 or 80 ppm Se as sodium selenite (SS) and in experiment II diets were supplemented with 0.1, 5.0 or 10.0 ppm as SS or selenomethionine (SM). Blood and tissue Se concentrations and glutathione peroxidase (GSH-Px) activity were measured at the termination of the feeding period. In both studies growth rate was depressed and food consumption decreased in hamsters given diets supplemented with 10 ppm or greater SS. Mortality associated with Se toxicity occurred only in females fed the 80 ppm Se-supplemented diet. Whole blood and tissue Se concentrations rose with increasing dietary Se and occurred up to the 80 ppm Se level in blood. Liver, kidney and lung Se concentrations were higher in hamsters fed SM than for those fed SS. Plasma GSH-Px activity was not significantly affected by increasing dietary Se levels, and hamsters fed dietary Se levels above 10 ppm did not have increased erythrocyte GSH-Px activity associated with increased blood Se concentrations. Liver GSH-Px activity was higher in SM-fed hamsters. The results suggest that dietary Se, fed as SS, becomes toxic for Syrian hamsters at levels of 10 ppm and above.

Animals↗
PubMed1983

Interaction of dietary fat and protein on pancreatic carcinogenesis in Syrian golden hamsters.

The role of interactions between dietary fat and protein in experimental pancreatic cancer was determined in Syrian golden hamsters treated with N-nitrosobis(2-oxopropyl)amine (BOP). Two levels of corn oil [4.5 and 18 g/385 kilocalorie (kcal)] were fed with each of two levels of casein (9 g/385 kcal and 36 g/385 kcal), either before or after a single sc injection of BOP (10 mg/kg body wt) at 8 weeks of age. Control diet was fed at other times (9 g corn oil and 18 g casein/385 kcal). The pancreatic ductular carcinoma incidence and multiplicity (average No. of tumors/tumor-bearing animals) increased as dietary fat and protein levels rose in hamsters fed the four diets after carcinogen treatment. Enhanced carcinogenesis by high-fat (HF) diets occurred only in hamsters fed the high-protein (HP) level, and protein effects were seen only with the HF diets. The low-fat-low-protein (LF-LP) diet inhibited pancreatic carcinogenesis among the hamsters given the four diets before BOP treatment. Pancreatic adenoma yields were elevated in hamsters given either HF or HP diets following BOP treatment, by comparison with the low levels. However, when diets were fed before BOP treatment, an increased yield occurred with the rise in protein, but the yield was reduced in males with the increase in fat. Acinar cell nodules were observed primarily in hamsters fed LP levels after BOP, and their multiplicity was highest in those given the HF diet. The interaction between dietary fat and protein demonstrated the interdependence of the effects of these two nutrients on pancreatic carcinogenesis in hamsters.

Adenoma, Islet Cell↗
PubMed1983

Modifying factors in pancreatic carcinogenesis in the hamster model. I. Effect of protein-free diet fed during the early stages of carcinogenesis.

The role of protein in pancreatic carcinogenesis was examined in outbred Syrian golden hamsters treated with the pancreatic carcinogen N-nitrosobis(2-oxopropyl)amine (BOP) and fed a purified protein-free diet (PPFD). The PPFD was fed for 28 days from 8 weeks of age; before and after animals were fed PPFD, they were given a commercial diet (CD). BOP was given before PPFD feeding (group 1) or at 18 days (group 2) and 28 days (group 3) from the beginning of the PPFD feeding. BOP-treated control hamsters (group 4) were pair-fed a purified control diet (PCD) instead of PPFD. All animals fed PPFD and PCD were returned to a CD for the rest of the experiment, which was terminated in each group 52 weeks after BOP treatment. The results showed a highly significant reduction of tumor incidence (P less than 0.0001) in hamsters that received PPFD, when compared to those fed PCD, regardless of the time of carcinogen administration during the dietary regimen. Hamsters treated with BOP at 18 days of PPFD (group 2) developed neither benign nor malignant pancreatic tumors. The inhibition of pancreatic neoplasms was not related to reduced calorie consumption, since this occurred in the BOP-treated hamsters that were pair-fed the PCD diet. The results indicated that both the initiation and promotion of pancreatic carcinogenesis with BOP in hamsters can be inhibited by lack of protein in the diet given for 4 weeks during the early stages of the neoplastic process.

Animals↗
PubMed1983

Increased tumorigenesis induced by N-nitrosobis(2-oxopropyl)amine in Syrian golden hamsters fed high-fat diets.

The effects of dietary fat on carcinogenesis were presented, with the pancreas excluded, in randombred Syrian golden hamsters after administration of N-nitrosobis(2-oxopropyl)amine (BOP). Diets containing 4.5, 9, or 18 g corn oil/385 kilocalories [low-fat (LF), medium-fat (MF), or high-fat (HF) diet, respectively] were fed in two sequences. In the first sequence during which the effects of fat on the initiation phase of BOP carcinogenicity were examined, LF or HF diets were fed to hamsters 3-7 weeks of age and for 2 days after a single sc BOP treatment (10 mg/kg body wt) to 8-week-old hamsters. These hamsters were then given MF diet for the remainder of their lives. In the second sequence during which the role of fat on the promotional phase (development) of BOP-induced cancer was evaluated, MF diet was fed during the weeks preceding BOP treatment and LF or HF levels were given after BOP treatment. Separate groups were fed MF diet throughout both phases, and parallel animal groups received each diet sequence and were treated with saline at 8 weeks of age. Renal adenocarcinomas in males were observed only in those given HF diet either before or after BOP treatment (9% incidence). Similarly, pulmonary adenoma and intraphepatic biliary cystic adenoma (cholangioma) incidences were elevated above spontaneous rates in HF-fed groups. This study demonstrated that dietary fat enhanced BOP-induced tumorigenesis in the kidneys, lungs, and liver when fed, either during initiation (preceding carcinogen treatment) or at promotional stages (following carcinogen treatment).

Age Factors↗
PubMed1983

Modifying factors in pancreatic carcinogenesis in the hamster model. IV. Effects of dietary protein.

The possible effects of dietary protein on pancreatic cancer induced in outbred Syrian golden hamsters by N-nitrosobis(2-oxopropyl)amine (BOP) were studied. Three levels of casein as protein at low [LP = 9 g/385 kilocalories (kcal)], medium (MP = 18 g/385 kcal), or high levels (HP = 36 g/385 kcal) were fed in two sequences to 4 groups of hamsters. The effects of protein level on the initiation phase of BOP carcinogenesis were examined in hamsters fed LP or HP from 3 through 7 weeks of age, followed by MP for the remainder of their lives. The role of protein level on the promotional (developmental) phase of carcinogenesis was evaluated in hamsters fed (from 3 through 7 wk of age) MP, followed by LP or HP for the rest of their lives. One-half of the hamsters from each of the 4 groups received a single sc BOP injection (10 mg/kg body wt) at 8 weeks of age. Changes in diet from one type to the other occurred 2 days after BOP treatment. An MP diet fed before and after BOP served as the experimental control diet. The results demonstrated that the LP diet inhibited the developmental phase of carcinogenesis only in females, whereas the MP and HP diets did not affect initiation or promotion of cancer in either sex. The inhibitory effect of the LP diet in pancreatic carcinogenicity only in females calls for further studies.

Animals↗
PubMed1983

Influence of dietary fat on spontaneous lesions of Syrian golden hamsters.

Dietary corn oil was consumed by Syrian golden hamsters at levels of 4.5 g [low fat (LF)] or 18 g [high fat (HF)]/385 kilocalories (kcal) from 3 to 7 weeks of age followed by a diet containing 9 g [medium fat (MF)]/385 kcal for life. In other groups MF diet was given from 3 to 7 weeks of age and followed by either LF or HF for life. A separate group was fed MF continuously after 3 weeks of age. Spontaneous lesions, which were altered by these dietary protocols, are reported. An HF diet fed after 8 weeks increased the incidence of flank organ hyperplasia and prostatitis, but it decreased prostatic fibrosis in males. Consumption of HF diets after 8 weeks by females increased survival and resulted in an elevated incidence of thyroid adenomas, ovarian cell hyperplasia, vaginal papillomas, and adrenal cortical cell adenomas. In age-adjusted data the increase in ovarian cell hyperplasia and adrenal cortical cell adenomas was shown to be due to HF diet and not to be a consequence of extended survival. Periodontitis and calcification of cardiac tissues decreased in hamsters fed HF diets after 8 weeks, but cell vacuolization and hyperplasia of the anterior pituitary gland and epithelial hyperplasia in the forestomach were increased. Salivary gland adenocarcinomas were observed only in hamsters fed HF diets. Feeding HF levels, either during weeks 3-7 or after week 8, decreased osteofibrosis and otitis media and increased urinary bladder epithelial hyperplasia, adrenal cortical cell lipomatosis, and bone chondrosis. Calcification of gastric and renal arteries decreased as dietary fat levels increased either before or after 8 weeks of age in males and only when fed after 8 weeks in females. Colitis and focal glandular hyperplasia of the colon mucosa were increased in both sexes by an HF diet being given before or after 8 weeks of age.

Animals↗
PubMed1982

Nutritional evaluations of three dietary levels of lactalbumin throughout the lifespan of two generations of Syrian hamsters.

Syrian hamsters were fed one of three levels of lactalbumin (10, 20 or 40%) or a commercial diet from 4 weeks of age. The hamsters were mated at 12 weeks of age and parents (Fo generation) and offspring (F1 generation) remained for life on the assigned parental diet. Hamsters were killed to evaluate nutritional status from both generations at 4, 10, 22, 34 and 64 weeks of age. Remaining hamsters were allowed to live out their natural lifespan. Female hamsters generally grew faster with each increment in lactalbumin. Growth was greatest in male hamsters on the 20% lactalbumin diet and greater in the F1 than in the F0 generation. Reproduction was superior in hamsters fed the commerical diet and differed by season in those given purified diets, with the best performance following the autumn matings. Litter size and body weights of offspring at weaning increased from hamsters fed 10% of those fed higher levels. In the F0 generation, the longest female lifespans were observed in the 20 and 40% lactalbumin groups, respectively. The F1 generation females had longer survivals with each increase in lactalbumin. Male survival in both generations increased from the commercial diet to the 40 and 10% lactalbumin levels and was greatest in males fed 20% lactalbumin diet.

Animals↗
PubMed1982

Modification of circadian rhythms of drug metabolism in the Syrian hamster.

Male Syrian hamsters consumed one of three levels of lactalbumin (10, 20, or 40%) for 8 weeks prior to administration of a single dose of 20 mg/kg (sc) N-nitrosobis(2-oxopropyl)amine (BOP) at 0600 hr. Liver weights, liver microsomal protein, and cytochrome P450 content and the activities of microsomal ethylmorphine N-demethylase (EMND), aniline hydroxylase (ANH), and arylhydrocarbon hydroxylase (AHH) were determined in control and BOP-treated animals after 0 (0600), 3 (0900), 6 (1200), 12 (1800), and 24 (0600) hr. Circadian rhythms were observed in liver weights, contents of microsomal protein, and cytochrome P450 and in the activities of EMND and ANH. Cycles of liver weight, cytochrome P450, and EMND activity were present in animals fed the higher (20 and 40%) lactalbumin levels, but not in those fed the low level (10%). BOP treatment eliminated the circadian cycles of cytochrome P450 and EMND, and reduced liver weight, the content of microsomal protein, and the ANH activity at two or three of the measurement times. AHH activity did not exhibit a circadian cycle, but these values were consistently increased by feeding high protein and reduced by BOP.

Aniline Hydroxylase↗
PubMed1982

Dietary amino acids and hepatic microsomal drug metabolism in Syrian hamsters.

The source and level of amino acids fed to Syrian hamsters modified hepatic microsomal drug metabolism in this species, and the effects differed between the two sexes. Drug-metabolism systems of the liver were evaluated in Syrian golden hamsters fed three sources of amino acids, casein (C), lactalbumin (L) and supplemented casein (SC), each at four levels (4, 10, 20, and 40 gm/100 gm of diet). A protein-free (PF) diet was fed to an additional hamster group. Hepatic microsomal protein content, cytochrome P450 content, and aryl hydrocarbon hydroxylase (AHH) and aniline hydroxylase (ANH) activities were measured after three weeks of feeding the diets. Microsomal protein content generally rose with increasing protein levels in the diets from 0 to 20 gm/100 gm diet, except for C-fed females, in which values did not differ from those fed PF diet. Supplemented casein supported no increased levels of microsomal protein when fed from 4-40 gm/100 gm diet; however microsomal protein rose from increased dietary C and L up to 20 gm/100 gm diet in males and from increased L up to 20 mg/100 gm diet in females. Cytochrome P450 content was influenced in animals fed C and L by amino acid level in a manner similar to observed effects on microsomal protein. However, consumption of 10 gm SC/100 gm diet by males resulted in the highest cytochrome levels. AHH activity rose with increased dietary amino acids for both male and female hamsters; and maximal activities occurred in hamsters fed the 20 or 40 gm protein/100 gm diet levels. ANH activity was influenced both by amino acid source and level with both sexes; the feeding of C resulted in a higher activity of this enzyme than that of SC. ANH activity was highest in hamsters fed the 20 and 40 gm amino acid/100 gm diet levels.

Amino Acids↗
PubMed1982

Effects of the source and level of protein fed to Syrian hamsters on growth, protein utilization, and selected blood proteins.

Syrian hamsters were fed diets formulated with casein, lactalbumin, and casein supplemented with L-methionine and L-cysteine for 3 weeks. Each protein source was fed at 4, 10, 20, and 40 g/100 g diet and supplied 3.4, 9, 17, and 34% protein. A protein-free diet was given to separate groups. Maximal growth rates were obtained at the 10, 20, and 40 g/100 g diet levels, and protein efficiency ratios showed maximal protein utilization with the 10 g/100 g diet level of each protein source. Net protein utilization was influenced by both protein source and level. In both sexes, casein was less well-utilized than either lactalbumin or supplemented casein when the protein sources were fed at the 4 or 10 g/100 g diet levels. Whole blood hemoglobin increased with increasing dietary protein levels, irrespective of protein source. Protein source influenced serum albumin concentrations in female hamsters at the 4 and 10 g/100 g levels and in male hamsters at the 40 g/100 g level. The highest albumin concentrations were observed in females fed 10 g lactalbumin/100 g diet or 20 or 40 g casein/100 g diet. Maximal concentrations of serum alpha one globulin were observed in female hamsters at the 4 or 10 g/100 g diet and in male hamsters at the 0 or 4 g/100 g levels. Serum beta globulins were influenced by protein level. The highest concentrations were observed in the animals fed 10 to 40 g protein source/100 g diet. Serum protein changes were not consistently related to differences in growth or protein utilization.

Animal Nutritional Physiological Phenomena↗
PubMed1982

Survival of hamsters fed graded levels of two protein sources.

Two protein sources (supplemented casein and lactalbumin), which were well-utilized by Syrian hamsters in previous 3-week experiments, were fed in long-term studies. Casein supplemented with methionine and cysteine was fed for 20 weeks at levels of 4, 20, and 40 g/100 g diet. The lowest level did not support normal growth and resulted in the highest mortality rate during the first 10 weeks of feeding. The higher levels caused increased mortality in females, in association with decreasing body weights between 16 and 20 weeks. Kidney weights and incidences of lower nephron nephrosis at 20 weeks were elevated in both sexes fed the 40 g/100 g levels of supplemented casein by comparison with the 10 g/100 g level. In a separate experiment, lactalbumin was fed for life at 10, 20, and 40 g/100 g diet levels, and its effects compared to those with a commercial diet. The lactalbumin diet supported somewhat slower growth rates, but improved survival when compared to commercial diet-fed groups. Survival was longest in both sexes fed the 20 g lactalbumin/100 g diet levels for life.

Animal Nutritional Physiological Phenomena↗
PubMed1981

Sex differences in the effects of retinoids on carcinogenesis by N-nitrosobis(2-oxopropyl)amine in Syrian hamsters.

Syrian hamsters were given in a single dose of N-nitrosobis(2-oxopropyl)-amine (BOP) (40 mg/kg, s.c.) and 1 week later were fed 1 of 4 retinoid types (13-cis-retinoic acid (13-cis-RA), N-ethylretinamide (ERA), 2-hydroxyethylretinamide (OH-ERA), or 4-hydroxyphenylretinamide (PRA)) each at 3 levels (0.05, 0.1, 0.2 mM/kg diet). The pancreatic carcinoma incidence was not influenced significantly by feeding retinoids. The pancreatic adenoma incidence, however, was reduced by feeding each of the retinoids to female hamsters, with the reduction varying with the retinoid fed (13-cis-RA greater than ERA and OH-ERA greater than PRA). In male hamsters increased numbers of pancreatic adenomas were observed after feeding OH-ERA and PRA. Tumors induced in other tissues were reduced by retinoids in females, but not in males. Females fed 13-cis-RA and ERA had a lower incidence of gall bladder polyps, and feeding OH-ERA reduced the liver tumor incidence. Food consumption and serum alkaline phosphatase ans aspartate amino transferase activities were not influenced by BOP or retinoid type or level. Body and pancreas weight were influenced by retinoid level, but the effects were not consistently dose-related.

Animals↗
PubMed1981

Enhancement of experimental pancreatic cancer in Syrian golden hamsters by dietary fat.

The effects of dietary fat on the induction and development of pancreatic ductular adenocarcinoma were studied in randombred Syrian golden hamsters. Diets containing low-fat (LF) or high-fat (HF) levels of corn oil [4.5 or 18.0 g/385 kilocalorie (kcal)], contributing 10 or 41% of the calories, respectively, were fed either before or after a single injection of N-nitrosobis(2-oxopropyl)amine (BOP) (10 mg/kg body wt). Control hamsters were fed corn oil at a medium-fat (MD) level (9 g/385 kcal) for life. The incidence of ductular adenocarcinomas increased in both males and females (LF diet, 16%; HF diet, 34%) when the HF diet was fed after BOP treatment. The average number of carcinomas per carcinoma-bearing animal also increased (LF diet, 1.3; HF diet, 3.0), but the carcinoma incidence was not influenced by these diets being fed before carcinogen treatment. The incidence of ductular adenomas was high with all treatments and was not influenced by diet. However, the number of adenomas was increased in animals fed HF diets. In addition, the incidence of acinar cell nodules was elevated in animals fed the MF and HF diets after BOP administration. These results showed that dietary fat modified the development of experimental ductular adenocarcinoma of the pancreas.

Adenoma↗