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PubMed1990

Energy expenditure in humans: effects of dietary fat and carbohydrate.

A high-dietary fat intake may be an important environmental factor leading to obesity in some people. The mechanism could be either a decrease in energy expenditure and/or an increase in caloric intake. To determine the relative importance of these mechanisms we measured 24-h energy expenditure in a whole body calorimeter in 14 nondiabetic subjects and in six subjects with non-insulin-dependent diabetes mellitus, eating isocaloric, weight-maintenance, high-fat, and high-carbohydrate diets. All subjects were Pima Indians. In nondiabetics, the mean total 24-h energy expenditure was similar (2,436 +/- 103 vs. 2,359 +/- 82 kcal/day) on high-fat and high-carbohydrate diets, respectively. The means for sleeping and resting metabolic rates, thermic effect of food, and spontaneous physical activity were unchanged. Similar results were obtained in the diabetic subjects. In summary, using a whole body calorimeter, we found no evidence of a decrease in 24-h energy expenditure on a high-fat diet compared with a high-carbohydrate diet.

Adult↗
PubMed1998

Chronic ingestion of dietary fat is a prerequisite for inhibition of feeding by enterostatin.

Enterostatin (Ent), the activation pentapeptide from procolipase, inhibits the intake of dietary fat. The selectivity of the response to fat suggests that the rat must recognize a permissive signal related to dietary fat for the Ent biological response. To investigate the nature of this signal, we studied the effects of Ent in rats that were adapted to either a high-fat (HF) or high-carbohydrate/low-fat (HC) diet and then naively exposed to either HF or HC diets. Ent (1 nmol) was injected into the lateral ventricle of overnight-fasted rats, and food intake was measured. Rats adapted to HF diet and tested with HC diet responded to Ent, but rats adapted to HC diet and tested with HF did not respond to Ent. The groups were maintained on their new test diets for up to 21 days and tested again for their response to Ent at 3, 7, 14, and 21 days. Ent response did not appear in HC-adapted rats switched to HF diet before 21 days. Conversely, the HF-adapted rats, which responded to Ent when tested with HC diet for the first time, did not respond at any subsequent testing time. The data suggest that chronic ingestion of dietary fat is required for Ent action and that chronic consumption of fat initiates a postingestion metabolic, endocrine, or neurochemical change that is required for the biological response to Ent.

Acclimatization↗
PubMed1999

Transcriptional regulation of cellular retinol-binding protein, type II gene expression in small intestine by dietary fat.

We have previously demonstrated that dietary fat, especially unsaturated fatty acids, induces cellular retinol-binding protein, type II (CRBPII) gene expression in rat jejunum. In the present study, we showed that feeding a high-fat diet caused parallel increases in jejunal CRBPII mRNA and CRBPII pre-mRNA levels. Nuclear run-on assay also revealed that this increase of CRBPII mRNA level by high-fat diet was, at least in part, triggered at a transcription level. Moreover, peroxisome proliferator-activated receptor alpha (PPARalpha) mRNA level was also increased in the jejunum by high-fat diet. Gel shift assay showed that the binding activity of rat jejunal nuclear protein to the nuclear receptor response elements located in the rat CRBPII gene (RXRE and RE3) was greater in rats fed high-fat diet than in those fed fat-free diet and were enhanced by addition of bacterially expressed PPARalpha protein. Also PPARalpha-retinoid X receptor alpha (RXRalpha) heterodimer was capable of binding to the CRBPII-RXRE and RE3 elements and these binding activities were enhanced by addition of some PPARalpha ligands in the gel shift assay. Taken together, these studies suggest that dietary fatty acids may lead to induction of CRBPII gene transcription through increases of PPARalpha as well as its ligand levels.

Animals↗
PubMed1995

Review of the effects of dietary fat on experimental mammary gland tumorigenesis: role of lipid peroxidation.

The purpose of this communication is threefold, that is, (1) to review and critique the studies designed to examine the interrelationship between dietary fat and experimental rodent mammary gland tumorigenesis, (2) to assess the influence of dietary fat on growth of human breast carcinoma transplants in immunodeficient mice, and (3) to examine and discuss the role of products of lipid peroxidation in these tumorigenic processes. It is concluded from this review and critique that the amount and type of dietary fat can significantly influence the development and/or growth of rodent mammary gland tumors and growth of human breast carcinomas in immune deficient mice. Dietary fat can be either stimulatory or inhibitory to these tumorigenic processes, phenomena that could be a function, at least in part, of the generation of products of lipid peroxidation.

Animals↗
PubMed1998

Dietary fat type and level influence adiposity development in obese but not lean Zucker rats.

The development of obesity is influenced by a variety of factors including genetics and dietary fat type and level. To examine the interaction between these factors, male lean and obese Zucker rats (5 weeks initial age) were fed either a low-fat (15% calories) or one of two high-fat diets (65% calories; predominant fat source of either soybean oil or palm olein) for 8 weeks. Body weight, food intake, indirect calorimetry, and body composition determinations were performed. As expected, food intake, body weight, feed efficiency, oxygen consumption, heat production and carcass lipid were all significantly higher in obese compared to lean rats. Dietary fat level and/or type influenced body weight gain, oxygen consumption, heat production, energy balance, and carcass weight and lipid content in the obese but not in the lean Zucker rats. Oxygen consumption and carcass weight were increased approximately 25% and 10% respectively in obese rats fed either of the two high-fat diets as compared to those fed the low-fat diet. The type of fat fed in the high-fat diets also influenced body weight gain, heat production, energy balance, and carcass lipid content of the obese rats. Body weight gain and carcass lipid content were increased (16%-17%; P < 0.005) in obese rats fed the high-fat palm olein diet as compared to those fed the low-fat diet. These parameters were not increased in obese rats fed the high-fat soybean oil diet. In contrast, indirect calorimetry measurements indicated a moderate increase in heat production (Kcal/effective body mass/day; 14.5%) and decrease in energy balance (44.8%) in the obese rats fed the high-fat soybean oil diet as compared to those fed the low-fat diet. Energy expenditure and lipid accumulation were negligibly influenced by dietary fat level or type in the lean Zucker rats. The differential response of the lean and obese Zucker rats to this short-term dietary manipulation demonstrate that genetic background can influence an individual's response to dietary fat type and level. The genetically obese Zucker rat appears to be a good model for further studies of high-fat diet-induced obesity.

Adipose Tissue↗
PubMed1978

Regulation by dietary fats of 3-hydroxy-3-methylglutaryl-Coenzyme A reductase in rat liver.

The effects of various dietary fats on the activity of 3-hydroxy-3-methylglutaryl-Coenzyme A (HMG-CoA) reductase in rat liver microsomes, the rate-limiting enzyme in cholesterogenesis, were examined. A series of experiments demonstrated the dependency of the HMG-CoA reductase activity on the nature of dietary fats. When saturated fats with chain length of 12 to 18 were the dietary sources and were fed at the 10% level for 19 days, feeding fats with shorter chain fatty acids caused a lower enzyme activity compared to those with longer chain fatty acids. The activity was also regulated by the degree of unsaturation of dietary fats; when safflower oil, camellia oil or tristearin were fed at the 10% level for 18 days, the higher the unsaturation, the lower the activity. When trimyristin or tripalmitin were fed at the 10% level for 14 days, addition of essential fatty acid, at the level of minimum daily requirement (1% was replaced by safflower oil), did not affect the enzyme activity. Through the rate of incorporation of mevalonate into cholesterol in the 12,500 x g supernatant fraction of the liver was also found to be influenced by the types of dietary fats, the extent of the response appeared much smaller than that of HMG-CoA reductase. No consistent correlation between the HMG-CoA reductase activity and the content of microsomal cholesterol or cholesteryl ester and the fatty acid composition of microsomal lipids was observed.

Animals↗
PubMed1993

Adipose tissue fatty acids and dietary fat sources in relation to endometrial cancer: a retrospective study of cases in remission, and population-based controls.

This study describes associations between early-stage endometrial cancer and type of dietary fat consumed, based on (i) adipose tissue fatty acid content (a biomarker for dietary fat) and (ii) self-reported frequencies of selected high-fat foods. Because obesity may be associated with high dietary fat intake as well as endometrial cancer, a secondary objective is to determine whether the observed dietary associations are statistically independent of body composition, assessed as percent body fat. To achieve these aims, we examined 20 cases of endometrial cancer in remission and 20 community controls, all aged 55-64. Abdominal adipose tissue biopsies from cases contained significantly higher concentrations of saturated fatty acids of intermediate chain length (C12-C16), lower ratios of polyunsaturated to saturated fatty acids (P:S ratio), and lower concentrations of C18 polyunsaturated as well as C18 saturated fatty acids. These differences were independent of degree of adiposity measured in a whole body 40K counter and several measurements of regional fat distribution. In addition, each subject's consumption of 20 high-fat items was reported by means of a semiquantitative food frequency questionnaire. Analysis of these data indicated that cases consumed more animal-derived fats, again independent of obesity. In particular, cases used more butter in cooking, ate more bacon, and drank more whole milk. Animal-derived fat intake displayed an inverse association both with the P:S ratio and the C18 polyunsaturated fatty acid content of adipose tissue, lending internal validity to the dietary data. These findings are consistent with the hypothesis that the type of dietary fat consumed may influence the occurrence of endometrial cancer.

Adipose Tissue↗
PubMed2006

Telephone-based counseling improves dietary fat, fruit, and vegetable consumption: a best-evidence synthesis.

Eating more fruits/vegetables and less dietary fat rank among the most important nutrition recommendations for health improvement. Telephone counseling is an increasingly popular means of delivering support for diet modification. Using a best-evidence synthesis, the purpose of this review was to assess the effectiveness of telephone-based counseling on improving dietary fat, fruit, and vegetable consumption for adults. Online databases and article bibliographies were searched to produce relevant randomized-controlled trials published during the past 5 years. Nine studies were ultimately included and the weight of the evidence indicated that telephone-based counseling promotes significantly greater improvements in fruit/vegetable consumption (median effect size=0.41) and dietary fat intake (median effect size=0.22) relative to usual care. Improvements were especially pronounced among women with (or at high risk for developing) cancer. In some studies, telephone-based counseling was also associated with greater improvement in blood lipid levels and weight. Based on these findings, several design considerations (eg, population focus, counseling intensity) for program managers are proposed. Telephone-based counseling was found to be a moderately effective intervention, but there are not enough studies yet to draw conclusions on other research questions, such as how advantageous telephone-based counseling is over traditional forms of dietary counseling. At present, telephone-based counseling may best be used as a complement to clinical care and a means to broaden the outreach of nutrition services.

Counseling↗
PubMed2005

Effects of increased dietary fat and exercise on skeletal muscle lipid peroxidation and antioxidant capacity in male rats.

BACKGROUND: Elevated dietary fat increases oxidative metabolism and has been linked to increased oxidative stress, while exercise training may augment antioxidant capacity. Most studies examining oxidative stress in skeletal muscle employ extremely high levels of dietary fat and/or intense exercise training that may not adequately model human diet and activity patterns. AIM: The purpose of this study was to examine the interaction between an elevated (40% of calories) monounsaturated fat diet and a moderate-intensity exercise program similar to recommended human exercise prescriptions, on skeletal muscle oxidative stress and antioxidant defenses. METHODS: Twenty-four male Sprague-Dawley rats (approximately 500 g) were randomly divided into 4 groups (n = 6/group): Standard Diet-Sedentary (SD-Sed), Standard Diet-Exercise (SD-Ex), Elevated Fat Diet-Sedentary (EFD-Sed), and Elevated Fat Diet-Exercise (EFD-Ex). The SD groups consumed 76% of calories from CHO, 14% from protein, and 10 % from fat, while the EFD groups received a diet of 46% of calories from CHO, 14% from protein, and 40 % from fat (high oleic sunflower oil). The exercise groups were progressively treadmill trained at 20 m/min, 4 days/week increasing from 15 min/day to 35 min/day by the end of 4 wks. RESULTS AND CONCLUSION: Antioxidant adaptations associated with exercise training or an elevated fat diet individually reduced basal lipid peroxidation levels in the plantaris muscle. However, the combination of exercise plus a monounsaturated fat diet increased lipid peroxidation levels above that with either treatment alone. This suggests an exhaustion of the antioxidant capacity in the plantaris muscle when both exercise and increased dietary fat diet are combined.

Animals↗
PubMed2006

Biologically based complementary and alternative medicine use among breast cancer survivors: relationship to dietary fat consumption and exercise.

Previous literature has shown that more than half of all female cancer survivors use some form of complementary and alternative medicine (CAM). Although the prevalence of CAM use in this population is becoming apparent, few researchers have examined the relationship between CAM use and lifestyle factors that could influence patients' well-being. The present study examined whether breast cancer survivors who use biologically based CAM are more likely than CAM nonusers to follow a low-fat diet and maintain moderate or vigorous exercise. Sixty-five female breast cancer survivors who were within 3 months of completing primary treatment were recruited. CAM use was measured by self-reported use of one or more of a list of 15 supplements. Dietary fat was measured by a 23-item self-report measure estimating fat consumption in the past month. Dietary fat stage of change and moderate and vigorous exercise stage of change were assessed using measures based on the Transtheoretical Model of Behavior Change. Results showed that biologically based CAM users maintained a lower percentage of calories from fat in their diet (t=2.12, p<0.05), and there was a trend for CAM users to be more likely than CAM nonusers to be in the action or maintenance stage for dietary fat consumption (p<0.09). However, this study did not find that CAM users were more likely to be in the action or maintenance stage of change for moderate or vigorous exercise. These findings suggest that biologically based CAM use among breast cancer survivors is associated with some, but not all, healthy lifestyle behaviors.

Adult↗
PubMed1976

Effect of dietary fats on ovine adipose tissue metabolism.

The effects of different dietary fats on ovine adipose tissue metabolism have been investigated. Six-month old sheep were fed for 6 weeks a control diet or diets supplemented with either tallow or a mixture of sunflower seed oil and soybean oil, treated to protect the fats from hydrolysis and hydrogenation in the rumen, or with maize oil. The rates of fatty acid, glyceride glycerol, and CO2 formation were measured in perirenal and subcutaneous adipose tissue slices by following the incorporation of either 14C from labeled acetate or glucose, or 3H from tritiated water into the appropriate product. Feeding protected tallow or maize oil but not protected sunflower seed oil plus soybean oil resulted in reduced rates of fatty acid biosynthesis in both perirenal and subcutaneous adipose tissue slices and CO2 formation in perirenal adipose tissue. Feeding the fat-supplemented diets had no effect on the rate of glyceride glycerol formation. The fat-supplemented diets also resulted in reduced activities of various enzymes, thought to be involved in lipogenesis, measured in 105,000 x g supernatant fractions from adipose tissue homogenates. The results suggested that ovine adipose tissue lipogenesis is sensitive to both the amount and the nature of dietary fat.

Acetate-CoA Ligase↗
PubMed1986

Modulation of putative preneoplastic foci in exocrine pancreas of rats and hamsters. I. Interaction of dietary fat and ethanol.

The effect of dietary fat and ethanol and their interactions on the development of putative, preneoplastic foci in exocrine pancreas was investigated in rats and hamsters. Rats were given a single i.p. injection of 30 mg azaserine per kg body wt at 19 days of age. Hamsters were injected s.c., with 20 mg N-nitrosobis(2-oxopropyl)amine (BOP)/kg body wt at 6 and 7 weeks of age. The animals were fed a low fat (LF) control diet (5% corn oil) or a high fat (HF) diet (25% corn oil). Ethanol was provided in drinking water at a 15% (w/v) concentration. The animals were given the respective diets and ethanol after the treatment with carcinogen. At 4 months post-initiation, the pancreata were quantitatively examined for the number and size of preneoplastic foci. In rats, acidophilic as well as basophilic foci were subject to modulation by HF and ethanol. The results point to a specific promoting effect of unsaturated fat on the growth potential of azaserine-induced acidophilic acinar cell foci in rat pancreas. There was no evidence of an interaction between HF and ethanol as far as acidophilic foci are concerned. Evaluation of the number and size of the basophilic foci demonstrated an enhancing effect of ethanol on the modulation of pancreatic carcinogenesis by fat, pointing to a possible interaction between these two lifestyle factors. This suggestion was supported by the finding that six out of 20 rats in the HF with ethanol group exhibited a carcinoma in situ, whereas in the HF and in the ethanol group such an advanced lesion was found in one animal only. Unlike in rats, ethanol had no modulating effect on number and growth of putative, preneoplastic lesions in hamsters, either in combination with LF or in combination with HF. A HF diet, however, caused a significant increase in number as well as an increase in percentage of pancreatic tissue occupied by early lesions induced in hamster pancreas by BOP.

Adenosine Triphosphatases↗
PubMed1990

Use of fat-modified food products to change dietary fat intake of young people.

Food purchasing and preparation practices were modified in two boarding high schools to increase the polyunsaturated-to-saturated fat ratio (P/S) of the diet of students by changing food products rather than attempting to change eating behaviors. During years when fat-modified products were served, the P/S of males increased by 75 percent, versus a decrease of 6 percent during control years. For females, P/S increased by 53 percent during intervention years, versus an increase of 6 percent during control years.

Adolescent↗
PubMed2000

Dietary fat and breast cancer.

One of the most often studied associations in epidemiology is dietary fat and breast cancer risk. That migrants from low-risk countries increase their risk on immigrating to higher-risk countries suggests that some modifiable lifestyle or environmental factor is responsible for the development of breast cancer. Although early international correlational studies and experimental animals studies support dietary fat as a risk factor for breast cancer, more recent data from case-control studies and cohort studies have been equivocal, thus the analytical data do not support a strong positive association. The conflicting results from analytic studies may be due to methodologic issues associated with study design, dietary assessment tools, measurement error, improper statistical analyses, and a lack of heterogeneity in fat intake among the study population. Moreover, current dietary questionnaires may be inadequate in capturing true dietary intakes or capturing the risk with exposure during earlier periods of a woman's life. Although two large clinical trials investigating the fat/breast cancer relationships issue are underway, researchers are generally skeptical at their ability to detect an independent association between fat and breast cancer risk. Further epidemiologic studies using current methodology may not prove to be fruitful in generating definitive answers to shed light on this controversial issue. In addition, rather than concentrating on dietary fat, researchers should focus on diets that are not only low in saturated fat, but also high in fruit and vegetable consumption. Researchers should take advantage of advances in molecular and genetic technology for a different perspective in examining the issue. For example, markers of susceptibility to breast cancer that can detect women at higher risk for breast cancer may be helpful in clarifying the role of dietary fat. More comprehensive and multiple approaches to studying dietary factors and breast cancer are recommended.

Age Factors↗
PubMed1993

Dietary fat exacerbates liver disease in bile duct-ligated rats.

Previous studies have suggested that the mortality of bile duct-ligated (BDL) rats is related to the amount of dietary fat consumed. We investigated the influence of dietary fat concentration on liver disease in BDL rats. Groups of rats were fed for 4 wk either a low fat diet (LF, 0.92 kJ/g; 3% of total energy from fat), a high fat diet (HF, 1.07 kJ/g; 30% fat), a high fat diet with energy density equivalent to that of the LF diet (HFIB, 0.92 kJ/g; 30% fat) or a diet based on the composition of commercial nonpurified diets (COMP, 0.90 kJ/g; 10% fat). Energy intake, body weight gain, plasma biochemical indices and hepatic histology were compared in BDL and sham-operated control rats. Bile duct-ligated animals consuming the LF diet showed a faster recovery of energy intake and greater body weight gain following surgery than did BDL animals fed the other three diets. Plasma alkaline phosphatase activity was significantly greater in BDL animals fed either of the high fat diets than in those fed the LF or COMP diet starting 1 and 2 wk, respectively, after surgery. Hepatic fibrosis and bile duct proliferation at d 28 post-ligation were greater in rats fed a 30% fat (HF) diet than in rats fed the 3% fat (LF) diet. These results suggest that dietary fat concentration can influence the severity of liver dysfunction in extrahepatic biliary obstruction.

Alkaline Phosphatase↗
PubMed2000

Nutrition intervention group program based on preaction-stage-oriented change processes of the Transtheoretical Model promotes long-term reduction in dietary fat intake.

OBJECTIVE: To develop and evaluate the long-term effectiveness of an intervention program, based on preaction-stage-oriented change processes of the Transtheoretical Model of Behavior Change, that could be delivered in a group setting to help participants lower dietary fat intake. DESIGN: An enhanced version of the nonequivalent control group experimental design was used. Entire sections of an undergraduate introductory nutrition science course were assigned to an experimental, pretest/posttest control, or posttest-only control group. Daily fat intake and stage of change of the experimental and pretest/posttest control groups were determined at the pretest and posttest and 1-year later at a follow-up test. Every 1 to 2 weeks during the study, stage of change of the experimental group was assessed. Daily fat intake of the experimental group was assessed at study midpoint. Daily fat intake and stage of change of the posttest-only control group was determined at the posttest. Pretest results were used to place participants of the experimental and pretest/posttest control groups in either the preaction stage (i.e., precontemplation, contemplation, or preparation) or the action/maintenance stage. SUBJECTS/SETTING: The sample consisted of 38, 30, and 42 undergraduate students who were assigned to the experimental, pretest/posttest control, and posttest-only control groups, respectively. INTERVENTION: The experimental group participated in a group-based, dietary fat intake intervention that included a series of 11 lessons taught over a 14-week period. Each lesson was based on 1 or 2 of the preaction-stage-oriented change processes of the Transtheoretical Model. MAIN OUTCOME MEASURES: Data were evaluated to determine the effects of the intervention program on long-term dietary fat reduction and stage of change progression. STATISTICAL ANALYSIS PERFORMED: Analysis of variance, repeated-measures analysis of variance, and paired t tests. RESULTS: For pretest and posttest dietary fat intake scores, stage and time were significant, and there was a significant time-by-stage interaction. Time was significant for pretest and posttest stage scores. Subjects in the preaction-stage experimental group significantly increased their mean stage of change and reduced their fat intake between the pretest and posttest; these changes persisted for 1 year. Pretest/posttest control group participants who began in a preaction stage also significantly increased their mean stage and reduced fat intake by the posttest, but these changes did not endure until the follow-up test. APPLICATIONS/CONCLUSIONS: This intervention program produced an enduring, significant reduction in mean dietary fat consumption and a significant progression in mean stage of change of subjects in the experimental group who were in the preaction stage. It may be appropriate to design group interventions to use preaction stage processes rather than the more traditionally used action and maintenance stages change processes.

Adolescent↗
PubMed2001

Is the association between dietary fat intake and insulin resistance modified by physical activity?

The rising prevalence of type 2 diabetes, a condition associated with insulin resistance, is commonly attributed to changes in dietary patterns and physical activity levels in susceptible populations. However, few studies have described the independent effects of dietary intake and physical activity on the degree of insulin sensitivity within populations or examined the possibility of interactions between dietary factors and physical activity. This study was undertaken to describe the relationship between the quantity and pattern of dietary fat intake on fasting insulin levels (a marker of insulin sensitivity) and to investigate whether the association was modified by physical activity. A cross-sectional study of 815 nondiabetic men and women (30 to 71 years) recruited from a population-based sampling frame was undertaken. Diet was characterized using a semiquantitative food frequency questionnaire. Physical activity level (PAL), the ratio of total energy expenditure to basal metabolic rate, was estimated using individually calibrated heart rate monitoring, a method previously shown to be an objective and valid method for assessing total energy expenditure. In a linear regression model adjusted for total energy intake, total fat intake bordered on a significant association with fasting insulin (b = 0.000081; P =.058), and the polyunsaturated to saturated fat ratio (P:S ratio) of the diet was negatively associated with fasting insulin concentration (b = -0.37, P <.001). A negative association was observed between the PAL and fasting insulin (b = -0.12, P =.025). The association of the P:S ratio and PAL with fasting insulin remained significant when adjusted for each other and for total fat, total energy intake, body mass index (BMI), waist-to-hip ratio (WHR), age, sex, family history of diabetes, smoking status, and alcohol intake (P:S ratio, b = -0.24, P =.003; PAL, b = -0.13; P =.007). The association with total fat intake was no longer significant in this multivariate model (b = 6.7 x 10(-6); P =.858). There was no evidence for an interaction between total dietary fat intake and PAL (b = -0.000048; P =.243) or between the P:S ratio and PAL (b = -0.013; P =.949). These data demonstrate an independent association between the P:S ratio of the diet, the overall level of physical activity, and the fasting insulin concentration, a marker of insulin sensitivity. There was no evidence that the association between dietary fat intake and insulin resistance was modified by physical activity. The findings provide further support for efforts to promote increases in overall physical activity and modifications in the pattern of dietary fat intake in the whole population.

Adult↗
PubMed1983

Influence of dietary fat and indomethacin on the growth of transplantable mammary tumors in rats.

Studies were designed to determine if treatment with indomethacin influenced the growth of a transplantable, metastatic, rat mammary tumor. Female, Wistar-Furth inbred rats were fed either a standard chow diet or a semipurified diet containing 2, 5, 10, or 20% stripped corn oil. Indomethacin was given in drinking water, and rats consumed between 2.5 and 3.0 mg indomethacin/kg body weight/day. Feeding of diets and initiation of treatment with indomethacin were started when rats were weaned (21 days old) and continued until they were killed. Approximately 5 X 10(3) mammary tumor cells (DMBA-4) were injected into the fat pad of the sixth mammary gland which is adjacent to the right inguinal lymph node. Each dietary/treatment group consisted of at least 10 rats. Since indomethacin inhibits prostaglandin synthesis, two other groups of non-tumor-bearing rats were used to determine if dietary fat and treatment with indomethacin either influenced prostaglandin E2 production (in vitro) by mononuclear cells from the spleen or altered serum levels of fatty acids. Results indicated that: (a) the rate of tumor growth in untreated rats was significantly greater when the dietary fat content was either 10 or 20% compared to diets containing either 2 or 5% fat; (b) the tumor growth-promoting effects of 10 and 20% fat diets were completely abrogated in rats treated with indomethacin; (c) treatment with indomethacin also inhibited tumor growth in rats fed diets containing either 2 or 5% fat; (d) synthesis of prostaglandin E2 by mononuclear cells from the spleens of untreated rats increased as the dietary fat content increased; (e) in indomethacin-treated rats, prostaglandin E2 synthesis was inhibited in all dietary groups and was not dependent on dietary fat; and (f) in both untreated and indomethacin-treated rats, the serum concentrations of oleic and linoleic acids were influenced to the same extent by dietary fat.

Animals↗