Dietary fat and cecal microbial activity in the rat

Weanling rats were fed low-fat (1% w/w safflower oil) or high-fat (1% w/w safflower oil plus 35% w/w beef fat or cocoa butter) diets for 30 days, and the activities of five cecal microbial enzymes were determined. When compared with the low-fat diet, beef fat significantly increased total cecal beta-glucuronidase activity, but cocoa butter, with a similar fatty acid composition, did not. Both high-fat diets significantly decreased total cecal azoreductase, beta-glucosidase, and nitrate reductase activities, but neither significantly affected urease activity. When expressed as specific activities (per 10(11) bacteria), cocoa butter decreased azoreductase, and beef fat caused increases of beta-glucuronidase and urease. Beef fat, but not cocoa butter, significantly reduced cecal bacterial numbers when compared to the low-fat diet. Both high-fat diets led to equivalent reductions in the proportion of aerobic bacteria.     

Dietary fat and the beta-adrenergic-mediated chronotropic response in the rat

We have investigated the effect of dietary fat on isoproterenol-stimulated and propranolol-inhibited heart rate in the rat. In the first experiment, weanling male Sprague-Dawley rats were fed diets containing 10% butter (10B), 10% corn oil (10C) or 9% butter/1% corn oil (10M) for 4 wk. Heart rate was determined in response to increasing i.v. doses of isoproterenol. The percent stimulation at the highest dose of isoproterenol (100 microM) was found to be significantly higher (P less than 0.05) in the 10C-fed group than either the 10B- and 10M-fed groups. A similar study investigated the effect of propranolol inhibition of heart rate in low-fat (10C and 10B) as well as high-fat (25C) corn oil- and high-fat (25B) butter-fed animals. Heart rate was elevated with a constant i.v. infusion of isoproterenol and the inhibitory effect of propranolol was determined. The ED50 was found not to depend on the level of fat, but was found to be significantly lower in the corn oil-fed animals than in those red butter fat (P less than 0.05). Thus, animals appear to be more sensitive to these beta-adrenergic agonists/antagonists when fed a diet containing corn oil rather than butter fat as the lipid source.     

Dietary fat dose dependently increases spontaneous caloric intake in rat

OBJECTIVE: To characterize the dose-response relationship between dietary fat to carbohydrate ratio and spontaneous caloric intake. RESEARCH METHODS AND PROCEDURES: Male Long-Evans rats consumed milk-based liquid diets that differed in fat content (17% to 60% of kilocalories) but had equivalent protein content and energy density. In Experiment 1, rats consumed one of the diets (n = 9/diet group) as the sole source of nutrition for 16 days. In Experiment 2, diets were offered as an option to nutritionally complete chow for 4 days followed by a 3-day chow-only washout in a randomized within-subjects design (n = 30). In Experiment 3, nine rats received isocaloric intragastric infusions of diet overnight, with chow available ad libitum. At least two no-infusion days separated the different diet infusions, which were given in random order. Food intake was measured daily RESULTS: Dietary fat dose dependently increased total daily kilocalories in each of the three paradigms. DISCUSSION: These data imply that the postingestive effects of carbohydrate and fat differentially engage the physiological substrates that regulate daily caloric intake. These findings reiterate the importance of investigating macronutrient-specific controls of feeding, rather than prematurely concluding that dietary attributes that covary with fat content (e.g., caloric density and palatability) drive the overeating associated with a high-fat diet.     

Dietary fat

For the past two decades, epidemiologists have observed lower risks of lung, breast, prostate, colon, and other cancers in populations that frequently consume fruits and vegetables. Numerous phytoestrogens have been shown to be anticarcinogenic under experimental conditions and may account for at least part of the cancer‐prevention effects of fruit and vegetable consumption. These plant constituents include isoflavonoids, coumestans, lignans, phytosterols, and flavonoids. DietSys, the nutrient analysis program associated with the National Cancer Institute Health Habits and History Questionnaire (HHHQ), and other nationally available nutrient analysis databases do not fully assess these constituents. Therefore, we modified DietSys to include these components in foods on the basis of published values. In addition, as part of an epidemiological study of prostate cancer, we modified the food‐frequency component of the HHHQ to include the main foods contributing to phytoestrogen intake. Although there are limitations to the consistency and quality of many of the values because they were gathered from a variety of sources, our approach should provide a useful first tool for assessing the epidemiological association between phytoestrogen consumption and cancer risk. Furthermore, this work has already facilitated the identification of the major dietary contributors with phytoestrogen activity and prioritized future laboratory analyses of specific foods toward the development of a more complete and accurate database.     

Dietary fat and mammary carcinogenesis

Evidence that dietary fat has an influence on carcinogenesis comes from both epidemiological data and experiments with animals. The experimental studies have indicated that dietary fat acts primarily as a promoter of carcinogenesis and that the effect depends on the type as well as the amount of fat in the diet. Vegetable oils containing polyunsaturated fatty acids of the linoleic acid family (n‐6) have been shown to enhance mammary tumorigenesis, but a fish oil containing polyunsaturated fatty acids of the linolenic acid family (n‐3) had an inhibitory effect at higher levels of intake. These and other findings suggest that the effect may be related to prostaglandins or other biologically active products of polyunsaturated fatty acids. Epidemiological data show a positive correlation between dietary fat and mortality from cancer at various sites, and this is supported by results of animal experiments in the case of colon cancer and pancreatic cancer as well as breast cancer. In the epidemiological data, cancer mortality shows strong positive correlations with total dietary fat and with animal fat, but not with fat derived from plants. Fats and oils used as spreads, cooking fats, and salad oils are the main source of fat in the American diet. Other major sources are meats and dairy products. Fat intake could probably be reduced substantially without serious deleterious effects, and this might help to decrease the risk of developing certain types of cancer.

(Nutr Cancer 6, 254–259, 1985)     

Dietary fat and tumor metastasis

Evidence from several types of studies indicates a relationship between fat intake and occurrence of malignant tumors at specific sites. When rodents are fed high-fat diets, the incidence of mammary tumors sharply increases and latency of tumor appearance is greatly diminished, as compared with the same parameters in animals fed low levels of fat. Despite advances in surgical technique and the development of aggressive therapies for the treatment of primary cancers, most deaths in humans with cancer are caused by metastasis. Accordingly, we have reviewed the process of metastasis and have focused on the question of whether dietary fat can play a role. Metastasis is a complex, multistep, progressive process, and dietary fats may affect specific events such as implantation, survival, and proliferation of tumors. Finally, we discuss possible mechanisms by which dietary fat can modulate metastasis. Available data lead us to stress the importance of assessment of metastasis in studies of the effects of dietary fat on tumorigenesis.     

Dietary fat and mammary carcinogenesis

Evidence that dietary fat has an influence on carcinogenesis comes from both epidemiological data and experiments with animals. The experimental studies have indicated that dietary fat acts primarily as a promoter of carcinogenesis and that the effect depends on the type as well as the amount of fat in the diet. Vegetable oils containing polyunsaturated fatty acids of the linoleic acid family (n-6) have been shown to enhance mammary tumorigenesis, but a fish oil containing polyunsaturated fatty acids of the linolenic acid family (n-3) had an inhibitory effect at higher levels of intake. These and other findings suggest that the effect may be related to prostaglandins or other biologically active products of polyunsaturated fatty acids. Epidemiological data show a positive correlation between dietary fat and mortality from cancer at various sites, and this is supported by results of animal experiments in the case of colon cancer and pancreatic cancer as well as breast cancer. In the epidemiological data, cancer mortality shows strong positive correlations with total dietary fat and with animal fat, but not with fat derived from plants. Fats and oils used as spreads, cooking fats, and salad oils are the main source of fat in the American diet. Other major sources are meats and dairy products. Fat intake could probably be reduced substantially without serious deleterious effects, and this might help to decrease the risk of developing certain types of cancer.     

Dietary fat and natural-killer-cell activity

An intervention trial designed to lower the amount of fat in the diet was conducted to test the effect of reduced fat consumption (LF diet) on activity of natural killer (NK) cells in humans. Of 26 men enrolled initially, 17 successfully completed the intervention and lowered their fat intake to less than 30% of calories as fat. Data were analyzed in two ways. The paired t test showed a marked increase in NK-cell activity from baseline to the end of the LF-diet intervention (t = 4.77, p = 0.0002). Results of a general linear model showed an effect of lowering total dietary fat on increased NK-cell activity (approximately 0.53% increase for each absolute percent of calories as fat, p = 0.14) for all men and a highly significant effect in a subset of men who ate greater than 25% of calories as fat at baseline (approximately 1.22% increase, p = 0.009). These results were obtained after changes in total caloric intake, weight, exercise, and other fat-related covariates were accounted for.     

Dietary fat and physical performance

Although the relationship between dietary carbohydrate and physical performance is well described, there is much controversy about the relationship between dietary fat and physical performance. Recently, several studies have tried to clarify this relationship. Here the effects of acute fat on metabolism and performance will be discussed, as well as the effects of short-term and long-term high-fat diets.     

Dietary fat and insulin action in humans

A high intake of fat may increase the risk of obesity. Obesity, especially abdominal obesity, is an important determinant of the risk of developing insulin resistance and non-insulin-dependent diabetes mellitus. It is suggested that a high proportion of fat in the diet is associated with impaired insulin sensitivity and an increased risk of developing diabetes, independent of obesity and body fat localization, and that this risk may be influenced by the type of fatty acids in the diet. Cross-sectional studies show significant relationships between the serum lipid fatty acid composition, which at least partly mirrors the quality of the fatty acids in the diet, and insulin sensitivity. Insulin resistance, and disorders characterized by insulin resistance, are associated with a specific fatty acid pattern of the serum lipids with increased proportions of palmitic (16:0) and palmitoleic acids (16:1 n-7) and reduced levels of linoleic acid (18:2 n-6). The metabolism of linoleic acid seems to be disturbed with increased proportions of dihomo-gamma linolenic acid (20:3 n-6) and a reduced activity of the delta 5 desaturase, while the activities of the delta 9 and delta 6 desaturases appear to be increased. The skeletal muscle is the main determinant of insulin sensitivity. Several studies have shown that the fatty acid composition of the phosholipids of the skeletal muscle cell membranes is closely related to insulin sensitivity. An increased saturation of the membrane fatty acids and a reduced activity of delta 5 desaturase have been associated with insulin resistance. There are several possible mechanisms which could explain this relationship. The fatty acid composition of the lipids in serum and muscle is influenced by diet, but also by the degree of physical activity, genetic disposition, and possibly fetal undernutrition. However, controlled dietary intervention studies in humans investigating the effects of different types of fatty acids on insulin sensitivity have so far been negative.     

Dietary fat and the risk of breast cancer

Age-adjusted dietary fat intake of 133 incident Dutch breast cancer cases was significantly (p less than 0.01) higher than in 289 apparently healthy controls (mean and standard deviation: 102 +/- 36 g and 92 +/- 30 g, respectively). The age-adjusted relative odds of breast cancer showed a positive trend (p less than 0.05) with increasing fat intake. The multivariate adjusted relative odds was 3.5 (95% Cl = 1.6-7.6) for subjects in the highest quintile of fat intake (above 113 g) compared to those in the lowest quintile (below 65 g); this corresponds to a 30% increased risk per 10% of energy derived from fat. The association could not be attributed to energy intake, nor to the degree of saturation of the fat nor to any specific dietary source of fat.     

Dietary fat and the prevention of chronic disease

Chronic diseases are generally taken to include obesity (especially abdominal), diabetes, macrovascular disease (MVD), affecting all medium distributing arteries and the organs they supply, osteoporosis, and various cancers (notably breast, lung, colorectal, pancreatic, prostate and skin) and dementia. Unfortunately, they may not be so chronic, as their consequences for morbidity and mortality may occur early in adult life and proceed rapidly. Since they all, in one way or another, have food, nutritional and other environmental and lifestyle contributions, the term Eco-Nutritional disease may be preferred. Insofar as the nutritional basis of chronic disease is concerned, we may simply speak of nutritionally-related disorders or diseases (NRD). In regard to fat and END or NRD, the key considerations are how diverse the sources are and what it does to energy density (ED) and nutrient density (ND). These are reflected in the 2003 WHO report 9816 on "Diet, Nutrition and the Prevention of Chronic Disease".     

Dietary behaviors associated with total fat and saturated fat intake

OBJECTIVE: To estimate percentages of US adults who have adopted behaviors promoted by dietary guidance about how to reduce fat intake, and to assess relationships between these behaviors and intake of energy from total and saturated fat. DESIGN: Relationships were examined between intake of total and saturated fat from two 24-hour recalls in the US Department of Agriculture's 1994-1996 Continuing Survey of Food Intakes by Individuals and responses to 19 fat-related behavior questions on the follow-up Diet and Health Knowledge Survey (DHKS). SUBJECTS: Data are from a national sample of 5,649 individuals 20 years of age and older. STATISTICAL ANALYSES PERFORMED: Multiple regression models are used to identify dietary behaviors, demographic factors, and personal characteristics that are determinants of fat intake. RESULTS: In this study, the percentage of US adults who consistently followed the low-fat behaviors ranged from 8% to 70%. The most highly adopted behaviors (45% or more of adults) included trimming fat from meat, removing skin from chicken, and eating chips infrequently. The least highly adopted behaviors (15% or less of adults) included eating baked or boiled potatoes without added fat, avoiding butter or margarine on breads, eating low-fat instead of regular cheeses, and having fruit for dessert when dessert is eaten. Together, the 19 fat-related behavior questions on the DHKS formed a statistically significant predictor for total fat and saturated fat intake, expressed as a percent of energy (P<.0001). Key behaviors in terms of their predicted effect on lowering both total and saturated fat intake were never adding fat to baked or boiled potatoes, not eating red meats, eating less than 3 eggs per week, and never eating chicken fried. Predicted effects of these key behaviors in terms of lowering fat intake as a percentage of energy were > or = 1.5 percentage points for total fat and > or = 0.5 percentage point for saturated fat. CONCLUSIONS: Results have applications for designing brief fat assessment instruments and for identifying key nutrition education messages that promote important fat-lowering behaviors.     

Dietary fat reduction strategies.

In this study, we used computer modeling to identify which techniques designed to achieve dietary fat reduction were the most effective in meeting the dietary recommendations of the American Heart Association Step-One diet. Menus were developed for men and nonpregnant, nonlactating women, 25 to 50 years old, according to the Continuing Survey of Food Intakes by Individuals (with 36% and 37% of energy from fat for men and women respectively). The menus were modified realistically using the Minnesota Nutrition Data System. The following five strategies were applied: skim milk replaced whole milk and 2%-fat milk (SKM); medium-fat meat exchanges replaced higher-fat ones (MMtEx); lean meat exchanges replaced higher-fat ones (LMtEx); fat-modified products were used (FMP); and 2%-fat milk replaced whole milk (LFM). For men, strategies LMtEx, SKM + LMtEx, SKM + LMtEx + FMP, LMtEx + FMP, LMtEx + FMP + LFM, and LMtEx + LFM reduced energy by 195 to 415 kcal and achieved the targeted level of energy from fat (less than or equal to 30 +/- 1%) and cholesterol (less than 300 mg) while maintaining 67% or more of the Recommended Dietary Allowances for other nutrients. For women, however, no single strategy achieved the goal. Certain combinations of strategies, SKM + LMtEx, SKM + FMP, SKM + MMtEx + FMP, reduced energy by 150 to 268 kcal and achieved the targeted dietary fat and cholesterol goals while maintaining 67% or more of the Recommended Dietary Allowances for other nutrients. All strategies led to a reduction in both saturated fatty acids (to 9% to 10% of energy) and monounsaturated fatty acids.(ABSTRACT TRUNCATED AT 250 WORDS)