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PubMed1986

Influence of dietary retinyl acetate on normal rat mammary gland development and on the enhancement of 7,12-dimethylbenz[a]anthracene-induced rat mammary tumorigenesis by high levels of dietary fat.

The effect of high levels of dietary fat and retinyl acetate (ROA) on 7,12-dimethylbenz[a]anthracene (DMBA)-induced rat mammary tumor development and growth was examined. Female Sprague-Dawley rats, 51-53 days of age, were treated ig with 5 mg DMBA. At 55-57 days of age, the animals were divided into the following dietary treatment groups: A) 4.5% fat [control fat (CF)]; B) CF + 1.0 mmol ROA/kg diet (CF + ROA); C) 20.0% fat [high fat (HF)]; and D) HF + ROA. HF diets significantly increased mammary tumor multiplicity, with or without ROA, but did not significantly influence mammary tumor growth. ROA treatment reduced mammary tumor multiplicity regardless of the level of dietary fat and inhibited mammary tumor growth in the presence of normal levels of dietary fat. High levels of dietary fat did not significantly influence normal mammary gland growth and development. ROA significantly decreased normal mammary gland growth and development regardless of the level of dietary fat. Blood retinoids in rats fed ROA were primarily in the form of retinyl esters, i.e., retinyl linoleate, retinyl palmitate-oleate, and retinyl stearate. Free retinol levels in blood were not significantly influenced by ROA feeding. Blood retinyl ester levels were lower in rats fed the HF + ROA diet as compared to rats fed the CF + ROA diet.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed2001

Dietary fat supplementation effects on in vitro nutrient disappearance and in vivo nutrient intake and total tract digestibility by horses.

Addition of fat to the diet of the equine is a popular method of increasing energy density of the diet while reducing feed intake. Reducing feed intake is of interest to race horse trainers because additional feed is seen as additional weight and, therefore, a hindrance to performance. Limited information is available regarding the interactions of fat with other dietary components, particularly fiber, in the equine digestive system. The effect of dietary fat on in vitro nutrient disappearance in equine cecal fluid was studied in Exp. 1 using a split-plot design within a 2 x 2 Latin square. Two ponies were fed alfalfa (ALF) alone or alfalfa plus 100 g/d corn oil. Five substrates were used to determine in vitro DM disappearance, OM disappearance, NDF disappearance, and total dietary fiber (TDF) disappearance. The substrates included: ALF, tall fescue (TF), red clover (RC), soybean hulls (SBH), and rolled oats (RO). Fat supplementation did not affect in vitro DM, OM, or NDF disappearance. Addition of fat to the diet increased (P < 0.05) the disappearance of NDF in RO. Among substrates, in vitro DM and OM disappearance were highest (P < 0.05) for RO, followed by SBH, ALF, RC, and TF. In vitro NDF and TDF disappearance were highest (P < 0.05) for SBH, followed by RO, ALF, RC, and TF. In Exp. 2, the effects of varying levels of fat on nutrient intake and total tract digestibility were examined using a 4 x 4 Latin square design. Four mature mares were fed a 60% forage-40% concentrate diet containing different concentrations of fat: 0% supplemental fat control (C); 5% supplemental corn oil (5% CO); 10% supplemental corn oil (10% CO); or 15% supplemental corn oil (15% CO). Treatment did not affect intake of the concentrate portion of the diet or CP, gross energy, or NDF intake. Mares consuming the C diet had the highest (P < 0.05) intake of alfalfa cubes, DM, and OM, followed by those on the 10, 5, and 15% CO treatments, respectively. Treatment did not affect nutrient digestibility. Mares consuming the 15% CO diet had the highest (P < 0.05) fat digestibility, whereas those consuming C had the lowest fat digestibility. Fat in the form of CO generally had little effect on in vitro and in vivo nutrient digestibilities in horses.

Animals↗
PubMed2001

Dietary fat, cholesterol and colorectal cancer in a prospective study.

The relationships between consumption of total fat, major dietary fatty acids, cholesterol, consumption of meat and eggs, and the incidence of colorectal cancers were studied in a cohort based on the Finnish Mobile Clinic Health Examination Survey. Baseline (1967-1972) information on habitual food consumption over the preceding year was collected from 9959 men and women free of diagnosed cancer. A total of 109 new colorectal cancer cases were ascertained late 1999. High cholesterol intake was associated with increased risk for colorectal cancers. The relative risk between the highest and lowest quartiles of dietary cholesterol was 3.26 (95% confidence interval 1.54-6.88) after adjusting for age, sex, body mass index, occupation, smoking, geographic region, energy intake and consumption of vegetables, fruits and cereals. Consumption of total fat and intake of saturated, monounsaturated, or polyunsaturated fatty acids were not significantly associated with colorectal cancer risk. Nonsignificant associations were found between consumption of meat and eggs and colorectal cancer risk. The results of the present study indicate that high cholesterol intake may increase colorectal cancer risk, but do not suggest the presence of significant effects of dietary fat intake on colorectal cancer incidence.

Adult↗
PubMed2005

Dietary fat intake and proinflammatory cytokine levels in patients with heart failure.

BACKGROUND: Dietary fat intake affects proinflammatory cytokine levels of healthy adults. Whether dietary fats have similar effects in patients with heart failure (HF) is unknown. The purposes of this study were to determine (1) effect of dietary fat on interleukin (IL)-6, tumor necrosis factor (TNF)-alpha, and soluble receptors sTNF-R1 and sTNF-R2 levels in patients with HF and (2) subsequent impact of these levels on event-free survival. METHODS AND RESULTS: Forty-two patients provided 4-day food diaries and blood for cytokines. Event-free survival curves were calculated by Kaplan-Meier method and groups compared using log-rank test. IL-6 was not related to fat intake. TNF-alpha levels were elevated in patients with diets higher versus lower in saturated (6.9 +/- 5 versus 4.2 +/- 2 pg/mL) and trans fats (6.8 +/- 4.5 versus 4.5 +/- 2.8 pg/mL). Patients consuming diets higher in polyunsaturated fats had lower sTNF-R1 (2391 +/- 1010 versus 3373 +/- 2098 pg/mL) and sTNF-R2 (3803 +/- 1187 versus 5974 +/- 3275 pg/mL) levels. Higher omega-3 intake produced similar results: sTNF-R1 (2323 +/- 1304 versus 3307 +/- 1973) and sTNF-R2 (4117 +/- 2646 versus 5409 +/- 2801). Event-free survival was decreased in patients with higher TNF-alpha and sTNF-R1 levels. CONCLUSION: Dietary fat intake may affect proinflammatory cytokine levels in patients with HF. Research to determine whether changing composition of dietary fat can alter proinflammatory cytokine activity of HF patients is warranted.

Aged↗
PubMed1997

Psychological effects of dietary fat analysis and feedback: a randomized feedback design.

Excess consumption of dietary fat promotes chronic disease such as heart disease and cancer. Dietary analysis and feedback are often used to motivate dietary change; however, little is known about how people process, react to, and use this feedback to change behavior. This study used a randomized feedback design to examine psychological reactions to dietary fat feedback. Subjects were assessed for fat consumption and then randomly assigned to a high, moderate, or low percentage of calories from fat feedback group. Findings indicate that there are strong emotional, cognitive, and behavioral reactions to providing high-fat dietary feedback. Subjects that were told their diets were high in fat reported stronger negative emotional reactions and also reported they had stronger intentions to change than the other two feedback categories. These results are compared with studies providing nonrandomly assigned risk factor feedback.

Adolescent↗
PubMed1998

Dietary fat and obesity: an epidemiologic perspective.

The observation that dietary fat has an effect on weight gain and the development of obesity that is larger than would be expected on the basis of fat's energy value is mainly experimental. Several methodologic problems limit the interpretation of epidemiologic studies of the association between dietary fat intake and obesity. Among the issues relevant in this context are underreporting of energy and fat intakes, dieting behavior, inadequate control for variables such as energy expenditure, and limited between-subject variation in fat intake in developed countries. Different types of epidemiologic studies suffer from different types and magnitudes of bias and many conflicting results can be obtained. Ecologic and cross-sectional studies especially suffer from these biases. The more appropriate type of study (ie, prospective studies of fat intake and subsequent weight gain) was carried out in several countries but conflicting results were obtained. Overall, the observed associations seem to depend on the stage of cultural transition of the population studied (eg, modernization compared with postmodernization). Current epidemiologic methods are inadequate for performing valid studies of the relation between percentage of energy from dietary fat and obesity. Specifically designed prospective studies of unbiased estimates of energy balance are necessary. Appropriate control for confounders and emphasis on the possibility that genetic predisposition plays a role will also be necessary. At this stage there is no conclusive evidence from epidemiologic studies that under isoenergetic conditions dietary fat intake promotes the development of obesity more so than other macronutrients.

Body Mass Index↗
PubMedDate not supplied

Effect of dietary fat and cholesterol on dimethylbenz[a]-anthracene-induced mammary tumorigenesis in Sprague-Dawley rats.

The effect of dietary fats and cholesterol on dimethylbenz[a]-anthracene-induced mammary tumorigenesis was studied in female Sprague-Dawley rats. When the dietary fat source (at the 5% level) was palm oil (saturated fat) or corn oil (unsaturated fat), dietary cholesterol at the 0.2% level increased the tumor number of rats fed corn oil, but not those fed palm oil. Perilla oil (rich in alpha-linolenic acid) reduced tumor development as compared with safflower oil (rich in linoleic acid), but again dietary cholesterol at the 0.5% level diminished the favorable effect of n-3 polyunsaturated fatty acid (PUFA). The adverse effect of cholesterol was also observed in the n-6 PUFA fat. The promotive effect of dietary cholesterol was not necessarily associated with the change in the production of prostaglandin E2 by the tumor tissue or in the immunopotentiation. These results at least stress that the contrasting effects of dietary fats should be carefully evaluated whether cholesterol is present simultaneously or not.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1985

The relationship of dietary fat and cholesterol to mortality in 10 years: the Honolulu Heart Program.

This report examines the relationship of dietary fat and dietary cholesterol to mortality during a 10-year surveillance of a cohort of men of Japanese descent residing in Hawaii. The consumption of dietary fat (measured in grams) is related inversely and significantly to total mortality. No significant relationships exist between grams of dietary fat and any of the specific causes of death examined. No significant relationships are found between dietary saturated fatty acids (SFA, measured in grams) or dietary cholesterol (measured in milligrams) and any of the specific causes of death examined. In contrast, percentage of calories as fat is related inversely not only to total mortality, but to cancer mortality and to stroke mortality; and it is related directly to coronary heart disease (CHD) mortality. Percentage of calories as SFA is related inversely to cancer mortality and to stroke mortality, and it is related directly to CHD mortality. Only the relationship to stroke mortality remains significant in multivariate analysis if calories from alcohol are excluded from the computation. Dietary cholesterol per 1000 calories is related directly to CHD mortality. While these data provide support for the diet-heart hypothesis, they also suggest that men with low fat intakes have a higher total mortality rate than men with higher fat intakes. This increased risk, due to an excess risk of death from stroke and cancer, indicates that there is no overall beneficial effect from a low fat diet in this cohort.

Aged↗
PubMed1997

Does dietary fat influence insulin action?

What is clear from the research thus far is that dietary fat intake does influence insulin action. However, whether the effect is good, bad, or indifferent is strongly related to the fatty acid profile of that dietary fat. The evidence has taken many forms, including in vitro evidence of differences in insulin binding and glucose transport in cells grown with different types of fat in the incubation medium, in vivo results in animals fed different fats, relationships demonstrated between the membrane structural lipid fatty acid profile and insulin resistance in humans, and finally epidemiological evidence linking particularly high saturated fat intake with hyperinsulinemia and increased risk of diabetes. This contrasts with the lack of relationship, or even possible protective effect, of polyunsaturated fats. In particular, habitual increased n-3 polyunsaturated dietary fat intake (as fish fats) would appear to be protective against the development of glucose intolerance. It is reassuring that the patterns of dietary fatty acids that appear beneficial for insulin action and energy balance are also the patterns that would seem appropriate in the fight against thrombosis and cardiovascular disease. Mechanisms, though, still need to be defined. However, there are strong indicators that defining the ways in which changes in the fatty acid profile of membrane structural lipids are achieved, and in turn influence relevant transport events, plus understanding the processes that control accumulation and availability of storage lipid in muscle may be fruitful avenues for future research. One of the problems of moving the knowledge gained from research at the cellular level through to the individual and on to populations is the need for more accommodating research designs. In vitro studies may provide in-depth insights into intricate mechanisms, but they do not give the "big picture" for practical recommendations. On the other hand, correlational studies tend to be fairly blunt instruments, requiring large numbers that are very often not feasible if a greater depth of understanding of the biological processes is to be incorporated. There may be benefit in turning to the clinical case study as a framework for a more comprehensive analysis of the links between dietary fats and insulin action. The real challenge is to keep the depth of analysis rigorous enough to be able to explain and accommodate individual variation (i.e., the diversity of both environmental and genetic backgrounds) while at the same time satisfying the cultural need to provide appropriate overall dietary guidelines. Finally, David Kritchevsky brought to our attention a delightful quote from Mark Twain: "There is something fascinating about science. One gets such a wholesale return of conjecture for such a trifling investment of fact." In the field of dietary fats and the Metabolic Syndrome, this quotation is, unfortunately, apt. Much more research is necessary to define how dietary fats really work to affect insulin action. Well designed, long-term studies in "free range" humans must be undertaken if dietary guidelines for the Metabolic Syndrome are to be based on anything more than a "trifling" amount of "fact."

Animals↗
PubMed1993

Dietary fat increases high density lipoprotein (HDL) levels both by increasing the transport rates and decreasing the fractional catabolic rates of HDL cholesterol ester and apolipoprotein (Apo) A-I. Presentation of a new animal model and mechanistic studies in human Apo A-I transgenic and control mice.

In humans, diets high in saturated fat and cholesterol raise HDL-cholesterol (HDL-C) levels. To explore the mechanism, we have devised a mouse model that mimics the human situation. In this model, HuAITg and control mice were studied on low fat (9% cal)-low cholesterol (57 mg/1,000 kcal) (chow) and high fat (41% cal)-high cholesterol (437 mg/1,000 kcal) (milk-fat based) diets. The mice responded to increased dietary fat by increasing both HDL-C and apo A-I levels, with a greater increase in HDL-C levels. This was compatible with an increase in HDL size observed by nondenaturing gradient gel electrophoresis. Turnover studies with doubly labeled HDL showed that dietary fat both increase the transport rate (TR) and decreased the fractional catabolic rate of HDL cholesterol ester (CE) and apo A-I, with the largest effect on HDL CE TR. The latter suggested that dietary fat increases reverse cholesterol transport through the HDL pathway, perhaps as an adaptation to the metabolic load of a high fat diet. The increase in apo A-I TR by dietary fat was confirmed by experiments showing increased apo A-I secretion from primary hepatocytes isolated from animals on the high fat diet. The increased apo A-I production was not associated with any increase in hepatic or intestinal apo A-I mRNA, suggesting that the mechanism of the dietary fat effect was posttranscriptional, involving either increased translatability of the apo A-I mRNA or less intracellular apo A-I degradation. The dietary fat-induced decrease in HDL CE and apo A-I fractional catabolic rate may have been caused by the increase in HDL particle size, as was suggested by our previous studies in humans. In summary, a mouse model has been developed and experiments performed to better understand the paradoxical HDL-raising effect of a high fat diet.

Animals↗
PubMed1998

Factors affecting body tissue mobilization in early lactation dairy cows. 2. Effect of dietary fat on mobilization of body fat and protein.

Twenty-two multiparous Holstein cows were fed either a control diet or a control diet plus 3% added fat (dry matter basis) to determine the effect of added dietary fat on body tissue mobilization and milk production. Body composition measurements were taken using the D2O dilution technique at -2, 5, and 12 wk postpartum. Cows fed added fat produced 2.7 kg/d more milk than did those fed the control diet alone, but milk production, milk composition, and dry matter intake were not affected by diet. The maximum amount of body tissue loss occurred between -2 and 5 wk postpartum when cows fed both diets mobilized 46 kg of body fat and 12 kg of body protein. Between 5 and 12 wk postpartum, only small changes in both body protein and body fat were observed. Even though cows fed added fat showed a tendency toward reduced body fat mobilization (66 kg for cows fed the control diet vs. 37 kg for cows fed the control diet plus added fat) and increased body protein mobilization (4.8 kg for cows fed the control diet vs. 19.5 kg for cows fed the control diet plus added fat), the differences were not significant. Apparent differences in fat mobilization between diets might have been due to initial body fat stores (159 kg for cows fed the control diet vs. 126 kg for cows fed the control diet plus added fat). Across diets, one unit of change in body condition score corresponded to about 55 kg of empty body fat. Supplemental dietary fat did not reduce body tissue mobilization in early lactation.

Adipose Tissue↗
PubMed1993

Usual dietary fat intake and insulin concentrations in healthy women twins.

OBJECTIVE: To evaluate the associations between the usual intake of dietary fats and insulin concentrations. Insulin concentrations and insulin resistance have been positively related to risk for NIDDM, obesity, hypertension, dyslipidemia, and coronary heart disease, yet little is known of the environmental risk factors for relative hyperinsulinemia. Insulin resistance can be induced by high-fat feeding in laboratory animals; therefore, high-fat diets may increase risks for developing NIDDM. RESEARCH DESIGN AND METHODS: Subjects included 544 nondiabetic women who participated in the second examination of the Kaiser Permanente Women Twins Study (1989-1990). Fasting and 2-h post 75-g glucose load insulin levels were determined. Dietary fat intake was assessed by a food frequency questionnaire. Generalized least-squares regression analyses for unpaired twin data were used to determine the relationship between dietary fat intake and insulin levels after adjustment for total calories, age, several behavioral variables, and in some models, percentage of body fat and waist-to-hip ratio. Associations of dietary fat intake with insulin levels were also evaluated within the subset of monozygotic twin pairs (n = 164 pairs) after removal of genetic influences by regression analysis of intrapair differences. RESULTS: Among the 544 individual women, a 20 g/day increase in total dietary fat was associated with a higher fasting insulin level (9% [P < 0.001] before and 6% [P < 0.01] after adjustment for the obesity variables). Higher intakes of saturated fat, oleic acid, and linoleic acid were each positively related to higher fasting insulin values. The relation of dietary fat with fasting insulin was significantly attenuated among physically active women compared with those who were sedentary (P = 0.04), even after adjustment for obesity. Only saturated fat intake was significantly associated with 2-h postglucose load insulin level before (P = 0.004) but not after adjustment for obesity. Within identical twin pairs, total dietary fat was positively related to fasting insulin before (P = 0.03) but not after adjustment for obesity (P = 0.11). CONCLUSIONS: High intake of total dietary fat is positively related to relative fasting hyperinsulinemia in nondiabetic women, particularly those who are sedentary. This effect appears to be partly mediated by the relation of dietary fat with obesity.

Adult↗
PubMed1994

Hypercholesterolemic effect of dietary cholesterol in diets enriched in polyunsaturated and saturated fat. Dietary cholesterol, fat saturation, and plasma lipids.

Within the context of reduced-fat diets, the effects of incorporating a fat high in stearic acid and adding moderate amounts of dietary cholesterol were examined in 14 middle-aged and elderly women and men (range, 46 to 78 years) with low-density lipoprotein cholesterol (LDL-C) concentrations > 130 mg/dL (range, 133 to 219 mg/dL) at screening. The subjects consumed each of the five diets, which were as follows: (1) a baseline diet (35% fat with 13% saturated fatty acids [SFAs], 12% monounsaturated fatty acids [MUFAs], and 8% polyunsaturated fatty acids [PUFAs], and 128 mg cholesterol/1000 kcal); (2) a reduced-fat diet, in which two thirds of the fat was provided as corn oil (corn oil-enriched diet: 29% fat with 7% SFAs, 9% MUFAs, and 11% PUFAs and 85 mg cholesterol/1000 kcal), which met the National Cholesterol Education Program (NCEP) Step 2 guidelines; (3) a reduced-fat diet, in which two thirds of the fat was provided as beef tallow (beef tallow-enriched diet: 31% fat with 13% SFAs, 11% MUFAs, and 3% PUFAs and 109 mg cholesterol/1000 kcal); and two reduced-fat diets, one (4) enriched in corn oil and the other (5) enriched in beef tallow, to which moderate amounts of cholesterol in the form of egg yolk were incorporated (197 or 226 mg cholesterol/1000 kcal final cholesterol content in corn oil- or beef tallow-enriched diets, respectively). All diets were isocaloric and all food and drink were provided by the metabolic kitchen. Reducing the fat content of the diet resulted in decreased concentrations of LDL-C and high-density lipoprotein cholesterol (HDL-C).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed2003

Dietary fat intake--food sources and dietary correlates in the Malmö Diet and Cancer cohort.

OBJECTIVES: To identify food sources of fat, to compare food and nutrient intakes at different levels of relative fat intake, and to examine the contribution of different food groups to the variation in relative fat intake. Relative fat intake was expressed as energy contributed by fat in percentage of non-alcohol energy. DESIGN: Cross-sectional analysis of baseline data from the Malmö Diet and Cancer STUDY: An interview-based diet history method, a structured questionnaire and anthropometric measurements were used to obtain data. Analysis of variance compared food and nutrient intakes across quintiles of relative fat intake. Stepwise regression examined the contribution of food groups to the variation in relative fat intake. SETTING: Baseline examinations were conducted between 1991 and 1996 in the city of Malmö, southern Sweden. SUBJECTS: A sub-sample of 7055 women and 3240 men of the Malmö Diet and Cancer cohort. RESULTS: The major fat sources were dairy products, margarines, meat & meat products, and cakes & buns. Most plant foods, especially fruit, vegetables and breakfast cereals, were negatively associated with fat intake. Low fat consumers had significantly higher intakes of dietary fibre, vitamin C, beta-carotene, folic acid, iron, zinc and calcium. Intakes of all types of fatty acids and fat-soluble vitamins were positively associated with fat consumption. CONCLUSIONS: The results suggest that many food groups and nutrients may confound the associations between relative fat intake and disease. Plant foods, especially, are important to consider in studies of fat intake and disease risk.

Aged↗
PubMed1997

Dietary fats and colon cancer: assessment of risk associated with specific fatty acids.

There are many biological mechanisms whereby dietary fat and specific dietary fatty acids may alter risk of colon cancer in addition to their contribution to total energy intake. To evaluate these potential associations, we used detailed dietary intake data collected in a population-based study of 1,993 incident colon cancer cases and 2,410 controls conducted in 3 areas of the United States. The most commonly consumed fatty acid in the study population was oleic acid. One-third of dietary fats consumed came from additions to other foods at the table or from the preparation of other foods. After adjusting for total energy intake, physical activity and body size, neither total dietary fat nor specific fatty acids was associated with risk of colon cancer. However, among older women, fats from food preparation were associated with increased risk of colon cancer (OR 1.84, 95% CI 1.20-2.80), while fats from foods themselves or from additions to other foods were not. While dietary fats were not associated with colon cancer risk in the total population, subgroups of the population appeared to be at slightly greater risk if they consumed a high-fat diet. Women who consumed a diet high in mono-unsaturated fatty acids (MFAs) and poly-unsaturated fatty acids (PFAs) and who had a family history of colorectal cancer were at greater risk of colon cancer than those with similar intakes but without a family history of colorectal cancer. Similar associations with family history were noted among men diagnosed at younger ages for MFA, linolenic acid and 20-carbon PFA.

Adult↗
PubMed1995

Changes in dietary fat intake preceding the diagnosis of cancer.

We studied changes in dietary fat intake preceding the diagnosis of cancer in 96 men diagnosed with cancer during the Coronary Primary Prevention Trial and Post-trial Follow-up. Diet was assessed semiannually by 24-hour recall for the duration of the trial. Dietary fat intake was elevated in the interval 12-24 months before diagnosis compared with the interval 24-36 months before diagnosis [6.9 gm per day; 95% confidence interval (CI) = 0.04-13.7]. The percentage of calories as fat was also elevated (1.9%; 95% CI = 0.34-3.4). Fat consumption decreased in the 0- to 12-month prediagnostic interval. The basis for the elevation is unclear, but it may have been due to the metabolic effects of cancer before its diagnosis. Case-control studies of long-term diet may overestimate positive associations between dietary fat and cancer risk if the cases' recall includes the prediagnostic period, during which fat intake is elevated. In analyses of prospective studies of dietary fat and cancer, data from within the first 2-3 years of baseline should be examined separately to evaluate the potential for bias introduced by the inclusion of measurements representing transient elevations in dietary fat intake.

Adult↗
PubMed1995

Prediction of milk fatty acid profile in dairy cows fed dietary fat differing in fatty acid composition.

The objective of this work was to predict changes in milk fat composition caused by differences in dietary fat. Twenty-two references describing 35 experiments and 108 treatments were used in the analysis. For lauric, myristic, and palmitic acids in milk, proportions in the dietary fat and the total dietary fat concentration were important predictors for their concentrations in milk as well as for stearic and oleic acids in milk. Using a model that included these four parameters, the residual standard deviation around the observed versus predicted line within experiments was approximately 10% of the mean for short-chain fatty acids (< C12); for lauric, myristic, palmitic, and oleic acid; and for total C18 fatty acids in milk. The model also effectively predicted milk fatty acid profile with respect to lauric, myristic, palmitic, and oleic acid and total C18 fatty acids across experiments despite differences in breed, basal diet, and milk yield among experiments. The content of short-chain acids, stearic acid, and poly-unsaturated fatty acids were less effectively predicted across experiments. Possible explanations for the differing predictabilities for different milk fatty acids are discussed.

Animals↗
PubMed1987

Dietary fat, plasma lipoproteins, and immune function in middle-aged American men.

Dietary fat has been incriminated as a positive risk factor for the development of neoplasia in human populations. We used adipose tissue fatty acid analysis as an index of dietary fat intake to study the association between dietary fat and immune function in a group of 94 free-living American males (avg age 47 years). Immunocompetence was tested by a battery of T- and B-lymphocyte stimulation tests and also by natural killer (NK) cell activity. Correlations were sought between fatty acid composition, plasma lipids, and immune responsivity. The degree of unsaturation of the diet over a polysaturated-to-saturated fat ratio range of 0.54-1.01 had no predictable effect on the immune function. Stepwise regression analysis showed that the concentrations of plasma triglycerides and cholesterol and its subfractions did not explain any of the variance in the immune tests. Palmitic acid (16:0) was associated with 7% of the variance of the response to C. albicans and E. coli, perhaps through influencing B-cell activity. Stearic acid (18:0) was correlated negatively to concanavalin A responsivity (18% of the variance) and positively to NK activity (20% of the variance). If impaired in vitro immune function is a marker of increased risk for carcinogenesis, then our data do not support a role for dietary fat influencing in any systematic manner lymphocyte function in vitro, as reflected by proliferative response or NK activity. Further, plasma lipoproteins, in particular cholesterol levels, did not appear to affect any immune function test. It remains to be studied whether dietary fat, lipoproteins, or fat-soluble substances may influence membrane structure and function and prostaglandin formation as alternative pathways in the promotion of neoplasia.

Adipose Tissue↗