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PubMed2006

Gender differences in plasma lipid response to dietary fat.

The relationship between type of dietary fat, cardiovascular disease risk, and lipid/lipoprotein profiles has been studied since the early 1900s. For the most part, observational data from international comparisons, migration studies, and prospective studies have identified a positive relationship between saturated fatty acid (SFA) intake and coronary heart disease (CHD) risk, although in the latter case these observations were attenuated and in some cases became non-significant after adjusting for other dietary factors. Data from large-scale primary and secondary intervention studies support a positive relationship between CHD and SFA. The majority of data available were derived from male subjects, and if female subjects were included, few studies assessed the effect of gender on responsiveness. Recent evidence has emerged suggesting that females respond differently to diet with respect to CHD progression. This review discusses controlled clinical intervention studies that included data for both genders and their responses to dietary fat perturbations and lipoprotein profiles. The scope was limited for the most part to reports that included identifiers in the title or abstract that indicated data for female and male subjects were reported separately, although a statistical comparison between the genders may not have been reported. Overall, whether the studies assessed the effect of the ratio of SFA to monounsaturated fatty acids (MUFA), SFA to polyunsaturated fatty acids (PUFA), MUFA to PUFA, individual SFA, or SFA to trans fatty acids, female and male subjects responded similarly, and when differences were identified there was no consistent pattern.

Cardiovascular Diseases↗
PubMed1992

Plasma lipid composition in an elderly population: correlation with dietary fat.

The effects of dietary fat on plasma lipid composition were studied in a population of 51 elderly subjects (19 men, 32 women) who lived in a retirement home in the province of Jaén (southern Spain). Dietary intake of fat was elevated (106 and 115 g/day in men and women respectively), and fatty acid intake consisted of 40% oleic acid, 17% linoleic acid and 0.7% linolenic acid. Cholesterol intake was 506 and 518 mg/day in men and women respectively, whereas the plasma level of cholesterol was approximately 250 mg/dl in both sexes. In men and women, HDL-cholesterol levels were 71.5 and 62.2 mg/dl, and LDL-cholesterol levels were 153.5 and 152.3 mg/dl. The most abundant circulating fatty acid was palmitic acid (25%) in both sexes, followed by oleic (23%) and linoleic acid (15-16%), whereas linolenic acid represented only 0.3% of the plasma fatty acids. To determine whether plasma levels of fatty acids served as reliable biological markers of dietary fatty acid intake, we compared the two sets of values, and found that higher intake was reflected in higher plasma levels, although a significant linear correlation (p < 0.05) was found only for linolenic acid.

Aged↗
PubMed2006

Distinct modulation of angiotensin II-induced early left ventricular hypertrophic gene programming by dietary fat type.

Long-term dietary fatty acid intake alters the development of left ventricular hypertrophy, but the linking signaling pathways are unclear. We studied the role and underlying signaling mechanisms of dietary fat intake in the early phase of the hypertrophic process. Rats assigned for 4 weeks of high-oil, high-fat, or standard diet were subjected to angiotensin II (Ang II; 33 microg/kg/h, subcutaneous) or vehicle infusion for 24 h. The Ang II-induced increase in left ventricular mRNA levels of hypertrophy-associated genes was higher in rats fed the high-oil diet compared with the standard diet. Western blotting revealed that, in parallel with changes in gene expression, the high-oil diet increased c-Jun N-terminal kinase phosphorylation (P < 0.001). Ang II increased p38 mitogen-activated protein kinase (MAPK) phosphorylation in rats fed the high-fat diet (3-fold; P < 0.01). The increase in transcription factor activator protein-1 (AP-1) DNA binding activity in response to Ang II was higher in rats fed the high-oil diet compared with those fed the standard diet (P < 0.001). Ang II downregulated inducible nitric oxide synthase mRNA levels in fatty acid-supplemented groups compared with the standard diet group. These results show that dietary fat type modulates the early activation of hypertrophic genes in pressure-overloaded myocardium involving the distinct activation of AP-1 and MAPK signal transduction pathways.

Angiotensin II↗
PubMed1980

Influence of dietary fat concentration and saturation on immune ontogeny in mice.

Dietary fat modulation of immune responsiveness was studied using a murine model subjected to prenatal and postnatal dietary manipulation. The weight of lymphoid associated organs, particularly the spleen, thymus and liver were significantly influenced by dietary fat saturation and concentration whereas other organs studied were not influenced by this manipulation. The serum immunoglobulins IgG1 and IgG2, but not IgM or IgA, increased in mice fed the polyunsaturated fat (PUF) diet as compared to the levels in those mice fed the saturated fat (SF) diet. While dietary manipulation generally did not influence the peripheral differential blood cell counts, the percentage of immunoglobulin positive splenic cells changed with dietary manipulation; the percentage of T cells, however, was not influenced by the experimental diets. In contrast, T-cell blastogenesis was influenced by both saturation and concentration of dietary fat whereas B-cell transformation was influenced by neither variable. Changes in T-cell responses were manifested through changes in the lymphocytes, and not cell numbers; PUF, particularly high levels, suppresses lymphocyte blastogenesis whereas low levels or a deficiency of PUF intensify this response. It is concluded that dietary fats influence the modulation and level of immune function.

Animals↗
PubMed1985

Dietary fat in relation to mammary carcinogenesis.

The first evidence that dietary fat influences mammary carcinogenesis was provided by Tannenbaum, who showed that mice fed a high-fat diet developed spontaneous tumors more readily than those fed a low-fat diet. Similar observations have been made with various other animal models. Polyunsaturated vegetable oils enhance carcinogenesis more effectively than saturated fats, because of their higher linoleate content. Diets containing high levels of polyunsaturated fish oils do not stimulate carcinogenesis, however, perhaps because their polyunsaturated fatty acids belong mainly to the linolenate family. Dietary fat acts primarily as a promoting agent, but the exact mechanism is still unclear. The requirement for linoleate and the fact that the fat effect can be blocked by prostaglandin biosynthesis inhibitors suggests that it may be mediated by biologically-active compounds derived from linoleate. Other possibilities include changes in hormonal balance, alterations in the fatty acids of membrane lipids, effects on the immune system, modulation of intercellular communications, and metabolic alterations related to differences in fat and caloric intake. Interest in the role of dietary fat in mammary carcinogenesis has been greatly stimulated by epidemiological evidence of a strong, positive correlation between breast cancer and dietary fat. In these epidemiological data, total dietary fat shows a better correlation than fat from either plant or animal sources individually, and there is no apparent correlation with the polyunsaturated fatty acid content of the diet. Further studies are needed to investigate more thoroughly this apparent difference between experimental and epidemiological data.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Validation of the MEDFICTS dietary questionnaire: a clinical tool to assess adherence to American Heart Association dietary fat intake guidelines.

BACKGROUND: Dietary assessment tools are often too long, difficult to quantify, expensive to process, and largely used for research purposes. A rapid and accurate assessment of dietary fat intake is critically important in clinical decision-making regarding dietary advice for coronary risk reduction. We assessed the validity of the MEDFICTS (MF) questionnaire, a brief instrument developed to assess fat intake according to the American Heart Association (AHA) dietary "steps". METHODS: We surveyed 164 active-duty US Army personnel without known coronary artery disease at their intake interview for a primary prevention cardiac intervention trial using the Block food frequency (FFQ) and MF questionnaires. Both surveys were completed on the same intake visit and independently scored. Correlations between each tools' assessment of fat intake, the agreement in AHA step categorization of dietary quality with each tool, and the test characteristics of the MF using the FFQ as the gold standard were assessed. RESULTS: Subjects consumed a mean of 36.0 +/- 13.0% of their total calories as fat, which included saturated fat consumption of 13.0 +/- 0.4%. The majority of subjects (125/164; 76.2%) had a high fat (worse than AHA Step 1) diet. There were significant correlations between the MF and the FFQ for the intake of total fat (r = 0.52, P < 0.0001) and saturated fat (r = 0.52, P < 0.0001). Despite these modest correlations, the currently recommended MF cutpoints correctly identified only 29 of 125 (23.3%) high fat (worse than AHA Step 1) diets. Overall agreement for the AHA diet step between the FFQ and MF (using the previously proposed MF score cutoffs of 0-39 [AHA Step 2], 40-70 [Step 1], and > 70 [high fat diet]) was negligible (kappa statistic = 0.036). The MF was accurate at the extremes of fat intake, but could not reliably identify the 3 AHA dietary classifications. Alternative MF cutpoints of < 30 (Step 2), 30-50 (Step 1), and > 50 (high fat diet) were highly sensitive (96%), but had low specificity (46%) for a high fat diet. ROC curve analysis identified that a MF score cutoff of 38 provided optimal sensitivity 75% and specificity 72%, and had modest agreement (kappa = 0.39, P < 0.001) with the FFQ for the identification of subjects with a high fat diet. CONCLUSIONS: The MEDFICTS questionnaire is most suitable as a tool to identify high fat diets, rather than discriminate AHA Step 1 and Step 2 diets. Currently recommended MEDFICTS cutpoints are too high, leading to overestimation of dietary quality. A cutpoint of 38 appears to be providing optimal identification of patients who do not meet AHA dietary guidelines for fat intake.

Journal Article↗
PubMed1978

Prostaglandin production and lipolysis in isolated rat adipocytes as affected by dietary fat.

The influence of dietary fat on prostaglandin production and lipolysis was tested in basal and norepinephrine stimulated adipocytes isolated from the epididymal fat pads of fasted rats. Seven diets varying in fat calories and polyunsaturation were utilized. No basal differences were noted for prostaglandin E2 production or lipolysis. Norepinephrine stimulated prostaglandin E2 and F2alpha production was significantly (P less than 0.01) increased with greater polyunsaturation of fat, but not by increased fat calories. Norepinephrine stimulated lipolysis was depressed by an increase in fat calories but was unaffected by the degree of polyunsaturation of fat. This is in vitro evidence against the concept that prostaglandins play a feedback regulator role in fat cell lipolysis since no correlation could be made between the two parameters.

Adipose Tissue↗
PubMed1996

Dietary fat and colon cancer.

Dietary fat in general, and perhaps animal and polyunsaturated fats in particular, appear to increase colon carcinogenesis in animal models and epidemiologic studies. This observation holds the potential to shed light on the underlying mechanisms of colorectal carcinogenesis and reduce morbidity and mortality from the disease by dietary and chemoprevention. While research continues into the relationship between prostglandins and other putative mediators of the effects of fats on the colon, we can suggest that a diet which protects against colorectal cancer would be low in fat with most of that fat coming from vegetable sources. Prospective dietary trials are ongoing which may strengthen or modify these preliminary recommendations.

Animals↗
PubMed1991

[The effect of intestinal resection and dietary fat quality on the nutritional utilization of fat].

The influence of the quality of dietary fat on digestive and metabolic utilization of fat, serum levels of cholesterol and triglycerides and the relative percentages of serum fatty acids was studied in rats in which 50% of the distal small intestine (DSI) was resected and in sham-operated controls. Nutritive parameters were measured 1 month after surgery. The fat components of the diets were: olive oil, butter and equal parts of medium chain triglycerides (MCT), olive oil and sunflower seed oil. There was no changes in digestive utilization of fat in shamoperated controls with either dietary sources of fat, olive oil or butter. The removal of 50% of the distal small intestine led to a decline in the digestive utilization of fat (ADC) in both test diets. When dietary fat was supplied as equal parts of MCT, olive oil and sunflower seed oil instead of 100% olive oil (diet C), digestive utilization of fat was enhanced in resected rats. When ursodeoxycholic acid (UDCA) was added to diet C, digestive utilization of fat remained high, reaching values as elevated as those in sham-operated controls. At the metabolic level, resection of half the DSI led to a significant decrease in serum triglycerides and cholesterol levels, independently of type of dietary fat tested. The type of diet, as well as intestinal resection, do not led to an essential fatty acid deficiency in serum lipids; it is only a reflect of the supplemented diet fat contents.

Animals↗
PubMed1990

Effect of dietary fat on phospholipid class distribution and fatty acid composition in rat fat cell plasma membrane.

The effect of dietary fats on phospholipid class distribution and fatty acid composition was studied in rat fat cell plasma membrane. Three groups of male Wistar weanling rats were fed for 8 wk three diets differing in the amount and nature of the fats: 1.5% sunflower oil (low fat control; LFC), 10% sunflower oil (high fat, unsaturated; HFU), 1.5% sunflower oil + 8.5% cocoa butter (high fat, saturated; HFS). Plasma membranes were prepared from epididymal adipocytes. The amount and type of dietary fat significantly altered membrane phospholipid distribution. Phospholipid content was lowered with HFU as compared to LFC or HFS diets, but no changes were observed for cholesterol. Phosphatidylinositol (PI) and phosphatidylserine (PS) were less affected by dietary changes than were other phospholipid classes. Major changes were detected for phosphatidylcholine (PC), phosphatidylethanolamine (PE) and sphingomyelin (SM) contents. No large changes in PC and PE fatty acid compositions were observed between the LFC and HFS groups, but the HFU diet induced several changes. Correlations with plasma membrane 5'-nucleotidase activities are discussed.

Adipose Tissue↗
PubMed1989

Tumor necrosis factor-alpha-associated uterine endothelial injury in vivo. Influence of dietary fat.

The influence of dietary fat on recombinant human tumor necrosis factor-alpha (rHuTNF-alpha)-associated vascular endothelial injury in mice was examined. Histopathologic evaluation showed that greater injury was consistently observed in the uterus characterized by necrosis of endothelial cells lining small vessels in the endometrium and accompanied by multifocal hemorrhage and inflammatory cell accumulation. Mice fed standard animal diet, high corn oil diet, or high menhaden oil diet showed no differences in their susceptibility to the acute injury caused by rHuTNF-alpha injected alone or in combination with recombinant murine interferon-gamma. These results indicate that uterine endothelium may be a more sensitive target for rHuTNF-alpha-mediated endothelial injury and that high menhaden oil diet does not protect against tissue injury associated with the administration of rHuTNF-alpha alone or in combination with recombinant murine interferon-gamma.

Animals↗
PubMed1985

Dietary fat and blood pressure: an intervention study on the effects of a low-fat diet with two levels of polyunsaturated fat.

The role of dietary fat in human blood pressure control was studied among 84 middle-aged subjects (mainly couples) in two semirural communities in North Karelia, Finland. The families were randomly allocated into two groups that, after a baseline period of 2 weeks, changed their diet for a 12-week intervention period so that the proportion of energy derived from fats was similarly reduced in both groups, from 38 to 24%, but the polyunsaturated/saturated fatty acid (P/S) ratio was increased--from 0.2 to 0.9 in group I and to 0.4 in group II. After the intervention period, both groups switched back to their usual diet for a period of 5 weeks. During the intervention period, total serum cholesterol was reduced by 16% in group I and 14% in group II. Mean body weight and urinary sodium, potassium, calcium, and magnesium excretion changes were small or nonexistent. Mean systolic blood pressure decreased 4 mm Hg in group I (P less than 0.01) and 3 mm Hg in group II (P less than 0.01), and mean diastolic blood pressure decreased 5 mm Hg (P less than 0.001) and 4 mm Hg (P less than 0.01), respectively. The reductions were reversed during the switch-back period (P less than 0.01). These results confirm previous findings of the blood-pressure-reducing effect of a low-fat/high-P/S diet. Although a number of possible confounding factors can be ruled out, the dietary constituent accounting for the blood pressure change cannot be ascertained definitely. The results showed no significant further blood pressure reduction with more than a moderately increased P/S ratio when the saturated fat intake was markedly reduced.

Adult↗
PubMed1997

Mechanisms of the intestinal effects of dietary fats and milk products on colon carcinogenesis.

Dietary fat may promote colon cancer by increasing fatty acids (FA) and secondary bile acids (BA) in the colonic lumen. These cytotoxic surfactants can damage colonic epithelial cells and thus induce a compensatory hyperproliferation of crypt cells. Our studies show that the hyperproliferative effect of type and amount of dietary fat is not simply due to changes in colonic FA and BA. This indicates that an additional, at present unknown, cytotoxic factor is involved. The hyperproliferative effect of dietary fat is inversely related to the amount of calcium in the diet. In rat and man, dietary calcium precipitates colonic cytotoxic surfactants and thus inhibits luminal cytotoxicity. These inhibitory effects on metabolic risk factors suggest a preventive effect of dietary calcium on colon carcinogenesis.

Animals↗
PubMed2001

Moderate dietary fat consumption as a risk factor for ischemic heart disease in a population with a low fat intake: a case-control study in Korean men.

BACKGROUND: Dietary fat intake is associated with the incidence of ischemic heart disease (IHD) in Western countries. In populations in which both the average dietary fat consumption and the incidence of IHD are lower than in Western countries, the association of dietary fat intake with IHD incidence remains unknown. OBJECTIVE: We conducted a case-control study to examine the association of dietary fat with IHD incidence in Korean men. DESIGN: The case group consisted of 108 patients with electrocardiogram-confirmed myocardial infarction or angiographically confirmed (> or =50% stenosis) IHD who were admitted to a university teaching hospital in Seoul, Republic of Korea. The controls were 142 age-matched patients admitted to the departments of ophthalmology and orthopedic surgery at the same hospital. Dietary fat intake was assessed by a nutritionist using a semiquantitative food-frequency questionnaire. Body mass index (BMI), cigarette use, alcohol intake, exercise, and history of disease were determined during an interview and examination. RESULTS: In a univariate analysis, the mean percentages of energy from total fat, saturated fatty acids, and monounsaturated fatty acids were significantly higher in the cases than in the controls. BMI, smoking, and a history of hypertension were associated with the occurrence of IHD. In multiple logistic analyses, total fat intake was a significant risk factor (odds ratio: 1.08 for 1% of energy intake; 95% CI: 1.02, 1.14) after adjustment for BMI and smoking. CONCLUSION: In a population with a relatively low fat intake (19% of energy intake), a moderate increase in total fat intake may be a risk factor for IHD.

Alcohol Drinking↗
PubMed1999

Specific versus non-specific effects of dietary fat on carcinogenesis.

It will be apparent from this review that dietary fat can exert both specific and non-specific effects on carcinogenesis, at least in experimental animals. The non-specific effects appear to be related primarily to effects of dietary fat on energy balance. Although a positive energy balance can be achieved on a high-carbohydrate low-fat diet, it is much more likely to occur on a high-fat diet because of the high energy density of fat [101] and the fact that dietary fat is less capable of imparting a sense of satiety [102]. A continuing state of positive energy balance leads to obesity which has been associated with increased risk of cancer at a number of sites, including endometrium [103-106], postmenopausal breast cancer [107-113], renal cancer [114,115] and possibly cancers of the colorectum [116-122], pancreas [103,123] and prostate [124]. Whereas the non-specific effects of dietary fat appear to be deleterious for cancer, the specific effects in some cases can be beneficial. Examples are long-chain n-3 polyunsaturated fatty acids. CLA and tocotrienols. It is still too early to predict whether these may be of value in the prevention and/or treatment of human cancer but they seem worthy of further investigation. Knowledge of their mechanism of action may suggest novel approaches to the cancer problem and, as in the case of vitamins A and D, it may be possible to find analogues with more potent anti-cancer activity.

Animals↗
PubMed1990

Natural killer cell activity in a longitudinal dietary fat intervention trial.

It has been hypothesized that dietary fat may affect natural killer (NK) cell activity, a factor of potential importance in early tumor surveillance. Fourteen men successfully completed an intervention trial designed to test the effect of dietary fat on NK activity in humans. Study subjects lowered their fat intake to an average of 22% of calories as fat and consumed two dietary supplements (of coconut and safflower oils), in a cross-over design. These supplements resulted in large changes in the ratio of polyunsaturated to saturated fatty acids (1.73 to 0.34, on average). Results of a general linear model in which we fitted covariates on exercise, body mass, intervention sequence, and various dietary predictors revealed a significant effect of decreased total dietary fat intake on increased NK activity at an E/T ratio of 100:1 (about 0.79% increase for each absolute percent of calories as fat, P = 0.04). Similar results were obtained at E/T ratios of 50:1 and 25:1. No other nutritional predictor was significantly associated with NK activity at any E/T ratio.

Adult↗
PubMed1999

Dietary fat and carcinogenesis.

Epidemiologic investigations have suggested a relationship between dietary fat intake and various types of cancer incidences. Furthermore, epidemiologic studies as well as studies with animal models have demonstrated that not only the amount but also the type of fat consumed is important. At present, the mechanism by which dietary fat modulates carcinogenesis has not been elucidated. The effects of dietary fat on the development of tumours have been summarized in the present review with emphasis on colorectal, pancreas, breast and prostate cancer. It is concluded that influence on synthesis of prostaglandins and leukotrienes may be the universal mechanism by which dietary fats modulate carcinogenesis.

Animals↗
PubMed1994

Dietary fats, membrane phospholipids and obesity.

Modifications in dietary fat profile have been shown to affect body weight gain and adiposity. This may occur through changes in the partitioning between oxidation and storage and/or alterations in membrane structure, which may in turn influence metabolic rate. All the dietary fat classes are substrates for the biosynthetic elongase and desaturase enzymes. Obesity is associated with increased delta 9 desaturase activity, reduced delta 5 desaturase activity and perhaps reduced delta 6 desaturase activity. Dietary lipid profile can affect the activity of each of these enzymes. A number of possible mechanisms linking dietary fat subtypes with development of obesity are discussed, including modification of sodium potassium pump activity and alterations in mitochondrial proton leakage.

Animals↗