179 resultados para saturated fatty acids


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It is considered that consumption of very long chain (VLC, carbon chain length >= 20) n - 3 PUFAs in most Western populations is sub-optimal and benefits in relation to chronic disease would be gained from increased consumption. This review examines the current contribution that meat makes to dietary intake of VLC n - 3 PUFA and given its current low contribution, how ruminant meat may be enriched. Enrichment both directly with VLC n - 3 fatty acids and indirectly by increasing intake by the animals of alpha-linolenic acid (ALNA; C 18:3 n - 3) are considered. Since it now appears that dietary ALNA is a very limited source of VLC n - 3 PUFA in humans, the indirect route is controversial but since some forages-are rich sources of ALNA this route has many sustainability and environmental attractions. Consideration is also given to the increased concentrations of trans and conjugated fatty acids that will arise from enriching ruminant meat with PUFA.

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It is considered that consumption of very long chain (VLC, carbon chain length >= 20) n - 3 PUFAs in most Western populations is sub-optimal and benefits in relation to chronic disease would be gained from increased consumption. This review examines the current contribution that meat makes to dietary intake of VLC n - 3 PUFA and given its current low contribution, how ruminant meat may be enriched. Enrichment both directly with VLC n - 3 fatty acids and indirectly by increasing intake by the animals of alpha-linolenic acid (ALNA; C 18:3 n - 3) are considered. Since it now appears that dietary ALNA is a very limited source of VLC n - 3 PUFA in humans, the indirect route is controversial but since some forages-are rich sources of ALNA this route has many sustainability and environmental attractions. Consideration is also given to the increased concentrations of trans and conjugated fatty acids that will arise from enriching ruminant meat with PUFA.

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Previous experiments from our group have demonstrated that abomasal infusion of unsaturated free fatty acids (FFA) markedly decreases dry matter intake (DMI) in dairy cows. In contrast, experiments from other groups have noted smaller decreases in DMI when unsaturated triglycerides (TG) were infused postruminally. Our hypothesis was that unsaturated FFA would be more potent inhibitors of DMI than an equivalent amount of unsaturated TG. Four Holstein cows in late lactation were used in a single reversal design. Cows were fed a total mixed ration containing (DM basis) 23% alfalfa silage, 23% corn silage, 40.3% ground shelled corn, and 10.5% soybean meal. Two cows received soy FFA (UFA; 0, 200, 400, 600 g/d) and 2 received soy oil (TG) in the same amounts; cows then were switched to the other lipid source. Cows were abomasally infused with each amount for 5-d periods. The daily amount of lipid was pulse-dosed in 4 equal portions at 0600, 1000, 1700, and 2200 h; no emulsifiers were used and there was no sign of digestive disturbance. Both lipid sources linearly decreased DMI, with a significant interaction between lipid source and amount. Slope-ratio analysis indicated that UFA were about 2 times more potent in decreasing DMI than were TG. Decreased DMI led to decreased milk production. Milk fat content was increased linearly by lipid infusion. Milk fat yield decreased markedly for UFA infusion but was relatively unaffected by infusion of TG. Contents of short- and medium-chain fatty acids in milk fat decreased as the amount of either infusate increased. Contents of C-18:2 and C18: 3 in milk fat were increased linearly by abomasal infusion of either fat source; cis-9 C-18:1 was unaffected. Transfer of infused C18: 2 to milk fat was 35.6, 42.5, and 27.8% for 200, 400, and 600 g/d of UFA, and 34.3, 39.6, and 34.0% for respective amounts of TG. Glucagon-like peptide-1 (7-36) amide (GLP-1) concentration in plasma significantly increased as DMI decreased with increasing infusion amount of UFA or TG. Plasma concentration of cholecystokinin-octapeptide (CCK-8) was unaffected by lipid infusion. These results indicate that unsaturated FFA reaching the duodenum are more potent inhibitors of DMI than are unsaturated TG; the effect may be at least partially mediated by GLP-1.

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The effect of poultry species (broiler or turkey) and genotype (Wrolstad or BUT T8 turkeys and Ross 308 or Cobb 500 broilers) on the efficiency with which dietary longchain n-3 PUFA were incorporated into poultry meat was determined. Broilers and turkeys of both genotypes were fed one of six diets varying in FA composition (two replicates per genotype x diet interaction). Diets contained 50 g/kg added oil, which was either blended vegetable oil (control), or partially replaced with linseed oil (20 or 40 g/kg diet), fish oil (20 or 40 g/kg diet), or a mixture of the two (20 g linseed oil and 20 g fish oil/kg diet). Feeds and samples of skinless breast and thigh meat were analyzed for FA. Wrolstad dark meat was slightly more responsive than BUT T8 (P = 0.046) to increased dietary 18:3 concentrations (slopes of 0.570 and 0.465, respectively). The Ross 308 was also slightly more responsive than the Cobb 500 (P= 0.002) in this parameter (slopes of 0.557 and 0.449). There were no other significant differences between the genotypes. There was some evidence (based on the estimates of the slopes and their associated standard errors) that white turkey meat was more responsive than white chicken meat to 20:5 (slopes of 0.504 and 0.289 for turkeys and broilers, respectively). There was no relationship between dietary 18:3 n-3 content and meat 20:5 and 22:6 contents. If birds do convert 18:3 to higher FA, these acids are not then deposited in the edible tissues.

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Fatty acids are known to play diverse roles in immune cells. They are important as a source of energy, as structural components of cell membranes, as signaling molecules and as precursors for the synthesis of eicosanoids and similar mediators. Recent research has suggested that the localization and organisation of fatty acids into distinct cellular pools has a direct influence on the behaviour of a number of proteins involved in immune cell activation, including those associated with T cell responses, antigen presentation and fatty acid-derived inflammatory mediator production. This article reviews these studies and places them in the context of existing literature in the field. These studies indicate the existence of several novel mechanisms by which altered fatty acid availability can modulate immune responses and impact upon clinical outcomes

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Atherosclerosis, leading to cardiovascular disease, is a chronic condition involving a strong inflammatory component. There is evidence that the n-3 polyunsaturated fatty acids (PUFA) present in oily fish and fish oils protect against cardiovascular disease. While these fatty acids have well-recognised effects on plasma triacylglycerol concentrations, it is likely that they exert beneficial effects through other mechanisms in addition. A large body of evidence suggests that the n-3 PUFA have anti-inflammatory properties, some of which may be manifested in the arterial wall, either directly or indirectly, to modulate the progression of atherosclerosis. This review critically evaluates the evidence for the anti-inflammatory effects of the n-3 PUFA in cells and on pathways which have a direct influence on atherogenesis in the arterial wall.

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Over the last 25 years, the effects of fatty acids on the immune system have been characterized using in vitro, animal and human studies. Advances in fatty acid biochemistry and molecular techniques have recently suggested new mechanisms by which fatty acids could potentially modify immune responses, including modification of the organization of cellular lipids and interaction with nuclear receptors. Possibilities for the clinical applications of n-3 PUFA are now developing. The present review focuses on the hypothesis that the anti-inflammatory properties of n-3 PUFA in the arterial wall may contribute to the protective effects of n-3 PUFA in CVD, as suggested by epidemiological and secondary prevention studies. Studies are just beginning to show that dietary n-3 PUFA can be incorporated into plaque lipid in human subjects, where they may influence the morphology and stability of the atherosclerotic lesion.

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Fatty acids have diverse roles in all cells. They are important as a source of energy, as structural components of cell membranes, as signalling molecules and as precursors for the synthesis of eicosanoids. Recent research has suggested that the organization of fatty acids into distinct cellular pools has a particularly important role in cells of the immune system and that forms of lipid trafficking exist, which are as yet poorly understood. This Review examines the nature and regulation of cellular lipid pools in the immune system, their delivery of fatty acids or fatty acid derivatives to specific locations and their potential role in health and disease.

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The present review comes from the authors of the recent Scientific Advisory Committee on Nutrition (SACN) review Update on Trans Fatty Acids and Health, and focuses on assessing the strength of the evidence for a link between trans-fatty acid (trans-FA) intake and cancer. It evaluates a range of human ecological, case-control and prospective studies with trans-FA exposure assessed using either dietary assessment methods or trans-FA levels in tissues. Relevant animal studies are also presented in order to elucidate potential mechanisms. It concludes that there is weak and inconsistent evidence for a relationship between trans-FA and breast or colorectal cancer. Evidence for an association between trans-FA and prostate cancer is limited, but a recent large case-control study has shown a strong interaction between risk and trans-FA intake for the RNASEL QQ/RQ genotype that is present in about 35% of the population. This potential association requires further investigation. The single study on non-Hodgkin's lymphoma reported a strong positive association, but out), used a single assessment of dietary trans-FA made at the start of the study in 1980, and the significant changes it) trans-FA intakes between then and the end Of follow-up in 1994 limit the reliability of this observation. There is insufficient evidence to allow any differentiation between the effects of trans-FA from animal or vegetable origin on cancer risk.

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Background N-3 polyunsaturated fatty acids (PUFAs) from oily fish protect against death from cardiovascular disease. We aimed to assess the hypothesis that incorporation of n-3 and n-6 PUFAs into advanced atherosclerotic plaques increases and decreases plaque stability, respectively. Methods We did a randomised controlled trial of patients awaiting carotid endarterectomy. We randomly allocated patients control, sunflower oil (n-6), or fish-oil (n-3) capsules until surgery. Primary outcome was plaque morphology indicative of stability or instability, and outcome measures were concentrations of EPA, DHA, and linoleic acid in carotid plaques; plaque morphology; and presence of macrophages in plaques. Analysis was per protocol. Findings 188 patients were enrolled and randomised; 18 withdrew and eight were excluded. Duration of oil treatment was 7-189 days (median 42) and did not differ between groups. The proportions of EPA and DHA were higher in carotid plaque fractions in patients receiving fish oil compared with those receiving control (absolute difference 0.5 [95% CI 0.3-0.7], 0.4 [0.1-0.6], and 0.2 [0.1-0.4] g/100 g total fatty acids for EPA; and 0.3 [0.0-0.8], 0.4 [0.1-0.7], and 0.3 [0.1-0.6] g/100 g total fatty acids for DHA; in plaque phospholipids, cholesteryl esters, and triacylglycerols, respectively). Sunflower oil had little effect on the fatty acid composition of lipid fractions. Fewer plaques from patients being treated with fish oil had thin fibrous caps and signs of inflammation and more plaques had thick fibrous caps and no signs of inflammation, compared with plaques in patients in the control and sunflower oil groups (odds ratio 0.52 [95% CI 0.24-0.89] and 1.19 [1.02-1.57] vs control; 0.49 [0.23-0.90] and 1.16 [1.01-1.53] vs sunflower oil). The number of macrophages in plaques from patients receiving fish oil was lower than in the other two groups. Carotid plaque morphology and infiltration by macrophages did not differ between control and sunflower oil groups. Interpretation Atherosclerotic plaques readily incorporate n-3 PUFAs from fish-oil supplementation, inducing changes that can enhance stability of atherosclerotic plaques. By contrast, increased consumption of n-6 PUFAs does not affect carotid plaque fatty-acid composition or stability over the time course studied here. Stability of plaques could explain reductions in non-fatal and fatal cardiovascular events associated with increased n-3 PUFA intake.