Arachidonic acid and docosahexaenoic acid supplemented to an essential fatty acid–deficient diet alters the response to endotoxin in rats (original) (raw)
Related papers
The role of dietary polyunsaturated fatty acids in inflammation
Serbian Journal of Experimental and Clinical Research, 2013
Low-grade systemic infl ammation is at the base of the most chronic non-communicable diseases, which are reaching epidemic proportions worldwide. Key players in the regulation of infl ammation are n-6 and n-3 polyunsaturated fatty acids (PUFAs), in particular arachidonic acid (n-6) and eicosapentaenoic acid (n-3). Th ey are precursors of eicosanoids-signaling molecules involved in modulating the intensity and duration of infl ammatory responses. Eicosanoids derived from n-6 PUFAs have proinfl ammatory actions, while those derived from n-3 PUFAs act anti-infl ammatory. Th erefore, dietary intake of n-6 and n-3 PUFAs, as well as their ratio, could markedly aff ect the pathogenesis and manifestation of many chronic diseases associated with low-grade infl ammation. Th is review will focus on the relationship between dietary PUFAs and infl ammation, with reference to PUFAs status in plasma phospholipids in Serbian population.
Effect of Dietary Lipids on Endotoxemia Influences Postprandial Inflammatory Response
Journal of Agricultural and Food Chemistry, 2017
Metabolic syndrome (MetS) results in postprandial metabolic alterations that predisposes to a state of chronic low-grade inflammation and increased oxidative stress. We aimed to assess the effect of the consumption of the quantity and quality of dietary fat on fasting and postprandial plasma lipopolysaccharides (LPS). A subgroup of 75 subjects with metabolic syndrome was randomized to receive 1 of 4 diets: HSFA, rich in saturated fat; HMUFA, rich in monounsaturated fat; LFHCC n-3, low-fat, rich in complex carbohydrate diet supplemented with n-3 polyunsaturated fatty acids; LFHCC low-fat, rich in complex carbohydrate diet supplemented with placebo, for 12 week each. We administered a fat challenge reflecting the fatty acid composition of the diets at post-intervention. We determined the plasma lipoproteins and glucose, and gene expression in peripheral blood mononuclear cells (PBMC) and adipose tissue. LPS and LPS binding protein (LBP) plasma levels were determined by ELISA, at fasting and postprandial (4 hours after a fat challenge) states. We observed a postprandial increase in LPS levels after the intake of the HSFA meal, whereas we did not find any postprandial changes after the intake of the other three diets. Moreover, we found a positive relationship between the LPS plasma levels and the gene expression of IkBa and MIF1 in PBMC. No statistically significant differences in the LBP plasma levels at fasting or postprandial states were observed. Our results suggest that the consumption of HSFA diet increases the intestinal absorption of LPS, which, in turn, increases postprandial endotoxemia levels and the postprandial inflammatory response.
The American Journal of Clinical Nutrition, 2003
Background: Greatly increasing dietary flaxseed oil [rich in the nϪ3 polyunsaturated fatty acid (PUFA) ␣-linolenic acid (ALA)] or fish oil [rich in the long-chain nϪ3 PUFAs eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids] can reduce markers of immune cell function. The effects of more modest doses are unclear, and it is not known whether ALA has the same effects as its long-chain derivatives. Objective: The objective was to determine the effects of enriching the diet with ALA or EPA+DHA on immune outcomes representing key functions of human neutrophils, monocytes, and lymphocytes. Design: In a placebo-controlled, double-blind, parallel study, 150 healthy men and women aged 25-72 y were randomly assigned to 1 of 5 interventions: placebo (no additional nϪ3 PUFAs), 4.5 or 9.5 g ALA/d, and 0.77 or 1.7 g EPA+DHA/d for 6 mo. The nϪ3 PUFAs were provided in 25 g fat spread plus 3 oil capsules. Blood samples were taken at 0, 3, and 6 mo. Results: The fatty acid composition of peripheral blood mononuclear cell phospholipids was significantly different in the groups with higher intakes of ALA or EPA+DHA. The interventions did not alter the percentages of neutrophils or monocytes engaged in phagocytosis of Escherichia coli or in phagocytic activity, the percentages of neutrophils or monocytes undergoing oxidative burst in response to E. coli or phorbol ester, the proliferation of lymphocytes in response to a T cell mitogen, the production of numerous cytokines by monocytes and lymphocytes, or the in vivo delayed-type hypersensitivity response. Conclusion: An intake of ≤ 9.5 g ALA/d or ≤ 1.7 g EPA+DHA/d does not alter the functional activity of neutrophils, monocytes, or lymphocytes, but it changes the fatty acid composition of mononuclear cells.
Lipids, 1998
Weanling rats were fed on high-fat (178 g/kg) diets which contained 4.4 g α-linolenic (ALA), γ-linolenic, arachidonic (ARA), eicosapentaenoic (EPA), or docosahexaenoic acid (DHA)/100 g total fatty acids. The proportions of all other fatty acids, apart from linoleic acid, and the proportion of total polyunsaturated fatty acids (PUFA) (approximately 35 g/100 g total fatty acids) were constant, and the n-6 to n-3 PUFA ratio was maintained as close to 7 as possible. The fatty acid compositions of the serum and of spleen leukocytes were markedly influenced by that of the diet. Prostaglandin E 2 production was enhanced from leukocytes from rats fed the ARA-rich diet and was decreased from leukocytes from the EPA-or DHA-fed rats. Replacing dietary ALA with EPA resulted in diminished ex vivo lymphocyte proliferation and natural killer (NK) cell activity and a reduced cell-mediated immune response in vivo. In contrast, replacing ALA with DHA reduced ex vivo lymphocyte proliferation but did not affect ex vivo NK cell activity or the cell-mediated immune response in vivo. Replacement of a proportion of linoleic acid with either γ-linolenic acid or ARA did not affect lymphocyte proliferation, NK cell activity, or the cell-mediated immune response. Thus, this study shows that different n-3 PUFA exert different immunomodulatory actions, that EPA exerts more widespread and/or stronger immunomodulatory effects than DHA, that a low level of EPA is sufficient to influence the immune response, and that the immunomodulatory effects of fish oil may be mainly due to EPA.
Polyunsaturated fatty acids and inflammatory processes: New twists in an old tale
Biochimie, 2009
The n-6 fatty acid arachidonic acid (AA; 20:4n-6) gives rise to eicosanoid mediators that have established roles in inflammation and AA metabolism is a long recognised target for commonly used anti-inflammatory therapies. It has generally been assumed that all AA-derived eicosanoids are pro-inflammatory. However this is an oversimplification since some actions of eicosanoids are anti-inflammatory (e.g. prostaglandin (PG) E 2 inhibits production of some inflammatory cytokines) and it has been discovered quite recently that PGE 2 inhibits production of inflammatory leukotrienes and induces production of inflammation resolving lipoxin A 4. The n-3 fatty acids from oily fish and ''fish oils'', eicosapentaenoic acid (EPA; 20:5n-3) and docosahexaenoic acid (DHA; 22:6n-3), are incorporated into inflammatory cell phospholipids in a time-and dose-dependent manner. They are incorporated partly at the expense of AA, but also of other n-6 fatty acids. EPA and DHA inhibit AA metabolism. Thus production of AA-derived eicosanoids is decreased by these n-3 fatty acids; this occurs in a dose-dependent manner. EPA gives rise to an alternative family of eicosanoids (e.g. PGE 3), which frequently, but not always, have lower potency than those produced from AA. Recently a new family of EPA-and DHA-derived lipid mediators called resolvins (E-and D-series) has been described. These have potent anti-inflammatory and inflammation resolving properties in model systems. It seems likely that these mediators will explain many of the antiinflammatory actions of n-3 fatty acids that have been described. In addition to modifying the profile of lipid-derived mediators, fatty acids can also influence peptide mediator (i.e. cytokine) production. To a certain extent this action may be due to the altered profile of regulatory eicosanoids, but it seems likely that eicosanoid-independent actions are a more important mechanism. Indeed effects on transcription factors that regulate inflammatory gene expression (e.g. nuclear factor kB) seem to be important.
Prostaglandins, Leukotrienes and Essential Fatty Acids, 2000
Mice were fed a diet supplemented either with beef tallow (BT), BT plus ethyl eicosapentaenoate (EPA) or BT plus ethyl docosahexaenoate (DHA) for 9 weeks. EPA and DHA supplementation increased the content of the respective fatty acid in spleen leukocyte lipids, which was associated with the reduction in the arachidonate content. IL-1 mRNA induction upon lipopolysaccharide (LPS) stimulation in spleen leukocytes in the DHA diet group was significantly lower than in the BT diet group, but the EPA diet was without any significant effect. The amount of prostaglandin E2 (PGE2) released from LPS-stimulated spleen leukocytes was significantly lower in both the EPA and DHA groups than in the BT group. Thus, dietary EPA and DHA inhibited arachidonate metabolism similarly but had different effects on IL-1 mRNA induction in mouse spleen leukocytes.
Low-grade systemic infl ammation is at the base of the most chronic non-communicable diseases, which are reaching epidemic proportions worldwide. Key players in the regulation of infl ammation are n-6 and n-3 polyunsaturated fatty acids (PUFAs), in particular arachidonic acid (n-6) and ei-cosapentaenoic acid (n-3). Th ey are precursors of eicosanoids-signaling molecules involved in modulating the intensity and duration of infl ammatory responses. Eicosanoids derived from n-6 PUFAs have proinfl ammatory actions, while those derived from n-3 PUFAs act anti-infl ammatory. Th erefore, dietary intake of n-6 and n-3 PUFAs, as well as their ratio, could markedly aff ect the pathogenesis and manifestation of many chronic diseases associated with low-grade infl amma-tion. Th is review will focus on the relationship between dietary PUFAs and infl ammation, with reference to PUFAs status in plasma phospholipids in Serbian population.