Lipid Manipulation Research Articles

Tissue-Specific Fatty Acid and α-Tocopherol Profiles in Male Chickens Depending on Dietary Tuna Oil and Vitamin E Provision

The beneficial health-promoting effects of the long-chain polyunsaturated fatty acids (PUFA) of the n-3 series make them important constituents of human and animal diets. The effects of tuna oil or a combination of tuna oil with an increased level of vitamin E on the fatty acid profile and vitamin E distribution in tissues taken from cockerels were studied. Male chickens (Ross broiler breeders), penned on white wood shavings, were allocated into one of three groups with 12 birds per group and were fed from 10 wk of age on a commercial diet supplemented with 3% corn oil (control) or with 3% Tuna orbital oil (TO). Vitamin E was added at the rate of 40 mg/ kg, except in the third group in which the birds received a diet containing TO (3%) supplemented with 160 mg/kg vitamin E (TO+E). At 72 wk of age, the cockerels were killed, and tissues (liver, testes, heart, lung, kidney, spleen, thigh muscle, pancreas, internal fat, cerebellum, and cerebrum) were dissected for lipid and vitamin E analyses. Inclusion of TO in the cockerel diets significantly (P < 0.01) increased docosahexanoic acid (DHA) proportions in the major lipid fractions of the tissues with the brain being more resistant to lipid manipulation compared with the other tissues. Tissue enrichment with DHA took place at the expense of a decrease of n-6 PUFA. In the DHA-enriched tissues, vitamin E level decreased (P < 0.05), and susceptibility to peroxidation (TBARS accumulation) significantly (P < 0.01) increased. High vitamin E supplementation (160 mg/kg) in combination with TO prevented decrease of α-tocopherol concentration in the tissues and normalized or even increased their resistance to lipid peroxidation. There was tissue-specificity in response to dietary vitamin E supplementation; the liver was most responsive and the cerebellum was most resistant to vitamin E manipulation.

Relationship between the fatty acid composition of rat lymphocytes and immune functions.

The effects of dietary lipids on the fatty acid composition, activation and proliferation of lymphocytes were investigated. Weanling male Wistar rats were fed for 8 weeks on one of two low-fat diets which contained 50 g lipid/kg, or one of two high-fat diets containing 200 g lipid/kg, from either coconut oil or soyabean oil. The fatty acid composition of phospholipids from splenocyte membranes was affected by dietary lipid manipulation, and these differences influenced lymphocyte functions. Increased levels of linoleic acid in spleen lymphocytes correlated negatively with interleukin-2 receptor alpha-chain expression determined either by measuring the mean fluorescence or by the proportion of cells staining positive for CD25, and with the cell proliferation index. However, we found a positive correlation between interleukin-2 receptor alpha-chain expression determined by measuring the mean fluorescence and the cell proliferation index with the oleic acid concentration of spleen lymphocytes. Since phospholipid hydrolysis occurs early in lymphocyte activation, immunosuppressive effects induced by polyunsaturated fatty acids, described in the literature, could be due to an increase of linoleic acid or a decrease of oleic acid affecting many components of plasma-membrane-associated events involved in lymphocyte activation.

Determination of natural resistance of mice fed dietary lipids to experimental infection induced by Listeria monocytogenes.

Current understanding based on the effect of dietary lipid manipulation upon immune system function indicates that fatty acids are involved in the modulation of the immune response through different and complex pathways. Reduction of several immune parameters by fatty acid action may be applied in the treatment of diseases characterised by an overactivation of the immune system. As a consequence, a reduction of host resistance against infectious agents has been reported in animals fed dietary lipids. The present study confirms the action of dietary lipids on the survival of mice infected with the pathogenic bacterium Listeria monocytogenes. A significant increase in peritoneal cells from mice fed a hydrogenated coconut oil diet was found, while a significant reduction of bacterial recovery from spleens of these mice was observed in this group. In addition, both eicosanoid and phospholipase inhibitors did not promote any modification of lymphocyte proliferation from mice fed olive oil or fish oil.

Modulatory effects of dietary lipids on immune system functions.

Dietary lipid manipulation may affect a great number of immune parameters, such as lymphocyte proliferation, cytokine synthesis, natural killer (NK) cell activity, phagocytosis and so on. The immunomodulation induced by dietary fatty acids may be applied in the amelioration of inflammatory disorders, such as autoimmune diseases. However, the mechanisms that participate in these processes are still poorly understood. It is probable that modulation of immune system by fatty acids of the diet may occur by alteration of membrane fluidity, lipid peroxide formation, eicosanoid production or regulation of gene expression. However, recent studies have reported the effects of several free fatty acids on apoptosis induction of in vitro cultures. In fact, a possible explanation of the effects that fatty acids promote on the immune system cells could be associated with an apoptotic process performed in an irreversible way. In vivo studies have demonstrated the ability of fatty acids to alter the survival of animals fed diets containing oils and infected with a pathogenic bacterium. Experimental infection in animals fed dietary lipids produces a modification of resistance to micro-organisms. The present review analyses all of these parameters that dietary fatty acids are capable of altering in order to modify the immune response. Further studies will be needed to establish the mechanisms involved in immune system regulation, reduction of symptoms derived from autoimmune pathologies and so on.

Determination of natural resistance of mice fed dietary lipids to experimental infection induced by Listeria monocytogenes

Current understanding based on the effect of dietary lipid manipulation upon immune system function indicates that fatty acids are involved in the modulation of the immune response through different and complex pathways. Reduction of several immune parameters by fatty acid action may be applied in the treatment of diseases characterised by an overactivation of the immune system. As a consequence, a reduction of host resistance against infectious agents has been reported in animals fed dietary lipids. The present study confirms the action of dietary lipids on the survival of mice infected with the pathogenic bacterium Listeria monocytogenes. A significant increase in peritoneal cells from mice fed a hydrogenated coconut oil diet was found, while a significant reduction of bacterial recovery from spleens of these mice was observed in this group. In addition, both eicosanoid and phospholipase inhibitors did not promote any modification of lymphocyte proliferation from mice fed olive oil or fish oil.

Extracellular release of free fatty acids by rat T lymphocytes is stimulus-dependent and is affected by dietary lipid manipulation.

[(3)H]-Arachidonic acid-labelled rat T lymphocytes released radioactivity extracellularly when stimulated by the calcium ionophore A23187 or by monoclonal antibodies to some cell surface structures (CD2, CD5, CD11a, CD18, CD54, T-cell receptor) but not to others (CD49d, CD62L); release was greater with the calcium ionophore. Almost all of the radioactivity released from anti-CD2-stimulated lymphocytes was recovered in the free fatty acid fraction, whereas only about 50 per cent of that released after A23187 stimulation was recovered in this fraction. A23187 stimulation resulted in release of arachidonic acid from a variety of phospholipids (phosphatidylinositol, phosphatidylcholine and perhaps phosphatidylethanolamine), while the monoclonal antibody stimulation released arachidonic acid from phosphatidylinositol and perhaps phosphatidylcholine. Unstimulated lymphocytes released a range of fatty acids extracellularly, with palmitic acid accounting for 35-40 per cent and arachidonic acid for 5 per cent of released fatty acid. Stimulation of lymphocytes with either anti-CD2 or A23187 increased total fatty acid release 1.5- to 1.8-fold. In both cases palmitic acid remained the most predominant fatty acid released but the contribution of arachidonic acid increased. The type of lipid fed to the rats significantly influenced the amount and type of fatty acid released. Fish oil feeding significantly reduced extracellular fatty acid release by stimulated lymphocytes.

The effect of dietary lipid manipulation on murine splenic lymphocytes apoptosis and heat shock protein over expression.

In this study, we kept BALB/c mice on a hyperlipidic diet for 120 days and then assessed the predisposition to apoptosis and the appearance of heat shock protein (Hsp) on splenic lymphocytes. By immunoblot analysis, bands corresponding to Hsp 60 and Hsp 70 in cells from mice kept on a saturated fatty acid diet showed a greater expression already after 1 month while two other bands, which correspond to Hsp 25 and Hsp 27, were slightly present after 1 month of treatment. In cells from mice kept on a diet rich in unsaturated fatty acid, there was a marked expression of Hsp 25 and Hsp 27 after only 30 days of treatment, which was maintained constant for up to 4 months; while for bands corresponding to Hsp 60 and Hsp 70, a significant minor signal was only detectable after 2-4 months from the beginning of the treatment. Splenic lymphocytes from animals kept on a lipidic diet containing saturated fatty acids were more susceptible to death by apoptosis, while cells of animals treated with unsaturated fatty acid were shown to be more resistant.

The effect of dietary lipid manipulation on murine splenic lymphocytes apoptosis and heat shock protein over expression

In this study, we kept BALB/c mice on a hyperlipidic diet for 120 days and then assessed the predisposition to apoptosis and the appearance of heat shock protein (Hsp) on splenic lymphocytes. By immunoblot analysis, bands corresponding to Hsp 60 and Hsp 70 in cells from mice kept on a saturated fatty acid diet showed a greater expression already after 1 month while two other bands, which correspond to Hsp 25 and Hsp 27, were slightly present after 1 month of treatment. In cells from mice kept on a diet rich in unsaturated fatty acid, there was a marked expression of Hsp 25 and Hsp 27 after only 30 days of treatment, which was maintained constant for up to 4 months; while for bands corresponding to Hsp 60 and Hsp 70, a significant minor signal was only detectable after 2–4 months from the beginning of the treatment. Splenic lymphocytes from animals kept on a lipidic diet containing saturated fatty acids were more susceptible to death by apoptosis, while cells of animals treated with unsaturated fatty acid were shown to be more resistant.

Diabetes-induced impairment of macrophage cytokine release in a rat model: Potential role of serum lipids

Diabetes (type I and type II) affects approximately 13 million people in the United States. Delayed and incomplete healing of wounds can be a major problem for diabetic patients. Macrophages are an important cell in the complex process of wound repair representing the major source of cytokines throughout the wound healing process. Cytokines mediate many of the cellular responses critical to timely wound repair. It has been suggested that diabetes impairs wound healing through disruption of local cytokine production. We previously demonstrated that platelet-derived growth factor B chain (PDGF-B) levels are deficient at the wound site of diabetic rats. In the present study, we measured the levels of several marker cytokines released from cultured peritoneal macrophages of diabetic, nondiabetic hyperlipidemic, and normal rats. The diabetic condition was associated with a generalized reduction of macrophage cytokine release. Nondiabetic hyperlipidemic animals demonstrated similar cytokine reduction supporting the hypothesis that elevated serum lipids are the primary determinants of diabetes-induced reductions in macrophage cytokine release. Thus, manipulation of serum lipids may be a therapeutically useful modality for controlling macrophage cytokine release in the inflammatory and/or wound environment.

Effect of feeding different lipid sources on growth, feed efficiency and tissue fatty acid composition of Clarias batrachus fry and fingerlings

Summary Fry (0.46–0.53 g) and fingerlings (5.0–5.12 g) of the catfish Clarias batrachus were reared for 6 weeks on experimental diets differing in lipid sources. Triplicate groups of fish were fed ad libitum each of the four lipid sources (5 % of the diet), viz., (i) cod liver oil; (ii) sunflower oil; (iii) mixture (1:1) of cod liver oil/sunflower oil; and (iv) hydrogenated vegetable oil. These served mainly as sources of n-3; n-6; a mixture of n-3 and n-6; and saturated fatty acids, respectively. The results indicated that dietary lipid manipulation caused significant differences in weight gain, feed efficiency and tissue fatty acid profile of both fry and fingerlings. Deposition of fatty acids in the carcass very closely followed the fatty acid composition of the fed diet. The combination of n-3 and n-6 fatty acids elicited the best growth response, feed conversion and increased deposition of highly unsaturated fatty acids, suggesting the essential nature of both n-3 and n-6 fatty acids for maintenance of healthy stock and promotion of rapid growth in this species.

Influence of Diets Containing Olive Oil, Sunflower Oil or Hydrogenated Coconut Oil on the Immune Response of Mice.

The effect of diets containing olive oil, sunflower oil or hydrogenated coconut oil on immune cell function was investigated. Lipid administration in assays in vitro as well as in the diet has been demonstrated that affect to lymphocyte proliferation, cytokine synthesis, natural killer (NK) cell activity and antigen presentation. Therefore, unsaturated fatty acids may be used in the treatment of inflammatory diseases due to their immunomodulatory properties. Three groups of Balb/c mice were fed three diets at various times for 5, 15, 30, 60, or 90 days. Diets were different for each group, as each contained 15wt% olive oil, sunflower oil or hydrogenated coconut oil. The number of splenic cells showed significant differences with respect to the type of dietary lipid and the time of dietary administration. At the end of dietary lipid supplementation mitogen-stimulated lymphocyte proliferation from the spleens of mice fed diets that contained olive oil or hydrogenated coconut oil was significantly higher than that of mice fed diet that contained sunflower oil in which mitogen-stimulated proliferation of lymphocytes decreased lightly. Interleukin-2 (IL-2) production was significantly higher in mice fed the olive oil-or sunflower oil-enriched diets for 90 days when compared with that of mice fed the diet containing hydrogenated coconut oil. Dietary lipid manipulation also modified NK cell activity, since the results obtained showed a significant difference between the NK cell activity of mice fed the diet that contained olive oil and that observed in the mice fed the diet containing hydrogenated coconut oil. The results demonstrate that the addition to the diet of unsaturated fatty acids for different times may play an important role as a modulatory agent of immune cell function.

The effect of dietary fatty acid manipulation on phagocytic activity and cytokine production by peritoneal cells from Balb/c mice.

Previous studies have demonstrated that dietary lipid manipulation may modify immune response by affecting lymphocyte proliferation, phagocytosis, cytokine production, etc. In this paper, we investigated the effect of olive oil (OO) on the phagocytic activity and cytokine production by murine peritoneal cells. These results were compared with those obtained from mice fed diets containing sunflower oil (SO) or hydrogenated coconut oil (HCO). Balb/c mice were divided into three groups and fed diets containing 15% by weight of either OO, SO or HCO for 5, 15, 30, 60 or 90 d. Phagocytic activity and interleukin-1 (IL-1) production were increased in OO-fed mice as compared to the other groups. On the contrary, no significant differences were observed in the levels of tumor necrosis factor (TNF) production, although the levels of this cytokine were slightly increased in mice fed the OO diet. These observations suggest that OO is able to modify the immune response and therefore, it may be used as an immunomodulatory agent.

Manipulation of dietary lipids, fatty acids and vitamins in zooplankton cultures

1. A wide range of species that are cultivated in commercial mariculture are planktonic during at least part of their life cycle; for example, the larval stages of shellfish (shrimp and molluscs) and the live feeds (rotifers, brine shrimp, copepods) used in the larviculture of marine fish and shellfish. Over the last decades various techniques have been developed to deliver nutrients to these zooplanktonic organisms either through artificial diets or by manipulating the composition of the live prey fed to the carnivorous stages. This paper reviews the methodology that has allowed aquaculturists to gain knowledge of nutritional requirements and may offer interesting opportunities for ecologists to verify the importance of key nutrients in the natural food chain of marine as well as freshwater ecosystems.2. Live micro‐algae can be replaced partially or completely in the diet of filter‐feeders such as rotifers, Artemia, shrimp larvae and bivalves, by various types of preserved algae, micro‐encapsulated diets and yeast‐based diets, whereas lipid emulsions and liposomes may be utilized to supplement specific lipid‐and water‐soluble nutrients, respectively. Microbound and micro‐encapsulated diets have been designed to supplement live feed in the culture of micro‐predators such as fish and shrimp larvae.3. Live prey organisms, in particular rotifers and Artemia, can be ‘bio‐encapsulated’ with a variety of enrichment diets to manipulate their content in certain nutrients, including ω3 highly unsaturated fatty acids (FA) and the vitamins C, A and E. Nevertheless, the enrichment techniques are not applicable for all nutrients and prey organisms. Phospholipid composition is difficult to manipulate through the diet of live feed and the enrichment of the essential FA docosahexaenoic acid (DHA) is hampered in most Artemia species due to the catabolism of this FA following enrichment.

O.40 Effect of the manipulation of dietary lipids on mucosal fatty acid (FA) profile and intracolonic leukotriene (LT) release in experimental colitis

O.40 Effect of the manipulation of dietary lipids on mucosal fatty acid (FA) profile and intracolonic leukotriene (LT) release in experimental colitis

The effect of dietary lipid manipulation on the uptake of [3H]-triolein by tissues of the rat.

The effect of dietary lipid manipulation on the uptake of [3H]-triolein by tissues of the rat.

Characterization of lipoprotein composition in rats fed different dietary lipids and of the effects of lipoproteins upon lymphocyte proliferation

Weanling Lewis rats were fed for 10 weeks on a low fat (2.5% by weight; LF) diet or on diets containing 20% by weight of hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO), evening primrose oil (EPO), or menhaden (fish) oil (MO); all other components of the diets were identical. The chylomicron (CM), very low density lipoprotein (VLDL), low density lipoprotein (LDL), and high density lipoprotein (HDL) fractions were isolated from the serum. The serum from MO-fed animals had lower LDL and HDL cholesterol concentrations than the serum from animals fed each of the other diets. The apolipoprotein A-1 concentration in the HDL fraction from animals fed the MO diet was also low. The serum from HCO-fed animals had a higher CM triacylglycerol concentration than serum from animals fed each of the other diets. The serum from OO-fed animals had a higher VLDL triacylglycerol concentration than serum from animals fed each of the other diets. The concentration of apolipoprotein B was also high in the VLDL fraction from OO-fed animals. The fatty acid composition of each lipoprotein fraction was affected by the nature of the lipid in the diet; the greatest effects were observed in the CM and VLDL fractions. Each lipoprotein fraction isolated from LF-fed rats inhibited mitogen-stimulated rat spleen lymphocyte proliferation in a concentration-dependent manner; LDL and HDL caused greater inhibition than CM and VLDL. Dietary lipid manipulation did not alter the inhibitory effects of any of the lipoprotein fractions upon lymphocyte proliferation, except that CM and HDL from MO-fed animals and HDL from OO-fed animals resulted in enhanced proliferation compared with either CM or HDL from animals fed the other diets. We conclude that the inhibition of lymphocyte proliferation caused by feeding rats certain dietary lipids (OO, EPO, MO) may be mediated by non-lipoprotein serum components.

P-H3-01 Electrical manipulation of lipids and proteins in planar supported lipid bilayers: Boxer SG, Groves JT, Salafsky J., Wolfing C & and Ullman N. Department of Chemistry, Stanford University

P-H3-01 Electrical manipulation of lipids and proteins in planar supported lipid bilayers: Boxer SG, Groves JT, Salafsky J., Wolfing C & and Ullman N. Department of Chemistry, Stanford University

Effects of Dietary Lipid Manipulation upon Graft vs Host and Host vs Graff Responses in the Rat

The popliteal lymph node (PLN) assay was used to establish whether dietary lipids with differing fatty acid compositions could affect cell-mediated immunity in the rat. Weanling rats were fed for 4 weeks on a low-fat (2.5% by weight; LF) diet or on diets containing 20% (by weight) hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO), evening primrose oil (EPO), or menhaden (fish) oil (MO). Feeding the MO diet suppressed the graft vs host response compared with feeding the LF, HCO, SO, or EPO diets, while feeding the OO diet suppressed this response compared with feeding the LF or EPO diets. Feeding the MO diet suppressed the host vs graft response compared with feeding each of the other diets. Following the graft vs host reaction, PLN lymphocytes from animals fed the MO diet had significantly lower levels of expression of LFA-1 and CD2 compared with PLN lymphocytes from animals fed the LF diet; furthermore, they had lower levels of expression of T-cell receptor (TcR), CD4, CD8, LFA-1, and CD2 compared with lymphocytes from animals fed some, and in the case of CD2 each, of the other high-fat diets, Feeding the MO diet resulted in a lower proportion of cells expressing the interleukin-2 receptor, indicating an inhibition of lymphocyte activation, and a lower proportion of CD16 +/CD3 - cells, indicating a decrease in the proportion of NK cells within the PLN. Following the host vs graft reaction, PLN lymphocytes from animals fed the MO diet had significantly lower levels of expression of TcR and CD8 compared with lymphocytes from animals fed each of the other diets; furthermore, they had lower levels of expression of CD4, CD2, and LFA-1 compared with lymphocytes from animals fed the LF, HCO, OO, or SO diets. These observations indicate that the smaller PLN size of animals fed the MO diet results from an inhibition of activation and subsequent proliferation of cells within the node and perhaps also a suppression of movement of cells from the bloodstream to the PLN, due to decreased level of expression of adhesion molecules. These lowered levels of expression might be due to an inhibitory effect of the n-3 polyunsaturated fatty acids found in MO upon components of the signal transduction pathways involved in lymphocyte activation or upon expression of the genes for the surface molecules or both.

The effects of dietary lipid manipulation on the production of murine T cell-derived cytokines.

Lymphocytes play an important part in the development and progression of a number of autoimmune and inflammatory disorders, which are characterized by the presence of activated T cells and cytokines at the site of tissue injury and in the circulation. There has been considerable interest in using dietary polyunsaturated fatty acids (PUFA), particularly the n-3 PUFA found in fish oils, in the therapy of these conditions; such therapies aim, primarily, to suppress T-lymphocyte activity. While several studies have investigated the effects of fatty acids on the production of monocyte- and macrophage-derived cytokines, few have investigated their effects on the production of T cell-derived cytokines. Each of these studies have been restricted to IL-2 and have produced results which are not entirely clear. Moreover, there have been no studies to investigate the effects of dietary lipids other than fish oils on IL-2 production or the effects of dietary lipids on lymphokines other than IL-2. To investigate the effects of dietary lipid manipulation on the production of IL-2, IL-4, IL-10 and IFN-gamma by lymphocytes, mice were fed for 8 weeks on a low fat (LF) diet or one of 4 high fat diets, which contained 20% (by weight) hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO) or menhaden oil (MO). Culture medium of lymphocytes from mice fed the OO or SO diets contained significantly more IL-2 than that of lymphocytes from mice fed the LF or HCO diets.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of Dietary Lipid Manipulation upon Inflammatory Mediator Production by Murine Macrophages

This study investigated the effects of feeding mice lipids with different fatty acid compositions upon the ability of stimulated macrophages to produce inflammatory mediators. Weanling mice were fed for 8 weeks on a low-fat (LF; 2.5% by weight) diet or on diets containing 20% by weight of hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO), or menhaden (fish) oil (MO). Thioglycollate-elicited peritoneal macrophages were isolated. Macrophages isolated from MO-fed mice produced less PGE2, 6-keto-PGF1a, TXB2, and interleukin-6 in response to lipopolysaccharide (LPS) stimulation than those from mice fed each of the other diets. Macrophages from mice fed the OO, SO, or MO diets produced less tumor necrosis factor a in response to LPS stimulation than those from mice fed the LF or HCO diets. There was no effect of dietary lipid manipulation upon the production of interleukin-1 by LPS-stimulated macrophages. Macrophages from mice fed the MO diet produced more superoxide and hydrogen peroxide in response to phorbol ester stimulation than those from mice fed each of the other diets. In response to unopsonized zymosan, macrophages from mice fed the SO or MO diets produced more hydrogen peroxide than macrophages from mice fed the other diets. LPS-stimulated nitric oxide production was greater from macrophages from OO-, SO-, or MO- fed mice than from those fed the LF or HCO diets. Thus, the nature of the lipid consumed in the diet has significant effects upon the production of a variety of inflammatory mediators by macrophages. The most potent effect is caused by fish oil consumption. Possible mechanisms by which dietary fatty acids, particularly the n-3 polyunsaturated fatty acids found in fish oils, could affect mediator production by macrophages are described. The clinical relevance of such effects is discussed.