Response of (n-3) and (n-6) fatty acids in piglet brain, liver and plasma to increasing, but low, fish oil supplementation of formula.

Addition of fish oils to infant formula provides (n-3) long-chain polyenoic fatty acids (LCP), specifically 22:6(n-3), to infants fed formula rather than human milk. Most fish oils, however, contain high levels of 20:5(n-3) and low (n-6) LCP. These studies determined the brain total, synaptic plasma membrane phosphatidylethanolamine and phosphatidylcholine, and plasma and liver phospholipid fatty acids of piglets fed from birth to 15 d with formula containing (percent fatty acids) 34% 18:2(n-6), 0.8% 18:3(n-3) and 0, 2 or 6 g/L menhaden oil, or sow milk. The brain 22:6(n-3) was higher and 22:4(n-6) lower in piglets fed 6 g/L menhaden oil compared with sow milk. Brain levels of 20:5(n-3) did not increase, or levels of 20:4(n-6) decrease, with increasing dietary (n-3) LCP. A diet concentration-dependent increase in 20:5(n-3) and decrease in 20:4(n-6) (P less than 0.0001) in liver phospholipid showed no evidence of maximum saturation or depletion, respectively, over the range of (n-3) LCP intake studied. The fish oil supplementation was effective in supplying 22:6(n-3) to the developing brain. The accompanying increase in 20:5(n-3) and decrease in 20:4(n-6), important eicosanoid precursors, in plasma and liver phospholipid show the need for caution in the use of fish oils low in (n-6) LCP as a source of (n-3) LCP for infant formula.     

Dietary menhaden oil: effects on the rate and magnitude of modification of phospholipid fatty acid composition of mouse heart and brain

1. Male CD-1 white mice, 18-20 g body-weight, were given semi-purified diets containing 100 g menhaden oil (MO) or hydrogenated coconut oil (HCO)/kg for 23 d. Mice were killed on days 0, 3, 5, 7, 14, 23. After 23 d of MO supplementation the remaining mice were switched to the HCO diet for an additional 10 d. 2. The progressive change(s) in the polyunsaturated fatty acid (PUFA) composition of cardiac and brain phospholipid classes were followed during the MO supplementation and depletion periods. 3. The content of fatty acids 20:5n-3, 22:5n-3 and 22:6n-3 increased immediately following ingestion of the MO diet and continued to increase at a steady rate in both heart and brain phospholipid classes. 4. In general, the period required to reach steady-state was 1 week for n-3 PUFA and 18:2n-6, and 2 weeks for 20:4n-6. 5. Cessation of MO consumption for 10 d resulted in marked decreases in the content of n-3 PUFA and increases in n-6 PUFA in cardiac phospholipids in particular. Brain phospholipids were less responsive. 6. The results suggest that dietary fish oil must be consumed for at least 1 week before maximum changes in PUFA composition are observed, and fish oil ingestion must be continuous to maintain elevated n-3 PUFA levels in heart and brain phospholipids.     

Essential fatty acids in the liver and adipose tissue of genetically obese mice: effect of supplemental linoleic and gamma-linolenic acids

Genetically obese mice (ob/ob) and their lean litter-mates were given diets iso-energetically supplemented with sucrose, hydrogenated coconut oil, safflower oil or evening primrose (Oenothera biennis) oil. Weight gain over 15 weeks was significantly greater in the evening primrose oil-supplemented obese mice than in the other groups. In all the groups of obese mice, liver total phospholipids contained proportionally less linoleic acid and more dihomo-gamma-linolenic acid and arachidonic acid than did the lean controls. As a percentage of total fatty acids, n-3 essential fatty acids (EFA) in liver and adipose tissue lipids were significantly lower in the obese mice than in the lean controls. Supplementation with EFA-rich oils (safflower and evening primrose oil) increased the proportional composition of n-6 EFA and decreased the n-3 EFA more in the liver total phospholipids of the lean than the obese mice.     

Effects of repeated gestation and lactation on milk n-6 fatty acid composition in rats fed on a diet rich in 18:2n-6 or 18:3n-6.

The present study examined the effect of repeated gestation and lactation on the levels of long-chain n-6 polyunsaturated fatty acids in rat milk fat, and examined whether such levels might be modulated by supplementing the diet of the lactating dams with either (g/kg) 50 safflower oil (SFO; containing 800 g 18:2n-6/kg), or 50 evening primrose oil (EPO; containing 720 g 18:2n-6 and 90 g 18:3n-6/kg). The milk was collected at three different times (days 1, 8 and 15) in each given lactation period from female Sprague-Dawley rats which were successively bred for four pregnancies and lactations. Results showed that dietary fat and breeding frequency had no significant effects on milk triacylglycerol content, but they modified the pattern of milk fatty acids in both triacylglycerol and phospholipid fractions. After three or four successive breedings rats fed on EPO produced milk containing less saturated but more monounsaturated and polyunsaturated fatty acids compared with those fed on SFO. During the course of lactation the levels of n-6 metabolites, e.g. 18:3n-6, 20:3n-6 and 20:4n-6, in milk fat declined progressively. However, they were consistently higher in the EPO group than in the SFO group. These findings suggest that the levels of long-chain n-6 metabolites in the milk fat may be increased through supplementing the maternal diet with 18:3n-6.     

Dietary n-3 polyunsaturated fatty acids: rate and extent of modification of fatty acyl composition of lipid classes of mouse lung and kidney

The rate and extent of modification of fatty acid composition of mice lung and kidney by dietary menhaden oil (MO) was investigated. White mice were fed 2 wt% safflower oil and either 10 wt% MO or 10 wt% hydrogenated coconut oil (HCO) for 23 d. The stability of dietary MO-induced fatty acid modifications was assessed by replacing the MO diet of a group of mice after 23 d with the HCO diet for an additional 10 d. Mice were sacrificed on d 0, 1, 3, 5, 7, 14, 23 and 33. The n-3 polyunsaturated fatty acid (PUFA), 20:5n-3 and 22:6n-3 were rapidly incorporated into lung and kidney phosphoglyceride (PL) classes during the first 7 d of MO ingestion relative to the controls. After 1 wk of MO consumption, the rate of incorporation either plateaued at an elevated level or continued to increase at a much more gradual rate. A marked increase in the content of 22:5n-3 in lung and kidney was observed. A concomitant and rapid decrease was observed in the n-6 PUFA, 20:4n-6, 22:5n-6 and 18:2n-6. The minimum content of 20:4n-6 was reached between 1 and 2 wk, whereas the minimum levels of 18:2n-6 and 22:5n-6 occurred within 72 h. The n-6/n-3 PUFA ratio in lung and kidney and PL classes increased in mice fed HCO and decreased in mice fed dietary MO. When dietary MO was removed, the n-3 PUFA levels decreased with a concomitant increase in n-6 PUFA after 10 d of HCO consumption.(ABSTRACT TRUNCATED AT 250 WORDS)     

n-3 Essential fatty acids decrease weight gain in genetically obese mice

1. Lean (ln/ln) and obese (ob/ob) mice were given diets containing a fat source of 100 g evening primrose (Oenothera biennis) oil (fatty acids 18:2n-6, 18:3n-6; EPO) or 100 g cod liver oil (20:5n-3, 22:6n-3; CLO)/kg diet. 2. Weight gain was lower in the ob/ob mice fed on CLO, an effect unrelated to food intake. 3. In the ob/ob mice fed on CLO, thromboxane synthesis by clotting platelets was reduced compared with that in ob/ob mice fed on EPO. 4. The ob/ob CLO-fed mice had lower arachidonic acid but higher levels of n-3 fatty acids in liver, brown adipose tissue and white adipose tissue. 5. The n-3 fatty acids in CLO therefore replaced the n-6 fatty acids in tissue lipids and reduced synthesis of '2 series' prostaglandins in addition to causing lower weight gain in the CLO-fed ob/ob mice.     

Dietary influences of evening primrose and fish oil on the skin of essential fatty acid-deficient guinea pigs

There have been reports that certain dietary lipids are capable of regulating cellular inflammation and hyperproliferation. To investigate further the role of dietary manipulation involving gamma-linolenic acid (18:3n-6) and eicosapentaenoic acid (20:5n-3) on hyperproliferative cellular components, the effects of orally administered primrose oil (containing 18:3n-6) and menhaden fish oil (containing 20:5n-3) were tested in a cutaneous system using the essential fatty acid (EFA)-deficient guinea pig fed a hydrogenated coconut oil (HCO) diet. The effects of the dietary crossover regimen were determined on epidermal 1) morphology, 2) DNA synthesis, 3) delta 6- and delta 5-desaturase activities and 4) fatty acid composition of skin and liver lipids. Our results demonstrated that dietary fish oil lacked the capacity to reverse the signs of epidermal hyperproliferation, acanthosis and hypergranulosis that are characteristic of EFA deficiency. In contrast, primrose oil feeding reversed the histological and biochemical signs of hyperproliferation. These results suggest that dietary fish oil, which contains largely the 20:5n-3 fatty acid, lacks EFA-functional properties in the skin. In addition, substitution of HCO with primrose or fish oil after 6 wk revealed incorporation of 18:3n-6 and 20:5n-3 into epidermal lipids, respectively. The significance of these altered epidermal fatty acid profiles is discussed.     

Intensification of essential fatty acid deficiency in the rat by dietary trans fatty acids

Two studies were conducted using male rats to assess the effect of trans fatty acids upon essential fatty acid (EFA) deficiency. In the first study 5% corn oil (CO), hydrogenated coconut oil (HCNO) or margarine stock (MS, partially hydrogenated soybean oil) were fed, and the levels of trans fatty acids in tissue lipids were measured. The trans fatty acids present in MS were found to intensify EFA deficiency and to be retained in tissue lipids to a high degree, especially in heart phospholipids (PL). In the second study, as the level of trans fatty acids increased in the diet, increasingly higher levels of trans fatty acids were deposited in the heart PL. As dietary trans acid increased, a decrease in total omega 6 fatty acids, and a decrease in the sum of 18:2 omega 6 + 20:4 omega 6 - 20:3 omega 9 fatty acids in heart PL occurred, both criteria indicating a shift toward an increasing EFA deficiency state. Studies of delta 5 desaturase activity of liver microsomes in selected groups showed an increase in the conversion of 20:3 omega 6 to 20:4 omega 6 as the trans fatty acid level in the diet increased.     

Abnormal essential fatty acid composition of tissue lipids in genetically diabetic mice is partially corrected by dietary linoleic and gamma-linolenic acids

Genetically diabetic mice (db/db) and their non-diabetic litter-mates were maintained for 15 weeks on diets supplemented with safflower oil or evening primrose (Oenothera bienis) oil, both essential fatty acid (EFA)-rich sources, or hydrogenated coconut oil (devoid of EFA). Plasma glucose was higher in the diabetic mice supplemented with the oils than in the unsupplemented diabetic mice. In the oil-supplemented non-diabetic mice, plasma glucose did not differ compared with the unsupplemented non-diabetic mice. The proportional content of arachidonic acid in the phospholipids of the pancreas was significantly decreased in diabetic mice, an effect which was completely prevented by supplementation with safflower or evening primrose oil but not hydrogenated coconut oil. In the liver phospholipids of the diabetic mice, dihomo-gamma-linolenic acid was proportionally increased, an effect reduced by supplementation with safflower oil but not evening primrose or hydrogenated coconut oils. In the liver triglycerides of the diabetic mice, gamma-linolenic acid, dihomo-gamma-linolenic acid and arachidonic acid were all proportionally decreased, effects which were also prevented by safflower or evening primrose oil but not hydrogenated coconut oil. Alopecia and dry scaly skin were prominent in the diabetic mice but less extensive in the diabetic mice supplemented with EFA.     

Plasma, platelet, and aorta fatty acids composition in response to dietary n-6 and n-3 fats supplementation in a rat model of non-insulin-dependent diabetes

Male Sprague-Dawley rats were injected with 90 mg/kg of streptozotocin at 2 days of age. After weaning, they were put on a fat-free diet supplemented with safflower oil (S), a combination of S and linseed oil (L) or a combination of evening primrose oil (E) and L for 8 weeks. Plasma glucose levels and glycosuria were significantly elevated in all 3 groups of diabetic rats in comparison with the corresponding control rats. The percentage of arachidonic acid (20:4n-6) in plasma phospholipids of the S + L and E + L groups was similar to that of the S group and did not differ between control and diabetic rats while adrenic acid (22:4n-6) and docosahexaenoic acid (22:6n-3) changed in proportion to dietary n-3 and n-6 fats content. Arachidonic acid in aorta phospholipids significantly reduced in all 3 groups of diabetic rats as compared to the corresponding control groups. Dihomo-gamma-linolenic acid (20:3n-6) and arachidonic acid in aorta phospholipids increased by the E + L treatment. These results suggest that arachidonic acid in plasma phospholipids is kept constant regardless of the presence of diabetes of non-insulin-dependent type or dietary n-3 and n-6 fats supplementation. In aorta phospholipids, arachidonic acid in diabetic animals reduced and this may be compensated by gamma-linolenic acid supplementation, which leads to increase of dihomo-gamma-linolenic acid and arachidonic acid levels.     

Changes in piglet tissue composition at birth in response to increasing maternal intake of long-chain n-3 polyunsaturated fatty acids are non-linear

Addition of marine oils containing long-chain n-3 polyunsaturated fatty acids to the diet of pregnant sows may reduce piglet mortality. In previous experiments, when marine oils have been fed to pregnant sows, improvements in piglet tissue 22 : 6n-3 status have been accompanied by potentially undesirable decreases in 20 : 4n-6. The objective of the present experiment was to establish an amount of dietary salmon oil which would enhance piglet 22 : 6n-3 status while minimising reductions in 20 : 4n-6. Twenty-four pregnant multiparous sows were used in the experiment which began on day 60 of pregnancy (gestation length 115 d). To give four diets, salmon oil was added in increasing amounts (0, 5, 10 and 20 g/kg diet) to a basal diet; the diets were made isoenergetic by adding palm oil to each diet to give a total of 20 g oil/kg diet. Diets were offered to the sows in fixed amounts (2.5 kg/d) until parturition. Piglet tissue samples (brain, liver and retina) were obtained at birth before consumption of colostrum. The greatest increase in piglet tissue 22 : 6n-3 proportions occurred between 0 and 5 g salmon oil/kg diet, with only small increases between 10 and 20 g salmon oil/kg diet. In contrast, tissue 20 : 4n-6 proportions declined progressively as the amount of salmon oil fed to the sow increased. In brain, the change in the value 22 : 6n-3/22 : 5n-6 was greatest between 0 and 5 g salmon oil/kg diet, whereas in liver the value increased linearly with added salmon oil. In addition, piglet brain weight (g/kg live weight) increased to a maximum at 10 g salmon oil/kg diet. The optimum amount of supplementary salmon oil in the current experiment, defined as that which gave the greatest response in brain 22 : 6n-3 proportions with minimum reduction in 20 : 4n-6,was 10 g salmon oil/kg diet. This corresponds to an intake of approximately 2.4 g 20 : 5n-3 plus 3.6 g 22 : 6n-3/d or 0.6 % digestible energy.     

Alteration of the lipid composition of rat testicular plasma membranes by dietary (n-3) fatty acids changes the responsiveness of Leydig cells and testosterone synthesis

Experiments were conducted to assess whether changing dietary fat composition altered phospholipid composition of rat testicular plasma membranes in a manner that altered receptor-mediated action of luteinizing hormone (LH)/human chorionic gonadotropin (hCG). Weanling rats were fed diets that provided high or low cholesterol intakes and that were enriched with linseed oil, fish oil or beef tallow for 4 wk. Feeding diets high in (n-3) fatty acids decreased plasma and testicular plasma membrane 20:4(n-6) content. A marked reduction of the 22:5(n-6) content and an increase in the 22:6(n-3) content of testicular plasma membrane was found only in animals fed fish oil. A decrease in binding capacity of the gonadotropin (LH/hCG) receptor in the plasma membrane, with no change in receptor affinity, was observed for animals fed either linseed oil or fish oil diets. Dietary treatments that raised plasma membrane cholesterol content and the cholesterol to phospholipid ratio in the membrane were associated with increased binding capacity of the gonadotropin receptor. Feeding diets high in 18:3(n-3) vs. those high in fish oil altered receptor-mediated adenylate cyclase activity in a manner that depended on the level of dietary cholesterol. Feeding diets high in cholesterol or fish oil increased basal and LH-stimulated testosterone synthesis relative to that in animals fed the low cholesterol diet containing linseed oil. It is concluded that changing the fat composition of the diet alters the phospholipid composition of rat testicular plasma membranes and that this change in composition influences membrane-mediated unmasking of gonadotropin receptor-mediated action in testicular tissue.     

Perturbation of phospholipid and triacylglycerol fatty acid positional location in the heart of rats depleted of n-3 long-chain polyunsaturates

Rats depleted of long-chain polyunsaturated n-3 fatty acids (n-3–D) display several features of the metabolic syndrome, including obesity, liver steatosis, insulin resistance, hypertension, and cardiac hypertrophy. In this study, the heart phospholipid (PL) and triacylglycerol (TG) fatty acid content and pattern were compared between female control rats (C) and n-3–D rats. The sole n-3 fatty acids found in n-3–D rats, C22:5(n-3) and C22:6(n-3), were 10 to 20 times lower than in C. The total fatty acid content of PL was lower in n-3–D rats than C. No ectopic TG accumulation was found in n-3–D rats. In both PL and TG, the C16:0/C16:1(n-7) and C18:0/C18:1(n-9) ratios suggested increased Δ9-desaturase activity in n-3–D rats. The PL C18:2(n-6)/C20:4(n-6) and C20:4(n-6)/C22:4(n-6) ratios were also lower in n-3–D rats than C. Prior intravenous injection of a medium-chain TG:fish oil emulsion to n-3–D rats 60 to 120 minutes before killing augmented the PL content in C22:5(n-3) and C22:6(n-3), minimized the age-related decrease in the PL C18:1(n-9) relative content, and increased the TG C22:4(n-6) content. The alteration of cardiac function in n-3–D rats and its improvement after injection of medium-chain TG:fish oil emulsion coincides with parallel changes in heart lipid fatty acid content and pattern.     

Ingestion of fish oil or a derived n-3 fatty acid concentrate containing eicosapentaenoic acid (EPA) affects fatty acid compositions of individual phospholipids of rat brain, sciatic nerve and retina

The effect of feeding redfish (Sebastes marinus or mantella) oil or a derived n-3 fatty acid concentrate containing eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on the fatty acid compositions of individual phospholipids in selected neural tissues was studied in growing male rats. Control animals were given sunflower oil in the diet for the 5-wk feeding trial. Lipid analyses revealed that EPA (20:5n-3) became significantly enriched in all phospholipid fractions (phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine and phosphatidylinositol) in the tissues studied (brain, retina and sciatic nerve) in the two n-3 fatty acid dietary groups relative to controls. Corresponding changes were also found in the 22:5n-3 contents of these tissues, whereas little or no significant elevation in DHA (22:6n-3) was found. In contrast, the percentages by weight of the n-6 fatty acids including 18:2n-6, 20:4n-6 (arachidonic acid, AA), 22:4n-6 and 22:5n-6 were generally lower in the various phospholipids/tissues of the animals given fish oil or the n-3 fatty acid concentrate; the levels of 22:5n-6 and 22:4n-6 were markedly affected in this regard. These results indicate that dietary n-3 fatty acids (as EPA plus DHA) can greatly affect the fatty acid compositions of the various membrane phospholipids in nervous tissues within a relatively short time. These biochemical alterations may be important for functional changes including altered membrane fluidity, cellular responses, ion transport and the biosyntheses of AA- and EPA-derived prostaglandins and leukotrienes.     

Dietary n-3 and n-6 fatty acids alter avian metabolism: molecular-species composition of breast-muscle phospholipids

The effects of diets high in n-3 polyunsaturated fatty acids (PUFA; provided by fish oil), n-6 PUFA (sunflower oil) or in more-saturated fatty acids (tallow) on the distribution of subclasses of choline phospholipids (PC) and ethanolamine phospholipids (PE) from the breast muscle of broiler chickens were examined. Supplementation with the different fatty acids had no effect on the distribution of phospholipid subclasses. Feeding sunflower oil or tallow gave a molecular-species profile similar in both fatty acid subtype and proportion. In the diacyl PC phospholipids, 16 : 0-18 : 1n-9 and 16 : 0-18 : 2n-6 accounted for approximately 60 % of the total molecular species, whereas for the alkylenyl PC the predominant species were 16 : 0-18 : 1n-9 and 16 : 0-20 : 4n-6. Of the diacyl PE the dominant species was 18 : 0-20 : 4n-6 which accounted for 50 % of the molecular species, and of the alkylenyl PE the dominant species were 16 : 0-18 : 1n-9, 16 : 0-20 : 4n-6 and 18 : 0-20 : 4n-6. Supplementation with fish oil significantly increased levels of both eicosapentaenoic acid (20 : 5n-3) and docosahexaenoic acid (22 : 6n-3) in PC and PE when compared with either sunflower oil or tallow supplementation. The increase in the n-3 PUFA incorporation was associated with a corresponding decrease in the proportion of arachidonic acid (20 : 4n-6) in both PC and PE. Different dietary fats induce different patterns of fatty acid incorporation and substitution in the sn-2 position of the diacyl and alkylenyl PC and PE of avian breast muscle, and this finding is indicative of selective acyl remodelling in these two phospholipids.     

Dietary polyunsaturated fatty acids modulate fatty acid composition and early activation steps of concanavalin A-stimulated rat thymocytes.

The early biochemical responses to concanavalin A (Con A) of thymocytes from rats fed a saturated (coconut oil), (n-6) (sunflower oil) or (n-3) (fish oil) fatty acid-enriched diet for 3 wk were investigated. Fish oil feeding resulted in greater (n-3) polyunsaturated fatty acid level (PUFA) at the expense of (n-6) PUFA in total and individual thymocyte phospholipids. Such alterations of the fatty acid composition did not affect basal ornithine decarboxylase (ODC), cyclic nucleotide phosphodiesterase (PDE) or gamma-glutamyl transferase activities. However, the fish oil-enriched diet impaired some of the early thymocyte responses to Con A, such as the rapid induction (30 min) of soluble ODC and PDE activities. Synthesis of [3H]20:4(n-6) oxygenated metabolites was not different between the dietary groups; however, the uptake of [3H]20:4(n-6) into phospholipid classes was significantly lower in phosphatidylcholine and greater in phosphatidylethanolamine and phosphatidylinositol after fish oil feeding. Similarly, the Con A-induced remodeling of the [3H]20:4(n-6) esterification in phospholipids differed in sunflower oil- vs. fish oil-fed rats, suggesting a modulation of acyl CoA synthase and/or acyl CoA transferase activities. Thus, the modulation of Con A-induced ODC and PDE stimulation upon in vivo changes of membrane phospholipid fatty acid composition is not related to eicosanoid formation, but rather to the modification of the fatty acid acylation processes, altering phospholipid composition and signal transduction.     

Dietary supplementation with eicosapentaenoic acid, but not with other long-chain n-3 or n-6 polyunsaturated fatty acids, decreases natural killer cell activity in healthy subjects aged >55 y

BACKGROUND: Animal studies showed that dietary flaxseed oil [rich in the n-3 polyunsaturated fatty acid alpha-linolenic acid (ALA)], evening primrose oil [rich in the n-6 polyunsaturated fatty acid gamma-linolenic acid (GLA)], and fish oil [rich in the long-chain n-3 polyunsaturated fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)] can decrease natural killer (NK) cell activity. There have been no studies of the effect on NK cell activity of adding these oils to the diet of humans. OBJECTIVE: Our objective was to determine the effect of dietary supplementation with oil blends rich in ALA, GLA, arachidonic acid (AA), DHA, or EPA plus DHA (fish oil) on the NK cell activity of human peripheral blood mononuclear cells. DESIGN: A randomized, placebo-controlled, double-blind, parallel study was conducted. Healthy subjects aged 55-75 y consumed 9 capsules/d for 12 wk; the capsules contained placebo oil (an 80:20 mix of palm and sunflower seed oils) or blends of placebo oil and oils rich in ALA, GLA, AA, DHA, or EPA plus DHA. Subjects in these groups consumed 2 g ALA, 770 mg GLA, 680 mg AA, 720 mg DHA, or 1 g EPA plus DHA (720 mg EPA + 280 mg DHA) daily, respectively. Total fat intake from the capsules was 4 g/d. RESULTS: The fatty acid composition of plasma phospholipids changed significantly in the GLA, AA, DHA, and fish oil groups. NK cell activity was not significantly affected by the placebo, ALA, GLA, AA, or DHA treatment. Fish oil caused a significant reduction (mean decline: 48%) in NK cell activity that was fully reversed by 4 wk after supplementation had ceased. CONCLUSION: A moderate amount of EPA but not of other n-6 or n-3 polyunsaturated fatty acids can decrease NK cell activity in healthy subjects.     

Repletion with (n-3) fatty acids reverses bone structural deficits in (n-3)-deficient rats

(n-3) PUFA deficiency and repletion effects on bone mechanical properties have not been examined. The primary research aim was to evaluate whether changes in the fatty acid composition of bone tissue compartments previously reported to influence bone formation rates would affect bone modeling and mechanical properties. In this investigation, three groups of rats were studied, second generation (n-3)-deficient, (n-3)-repleted, and a control (n-3)-adequate. The (n-3)-adequate diet contained alpha-linolenic acid [LNA, 18:3(n-3), 2.6% of total fatty acids] and docosahexaenoic acid [DHA, 22:6(n-3), 1.3% of total fatty acids]. Fatty acid composition of the hindlimb tissues (bone and muscle) of chronically (n-3)-deficient rats revealed a marked increase in (n-6) PUFA [20:4(n-6), 22:4(n-6), and 22:5(n-6)] and a corresponding decrease in (n-3) PUFA [18:3(n-3), 20:5(n-3), 22:5(n-3) and 22:6(n-3)]. Measurement of bone mechanical properties (energy to peak load) of tibiae showed that (n-3) deficiency diminished structural integrity. Rats repleted with (n-3) fatty acids demonstrated accelerated bone modeling (cross-sectional geometry) and an improved second moment in tibiae compared with control (n-3)-adequate rats after 28 d of dietary treatment. This study showed that repletion with dietary (n-3) fatty acids restored the ratio of (n-6)/(n-3) PUFA in bone compartments and reversed compromised bone modeling in (n-3)-deficient rats.     

Effect of dietary n-3 fatty acids on weight gain and liver polar lipid fatty acid composition of fingerling channel catfish

A 10-wk experiment was conducted to determine the effect of supplementing a 5% tristearin basal diet with linoleic acid [18:2(n-6)], linolenic acid [18:3(n-3)], an n-3 highly unsaturated fatty acid (n-3 HUFA) mixture, cod liver oil, corn oil or linseed oil on growth and fatty acid composition of the liver polar lipid fraction of fingerling channel catfish (Ictalurus punctatus). The lowest weight gain was observed in fish fed the basal diet. Weight gain was improved by certain levels of supplemental n-3 fatty acids. Fish fed a diet containing 2% 18:3(n-3) grew at the same rate as fish fed a diet containing 2.5% cod liver oil plus 2.5% corn oil. The best growth rate was observed in fish fed diets containing either 5% cod liver oil or 5% linseed oil. Growth rate was depressed by supplementation with 4% 18:3(n-3) or 1.25% n-3 HUFA mix. No improvement in growth rate was observed with dietary 18:2(n-6). Dietary linolenate was converted to docosahexaenoic acid [22:6(n-3)]. The ratio of 20:3(n-9) to 22:6(n-3) of the fish showing good growth was less than 0.4. The data obtained in this experiment indicate that n-3 fatty acids are essential for channel catfish and that the 18:3(n-3) or n-3 HUFA dietary requirement is 1.0-2.0% or 0.5-0.75%, respectively.     

Brain cell and tissue recovery in rats made deficient in n-3 fatty acids by alteration of dietary fat

Rats were fed a purified diet containing either 1.5% sunflower oil [940 mg linoleic acid [18:2(n-6)]/100 g diet; 6 mg alpha-linolenic acid [18:3(n-3)]/300 g diet] or 1.9% soybean oil [940 mg 18:2(n-6)/100 g diet; 130 mg 18:3(n-3)/100 g diet]. In all cases and tissues examined 22:6(n-3) was lower and 22:5(n-6) was higher in rats fed sunflower oil than in rats fed soybean oil. Levels of 22:4(n-6) and 20:4(n-6) were largely unaffected. Expressed as a percentage of that in soybean oil-fed rats, 22:6(n-3) in sunflower oil-fed rats was as follows: neurons, 49; astrocytes, 47; oligodendrocytes, 10; lung, 27; testes, 32; retina, 36; liver, 35 and kidneys, 45. Ten wk after the change in diet of 60-d-old rats from one containing sunflower oil to one containing soybean oil, the fatty acid composition of the brain cells had not reached control values, e.g., that obtained in animals continuously fed soybean oil; 22:6(n-3) was 77, 65 and 80% of control levels for astrocytes, oligodendrocytes and neurons, respectively. In contrast, the recovery measured by the decay of 22:5(n-6) was complete within 10 wk. For 22:6(n-3), it took approximately 2 wk for liver and kidney to recover to the control value, 3 wk for lung, 6 wk for retina and 10 wk for testes. The decrease of 22:5(n-6) was rapid: the control values were reached within 2 wk for kidney, liver and lung and within 6 wk for retina.(ABSTRACT TRUNCATED AT 250 WORDS)