Dietary α-linolenic acid lowers postprandial lipid levels with increase of eicosapentaenoic and docosahexaenoic acid contents in rat hepatic membrane

This study was designed to examine the effects of dietary n−3 and n−6 polyunsaturated fatty acids (PUFA) on postprandial lipid levels and fatty acid composition of hepatic membranes. Male Sprague-Dawley rats were trained for a 3−h feeding protocol and fed one of five semipurified diets: one fat-free diet or one of four diets supplemented with 10% (by weight) each of corn oil, beef tallow, perilla oil, and fish oil. Two separate experiments were performed, 4-wk long-term and 4-d short-term feeding models, to compare the effects of feeding periods. Postprandial plasma lipid was affected by dietary fats. Triacylglycerol (TG) and total cholesterol levels were decreased in rats fed perilla oil and fish oil diets compared with corn oil and beef tallow diets. Hepatic TG and total cholesterol levels were also reduced by fish oil and perilla oil diets. Fatty acid composition of hepatic microsomal fraction reflected dietary fatty acids and their metabolic conversion. The major fatty acids of rats fed the beef tallow diet were palmitic, stearic, and oleic. Similarly, linoleic acid (LA) and arachidonic acid in the corn oil group, α-linolenic acid (ALA) and eicosapentaenoic acid (EPA) in the perilla oil group, and palmitic acid and docosahexaenoic acid (DHA) in the fish oil group were detected in high proportions. Both long- and short-term feeding experiments showed similar results. In addition, microsomal DHA content was negatively correlated with plasma lipid levels. Hepatic lipid levels were also negatively correlated with EPA and DHA contents. These results suggest that n−3 ALA has more of a hypolipidemic effect than n−6 LA and that the hypolipidemic effect of n−3 PUFA may be partly related to the increase of EPA and DHA in hepatic membrane.     

Dietary cod liver oil decreases arachidonic acid in rat gastric mucosa and increases stress-induced gastric erosions

The purpose of this study was to examine the influence of long-term feeding of dietary fat rich in either n−3 or n−6 fatty acids on the availability of arachidonic acid (20∶4n−6) in major phospholipids of gastric mucosa in rats. Three groups of male Wistar rats were fed either a standard diet, a cod liver oil-enriched diet (10% by weight), or a corn oil-enriched diet (10% by weight) for 8 mon. Dietary cod liver oil significantly reduced the level of 20∶4n−6 in phosphatidylcholine (PC) and in phosphatidylethanolamine (PE) of gastric mucosa. The loss of 20∶4n−6 was compensated for by eicosapentaenoic acid (20∶5n−3) in PC, whereas the decrease in 20∶4n−6 in PE corresponded to the increase in three n−3 fatty acids: 20∶5n−3, docosapentaenoic acid (22∶5n−3), and docosahexaenoic acid (22∶6n−3). The level of 20∶5n−3 was higher than the level of 22∶6n−3 both in PC and PE of mucosa in rats fed cod liver oil. Diets supplemented with corn oil increased the level of 18∶2n−6 but decreased the monoene fatty acids 16∶1 and 18∶1n−7 in PC but not in PE of gastric mucosa. The 20∶4n−6 levels of both PC and PE were markedly reduced by dietary cod liver oil, to about one-third of control levels. Similar changes were also observed in the stomach wall. Gastric erosions were observed in all rats exposed to restriction stress, but this form of stress induced twice the number of erosions in rats fed fish oil compared to control rats or rats fed corn oil. We conclude that a diet rich in fish oil altered the balance between n−6 and n−3 fatty acids in major gastric mucosal phospholipids, markedly reduced the availability of 20∶4n−6, and increased the incidence of gastric erosions induced by restriction or emotional stress.     

The effects of a dietary oxidized oil on lipid metabolism in rats

This study was carried out to investigate the effects of a dietary oxidized oil on lipid metabolism in rats, particularly the desaturation of fatty acids. Two groups of rats were fed initially for a period of 35 d diets containing 10% of either fresh oil or thermally treated oil (150°C, 6d). The dietary fats used were markedly different for lipid peroxidation products (peroxide value: 94.5 vs. 3.1 meq O₂/kg; thiobarbituric acid-reactive substances: 230 vs. 7 μmol/kg) but were equalized for their fatty acid composition by using different mixtures of lard and safflower oil and for tocopherol concentrations by individual supplementation with dl-α-tocopherol acetate. In the second period which lasted 16 d, the same diets were supplemented with 10% linseed oil to study the effect of the oxidized oil on the desaturation of α-linolenic acid. During the whole period, all the rats were fed identical quantities of diet by a restrictive feeding system in order to avoid a reduced food intake in the rats fed the oxidized oil. Body weight gains and food conversion rates were only slightly lower in the rats fed the oxidized oil compared to the rats fed the fresh oil. Hence, the effects of lipid peroxidation products could be studied without a distortion by a marked reduced food intake and growth. To assess the rate of fatty acid desaturation, the fatty acid composition of liver and heart total lipids and phospholipids was determined and ratios between product and precursor of individual desaturation reactions were calculated. Rats fed the oxidized oil had reduced ratios of 20∶4n−6/18∶2n−6, 20∶5n−3/18∶3n−3, 20∶4n−6/20∶3n−6, and 22∶6n−3/22∶5n−3 in liver phospholipids and reduced ratios of 20∶4n−6/18∶2n−6, 22∶5n−3/18∶3n−3, and 22∶6n−3/18∶3n−3 in heart phospholipids. Those results suggest a reduced rate of desaturation of linoleic acid and α-linolenic acid by microsomal Δ4-, Δ5-, and Δ6-desaturases. Furthermore, liver total lipids of rats fed the oxidized oil exhibited a reduced ratio between total monounsaturated fatty acids and total saturated fatty acids, suggesting a reduced Δ9-desaturation. Besides those effects, the study observed a slightly increased liver weight, markedly reduced tocopherol concentrations in liver and plasma, reduced lipid concentrations in plasma, and an increased ratio between phospholipids and cholesterol in the liver. Thus, the study demonstrates that feeding an oxidized oil causes several alterations of lipid and fatty acid metabolism which might be of great physiologic relevance.     

Lipid peroxidation in rat tissue slices: Effect of dietary vitamin E,corn oil-lard and menhaden oil

Rats were fed for 5 weeks either 10% (w/w) menhaden oil (MO) or a 10% corn oil-lard (COL) mixture (1∶1) in diets with ≤5 IU or ≤2 IU/kg vitamin E, respectively, or the same diets supplemented with d-α-tocopheryl succinate to a total of 35 and 180 IU vitamin E/kg, respectively. Slices of liver and heart from these rats were used to study lipid peroxidationin vitro. Thiobarbituric acid-reactive substances (TBARS) were measured in the medium after incubation of the slices at 37°C for 1 hr in the absence (uninduced) and presence of 0.5 mM tert-butyl hydroperoxide (induced). The release of TBARS from slices of heart and liver from rats fed either lipid decreased with increasing levels of dietary vitamin E. At the same level of dietary vitamin E, TBARS release was greater for slices of liver and heart from the MO-fed rats than from the COL-fed rats. Application of the TBARS data to a model simulating the experimental conditions showed a good correlation (r=0.95, p<0.001) between experimental and simulated values. Of the 16∶0–22∶6 fatty acids measured in liver from MO-fed rats, 15.4% was n−6 fatty acids and 29.9% was n−3 fatty acids; in liver from COL-fed rats, the respective values were 37.4% and 3.7%. Liver and kidney vitamin E levels were unaffected by the dietary lipid. This study demonstrated that a dietary fish oil increased the susceptibility of rat liver and heart toin vitro lipid peroxidation, and that vitamin E decreased TBARS in tissues from rats fed COL to lower levels than for tissues from rats fed MO. The results suggest that there might also be an increased requirement for dietary antioxidants by humans using fish oil supplements.     

The effect of enhanced intake of linoleic acid on the fatty acid composition of tissue polar lipids of post-smolt atlantic salmon (Salmo salar)

Duplicate groups of Atlantic salmon (Salmo salar) post smolts were given diets in which the lipid component was either fish oil or a mixture of corn oil and lard. This difference in the dietary lipid did not significantly affect growth over a period of sixteen weeks. Proportions of docosahexaenoic acid [22∶6(n−3)] and total (n−3) fatty acids in the polar lipids of liver and white muscle were unaffected by this difference in dietary lipid component over the time period used. Fish given the diet containing corn oil and lard had significantly higher levels of 20∶2(n−6), 20∶3(n−6) and 20∶4(n−6) in the polar lipids of these tissues than were present in the tissues of the fish given diets containing fish oil. There results suggest that linoleic acid [18∶2(n−6)] undergoes elongation and desaturation to arachidonic acid [20∶4(n−6)] in post-smolt Atlantic salmon.     

Response of urinary malondialdehyde to factors that stimulate lipid peroxidation in vivo

Malondialdehyde (MDA) derivatives occur as normal constituents of rat and human urine. In a previous study, it was found that MDA excretion in rats is responsive to MDA intake and to certain factors that increase lipid peroxidation in vivo: vitamin E deficiency, iron administration and a high concentration of cod liver oil (CLO) fatty acids in the tissues. In the present study, the effect on MDA excretion of several additional dietary and endogeneous factors was evaluated. The composition of dietary fatty acids had a major influence on MDA excretion in fed animals, being highest for animals fed n−3 fatty acids (20∶5 and 22∶6) from CLO, intermediate for those fed n−6 (18∶2) acids from corn oil (CO) and lowest for those fed saturated acids from hydrogenated coconut oil (HCO). Diet was the main source of urinary MDA in all groups. Fasting produced a marked increase in urinary MDA, which tended to be higher in rats previously fed CLO. Fasting MDA excretion was not affected by the level of CO in the diet (5, 10 or 15%), indicating that feeding n−6 acids does not increase lipid peroxidation in vivo. Adrenocorticotropic hormone and epinephrine administration increased urinary MDA, further indicating that lipolysis either releases fatty acid peroxides from the tissues or increases the susceptibility of mobilized fatty acids to peroxidation. A decrease in fasting MDA excretion was observed in rats previously fed a high level of antioxidants (vitamin E+BHT+vitamin C) vs a normal level of vitamin E. MDA excretion increased following adriamycin and CCl₄ administration. No increase was observed following short-term feeding of a choline-methionine-deficient diet, which has been reported to increase peroxidation of rat liver nuclear lipids. This study provides further evidience that urinary MDA can serve as a useful indicator of lipid peroxidation in vivo when peroxidation of dietary lipids is precluded. This research was performed in partial fulfillment of the requirements for the M.Sc. degree in Nutritional Sciences     

Dietary lipids modify the fatty acid composition of cartilage,isolated chondrocytes and matrix vesicles

The effects of dietary lipids on the fatty acid composition of hyaline cartilage, epiphyseal chondrocytes (EC) and matrix vesicles (MV) were evaluated in chicks. A basal semipurified diet was fed to chicks containing one of the following lipid sources at 70 g/kg: soybean oil, butter+corn oil, margarine+corn oil or menhaden oil+corn oil (MEC). Articular and epiphyseal growth cartilage were isolated from the proximal tibiotarsus; EC and MV were subsequently released by trypsin (EC 3.4.21.4) and collagenase (EC 3.4.24.3) digestion followed by ultracentrifugation. The fatty acid composition of polar lipids in chick epiphyseal cartilage at three and six weeks, as well as articular cartilage, EC and MV at eight weeks of age revealed the presence of high levels of saturated and monounsaturated fatty acids (up to 85.5%) but low levels of n−6 polyunsaturated fatty acids (PUFA) (2.6–10.2%). Mead acid (20∶3n−9,>3%) was also present in cartilage, EC and MV lipids, and was unaffected by the dietary lipid treatments. Total n−3 PUFA concentrations were the highest in cartilage, EC and MV of chicks consuming MEC. Feeding MEC lowered the levels of 20∶4n−6 in cartilage, but increased 20∶5n−3 levels. The data are consistent with those reported previously which showed that cartilage tissues are low in n−6 PUFA and that they contain 20∶3n−9. We furthermore demonstrated that the PUFA composition of cartilage can be modified by dietary lipids.     

Effects of dietary saturated fat on erucic acid induced myocardial lipidosis in rats

Male Sprague-Dawley rats were fed for one week diets containing 20% by weight fat/oil mixtures with different levels of erucic acid (22∶1n−9) (∼2.5 or 9%) and total saturated fatty acids (∼8 or 35%). Corn oil and high erucic acid rapeseed (HEAR) oil were fed as controls. The same hearts were evaluated histologically using oil red O staining and chemically for cardiac triacylglycerol (TAG) and 22∶1n−9 content in cardiac TAG to compare the three methods for assessing lipid accumulation in rat hearts. Rats fed corn oil showed trace myocardial lipidosis by staining, and a cardiac TAG content of 3.6 mg/g wet weight in the absence of dietary 22∶1n−9. An increase in dietary 22∶1n−9 resulted in significantly increased myocardial lipidosis as assessed histologically and by an accumulation of 22∶1n−9 in heart lipids; there was no increase in cardiac TAG except when HEAR oil was fed. An increase in saturated fatty acids showed no changes in myocardial lipid content assessed histologically, the content of cardiac TAG or the 22∶1n−9 content of TAG at either 2.5 or 9% dietary 22∶1n−9. The histological staining method was more significantly correlated to 22∶1n−9 in cardiac TAG (r=0.49;P<0.001) than to total cardiac TAG (r=0.40;P<0.05). The 22∶1n−9 content was highest in cardiac TAG and free fatty acids. Among the cardiac phospholipids, the highest incorporation was observed into phosphatidylserine, followed by sphingomyelin. With the addition of saturated fat, the fatty acid composition showed decreased accumulation of 22∶1n−9 and increased levels of arachidonic and docosahexaenoic acids in most cardiac phospholipids, despite decreased dietary concentrations of their precursor fatty acids, linoleic and linolenic acids.     

Effect of low levels of dietary fish oil on fatty acid desaturation and tissue fatty acids in obese and lean rats

The effect of very low levels of dietary long-chain n−3 fatty acids on Δ6 desaturation of linoleic acid (18∶2n−6) and α-linolenic acid (18∶3n−3), and on Δ5 desaturation of dihomo-γ-linolenic acid (20∶3n−6), in liver microsomes and its influence on tissue fatty acids were examined in obese and lean Zucker rats and in Wistar rats. Animals fed for 12 wk a balanced diet containing ca. 200 mg of long-chain polyunsaturated n−3 fatty acids per 100 g of diet were compared to those fed the same amount of α-linoleic acid. Low amounts of long-chain n−3 fatty acids greatly inhibited Δ6 desaturation of 18∶2n−6 and Δ5 desaturation of 20∶3n−6, while Δ6 desaturation of 18∶3n−3 was not inhibited in Zucker rats and was even stimulated in Wistar rats. Inhibition of the biosynthesis of long-chain n−6 fatty acids was reflected in a decrease in arachidonic acid (20∶4n−6) content of serum lipids when fasting, and also in the phospholipid fatty acids of liver microsomes. On the contrary, heart and kidney phospholipids did not develop any decrease in 20∶4n−6 during fish oil ingestion. Docosahexaenoic acid (22∶6n−3), present in the dietary fish oil, was increased in serum lipids and in liver microsome, heart, and kidney phospholipids.     

Digestion and absorption of free and esterified fish oil fatty acids in rats

This study was designed to test the hypotheses that digestibility and post-absorption metabolism of fish oil are influenced by impaired lipolysis and by the stereospecific composition of its triacylglycerols. Male Wistar rats were fed nonpurified diets containing one of the following fat sources: 9% native fish oil (NFO), 9% autorandomized fish oil (RFO), 8.1% fish oil-derived free fatty acids (FO-FFA) plus 0.9% glycerol, or 9% soybean oil (SO) as a reference fat. In a 24-day balance study, apparent digestibility of total dietary fat averaged 93.1% in the SO, NFO and RFO groups, and 90.9% in the FO-FFA group. Randomization of fish oil had no effect on apparent digestibility of individual fatty acids. In rats fed FO-FFA, apparent absorption of saturated and monounsaturated fatty acids was lower when compared to the NFO and RFO groups. Feeding the FO-FFA diet tended to increase plasma triglyceride content. The hypocholesterolemic effect of polyunsaturated n−3 fatty acids was not influenced by the dietary source. Similar effects on fatty acid profiles of plasma and liver phospholipids were caused by the NFO, RFO and the FO-FFA diets. We conclude that once polyunsaturated n−3 fatty acids are absorbed, their effect on lipid metabolism is not determined by the dietary source.     

Arachidonic acid,prostaglandin E2 and leukotriene C4 levels in gingiva and submandibular salivary glands of rats fed diets containing n−3 fatty acids

The effect of dietary n−3 fatty acids on prostaglandin E₂ (PGE₂) and leukotriene C₄ (LTC₄) levels in rat salivary glands and gingiva was examined in two separate nutritional studies. In the first set of experiments, two groups of male weanling Sprague-Dawley rats were fed semipurified diets containing 10% corn oil (control group) or 10% menhaden oil (experimental group). Rats were killed after 8 wk on the diets; the fatty acid composition of total phospholipids and the concentrations of PGE₂ and its precursor, arachidonic acid, were measured in gingiva and submandibular salivary glands (SMSG). Dietary n−3 fatty acids were incorporated into the tissue phospholipids. Arachidonic acid levels were reduced by 56% in gingiva and SMSG of rats fed menhaden oil compared with the control rats fed the diet containing corn oil. The concentrations of PGE₂ in SMSG and gingiva of rats fed the diet containing menhaden oil were reduced by 74% and 83%, respectively. In a subsequent nutritional study, we tested whether the diet-induced reduction in tissue arachidonic acid levels would also result in a corresponding decrease in LTC₄ production. Three groups of rats were fed diets containing 5% corn oil (group 1), 4% ethyl ester concentrate of n−3 fatty acids plus 1% corn oil (group 2), or 5% ethyl ester concentrate of n−3 fatty acids (group 3). After 6 wk of feeding, gingiva and SMSG were analyzed for arachidonic acid content andin vitro production of LTC₄. Arachidonic acid content of total phospholipids was about 60% lower in gingiva and 69% lower in SMSG of rats fed the ethyl ester concentrate of n−3 fatty acids (groups 2 and 3) than those of the control group fed the corn oil diet (group 1). Upon incubation with calcium ionophore, gingiva and SMSG from rats fed the n−3 fatty acids rich diet produced significantly less TLC₄ than those from rats of the control group. Because PGE₂ and LTC₄ are believed to be important biochemical mediators of periodontal disease, one may speculate that a diet-induced reduction in their levels may have a beneficial effect upon the course of the disease. The function of salivary glands may also be altered because of the role of these eicosanoids in salivary secretions. Presented in part for the Hatton Award Competition at the American Association for Dental Research Meeting, San Francisco, California, March 15–19, 1989, and at the International Association for Dental Research Meeting, Acapulco, Mexico, April 17–21, 1991.     

Black currant seed oil feeding and fatty acids in liver lipid classes of guinea pigs

Guinea pigs were fed one of three diets containing 10% black currant seed oil (a source of gamma-linolenic (18∶3 n−6) and stearidonic (18∶4 n−3) acids), walnut oil or lard for 40 days. The fatty acid composition of liver triglycerides, free fatty acids, cholesteryl esters, phosphatidylinositol, phosphatidylserine, cardiolipin, phosphatidylcholine and phosphatidylethanolamine were determined. Dietary n−3 fatty acids found esterified in liver lipids had been desaturated and elongated to longer chain analogues, notably docosapentaenoic acid (22∶5 n−3) and docosahexaenoic acid (22∶6 n−3). When the diet contained low amounts of n−6 fatty acids, proportionately more of the n−3 fatty acids were transformed. Significantly more eicosapentaenoic acid (EPA) (20∶5 n−3) was incorporated into triglycerides, cholesteryl esters, phosphatidylcholine and phosphatidylethanolamine of the black currant seed oil group compared with the walnut oil group. Feeding black currant seed oil resulted in significant increases of dihomogamma-linolenic acid (20∶3 n−6) in all liver lipid classes examined, whereas the levels of arachidonic acid (20∶4 n−6) remained relatively stable. The ratio dihomo-gamma-linolenic acid/arachidonic acid was significantly (2.5-fold in PI to 17-fold in cholesteryl esters) higher in all lipid classes from the black currant seed oil fed group.     

Dietary linoleic acid and the fatty acid profiles in rats fed partially hydrogenated marine oils

The influence of the linoleic acid levels of diets containing partially hydrogenated marine, oils (HMO) rich in isomeric 16∶1, 18∶1, 20∶1 and 22∶1 fatty acids on the fatty acid profiles of lipids from rat liver, heart and adipose tissue was examined. Five groups of rats were fed diets containing 20 wt% fat−16% HMO+4% vegetable oils. In these diets, the linoleic acid contents varied between 1.9% and 14.5% of the dietary fatty acids, whereas the contents oftrans fatty acids were 33% in all groups. A sixth group was fed a partially hydrogenated soybean oil (HSOY) diet containing 8% linoleic acid plus 32%trans fatty acids, mainly 18∶1, and a seventh group, 20% palm oil (PALM), with 10% linoleic acid and notrans fatty acids. As the level of linoleic acid in the HMO diets increased from 1.9% to 8.2%, the contents of (n−6) polyunsaturated fatty acids (PUFA) in the phospholipids increased correspondingly. At this dietary level of linoleic acid, a plateau in (n−6) PUFA was reached that was not affected by further increase in dietary 18∶2(n−6) up to 14.5%. Compared with the HSOY- or PALM-fed rats, the plateau value of 20∶4(n−6) were considerably lower and the contents of 18∶2(n−6) higher in liver phosphatidylcholines (PC) and heart PC. Heart phosphatidylethanolamines (PE) on the contrary, had elevated contents of 20∶4(n−6), but decreased 22∶5(n−6) compared with the PALM group. All groups fed HMO had similar contents oftrans fatty acids, mainly 16∶1 and 18∶1, in their phospholipids, irrespective of the dietary 18∶2 levels, and these contents were lower than in the HSOY group. High levels of linoleic acid consistently found in triglycerides of liver, heart and adipose tissue of rats fed HMO indicated that feeding HMO resulted in a reduction of the conversion of linoleic acid into long chain PUFA that could not be overcome by increasing the dietary level of linoleic acid.     

Conjugated linoleic acids alter bone fatty acid composition and reduce ex vivo prostaglandin E2 biosynthesis in rats fed n-6 or n-3 fatty acids

This study evaluated the effects of conjugated linoleic acids (CLA) on tissue fatty acid composition and ex vivo prostaglandin E₂ (PGE₂) production in rats given diets varying in n-6 and n-3 fatty acids. Four groups of rats were given a basal semipurified diet (AIN-93G) containing 70 g/kg of added fat for 42 d. The fat treatments were formulated to contain CLA (0 vs. 10 g/kg of diet) and n-6 (soybean oil having an n-6/n-3 ratio of 7.3) and n-3 fatty acids (menhaden oil+safflower oil having an n-6/n-3 ratio of 1.8) in different ratios in a 2×2 factorial design. Fatty acids in liver, serum, muscle, heart, brain, spleen, and bone (cortical, marrow, and periosteum) were analyzed by capillary gas-liquid chromatography. The various dietary lipid treatments did not affect growth; however, CLA improved feed efficiency. The CLA isomers were found in all rat tissues analyzed although their concentrations varied. Dietary CLA decreased the concentrations of 16∶1n−7, 18∶1, total monounsaturates and n−6 fatty acids, but increased the concentrations of n−3 fatty acids (22∶5n−3 and 22∶6n−3), and saturates in the tissues analyzed. Ex vivo PGE₂ production in bone organ culture was decreased by n−3 fatty acids and CLA. We speculate that CLA reduced the concentration of 18∶1 fatty acids by inhibiting liver Δ9-desaturase activity. The fact that CLA lowered ex vivo PGE₂ production in bone organ culture suggests that these conjugated fatty acids have the potential to influence bone formation and resorption.     

Effect of dietary n−3 and n−6 polyunsaturated fatty acids on lipid-metabolizing enzymes in obese rat liver

This study was designed to examine whether n−3 and n−6 polyunsaturated fatty acids at a very low dietary level (about 0.2%) would alter liver activities in respect to fatty acid oxidation. Obese Zucker rats were used because of their low level of fatty acid oxidation, which would make increases easier to detect. Zucker rats were fed diets containing different oil mixtures (5%, w/w) with the same ratio of n−6/n−3 fatty acids supplied either as fish oil or arachidonic acid concentrate. Decreased hepatic triacylglycerol levels were observed only with the diet containing fish oil. In mitochondrial outer membranes, which support carnitine palmitoyltransferase I activity, cholesterol content was similar for all diets, while the percentage of 22∶6n−3 and 20∶4n−6 in phospholipids was enhanced about by 6 and 3% with the diets containing fish oil and arachidonic acid, respectively. With the fish oil diet, the only difference found in activities related to fatty acid oxidation was the lower sensitivity of carnitine palmitoyltransferase I to malonyl-CoA inhibition. With the diet containing arachidonic acid, peroxisomal fatty acid oxidation and carnitine palmitoyltransferase I activity were markedly depressed. Compared with the control diet, the diets enriched in fish oil and in arachidonic acid gave rise to a higher specific activity of aryl-ester hydrolase in microsomal fractions. We suggest that slight changes in composition of n−3 or n−6 polyunsaturated fatty acids in mitochondrial outer membranes may alter carnitine palmitoyltransferase I activity.     

The effects of dietary fish oil on alveolar type II cell fatty acids and lung surfactant phospholipids

The purpose of this study was to determine the responsiveness of alveolar type II cells to dietary fish oil and the consequent effects on alveolar and lung surfactant. Rats were fed a corn oil or a fish oil diet for four weeks. Dietary n−3 fatty acids were readily incorporated into the type II cell phospholipids as indicated by higher levels of eicosapentaenoic acid (2.77±0.10%) and docosahexaenoic acid (1.63±0.10%) in the group receiving the fish oil diet. The elevated levels of n−3 fatty acids were accompanied by concomitant reduction in arachidonic acid and linoleic acid. Neither eicosapentaenoic acid nor docosahexaenoic acid was incorporated into type II cell triacylglycerols. Feeding a fish oil containing diet increased surfactant phospholipids, particularly 1,2-disaturated acyl phosphatidylcholines in whole lung compared to a corn oil diet. However, the amount of surfactant found in the alveolus was not different between the two diet treatment groups. The results suggest that dietary n−3 fatty acids stimulate synthesis and/or inhibit degradation of lung surfactant without altering surfactant secretion in alveoli.     

Asymmetric distribution of arachidonic and n−3 polyunsaturated fatty acids in rat liver microsomal membranes under a fat-free diet

Rats adapted to a corn oil or a fish oil diet were fed a fat-free diet, and changes in phospholipid polyunsaturated fatty acids (PUFA) in the inner and outer leaflets of liver microsomal membranes were followed for 18 wk. In rats previously adapted to a corn oil diet, arachidonic acid in phosphatidylcholine and phosphatidylethanolamine in the inner and outer leaflets did not decrease quickly; rather, linoleic acid decreased more than arachidonic acid for the first three weeks of feeding the fat-free diet. Even at 18 wk, 40–50% of the beginning arachidonic acid levels were still retained. In contrast, in rats previously adapted to a fish oil diet, the n−3 PUFA were quickly decreased by the fat-free diet to only 10–30% at 18 wk. Due to the appearance and increase of n−9 eicosatrienoic acid in the replacement of the n−3 and n−6 PUFA, total PUFA did not decrease in the inner and outer phosphatidylcholine in either group, but decreased somewhat in the phosphatidylethanolamine due to the insufficient increase of the n−9. On the other hand, the overall degrees of unsaturation in phosphatidylcholine fatty acids were always higher in the outer than in the inner leaflets and were not altered by feeding the fat-free diet even for 18 wk. Thus, the results appear to reveal the physiological importance of unsaturation ratio of fatty acids and the necessity of arachidonic acid in each membrane leaflet.     

Effects of dietary n−3 fatty acid-enriched chicken eggs on plasma and tissue cholesterol and fatty acid composition of rats

The purpose of this study was to examine the effects of feeding n−3 polyunsaturated fatty acid (PUFA)-enriched chicken eggs on plasma and liver cholesterol levels and fatty acid composition in rats. Eggs were collected from laying hens fed diets containing 10% flax seed (Hn−3), 12% sunflower seed (Hn−6), or wheat and soybean meal control (CON). Yolk powders were prepared and fed at the 15% level to weanling female Sprague-Dawley rats for 28 days. Consumption of n−3 PUFA-enriched yolks significantly reduced both plasma and liver total cholesterol. Liver total lipids and phospholipids of rats fed Hn−3 diet were enriched with linolenic, eicosapentaenoic, and docosahexaenoic acids with a concomitant reduction of arachidonic acid in liver phospholipids. The plasma cholesterol of rats fed yolk powders enriched with n−6 PUFA (mainly linoleic acid) was reduced to the same extent as in those fed the n−3 enriched, but the liver cholesterol was significantly increased, indicating differential effects of dietary n−3 and n−6 PUFA. The results demonstrated that the cholesterolemic and tissue lipid modulating properties of chicken eggs could be modified in a favorable way by altering the fatty acid composition of yolk lipids through manipulation of laying hen diets.     

Comparison of the effects of dietary fish oils with different n−3 polyunsaturated fatty acid compositions on plasma and liver lipids in rats

The effects of dietary fish oils with different n−3 polyunsaturated fatty acid compositions on plasma lipid profiles in rats have been studied. Forty-eight male rats, previously maintained on a cholesterol-free diet for 15 days, were fed for 60 days with diets supplemented with 10% fat of either marine hilsa fish (Hilsa ilisa, family clupeidae) or fresh-water chital fish (Notopterus chitala, family notopteridae). The diets had similar levels of total saturated (35–41%), monounsaturated (43–47%) and n−3 polyunsaturated (9–10%) fatty acids. Cholesterol contents of the diets were adjusted to 0.85%; γ-linolenic acid (3.3%) in chital oil and eicosapentaenoic acid (4.9%) in hilsa oil diets were the major n−3 contributors. The percentage of eicosapentaenoic acid in the chital oil diet was 0.57 times that of the hilsa oil diet, but the eicosapentaenoic (EPA) to arachidonic acid (AA) ratio in the latter (4.08) was 3.2 times that of the former (1.27). Sixty days of hilsa oil diet feeding decreased the levels of cholesterol (53.3±2.9 to 50.0±1.1 mg/dL), triacylglycerol (75.7±3.8 to 64.3±2.6 mg/dL) and phospholipid (55.8±1.5 to 51.7±3.1 mg/dL) in rat plasma. Similar treatment with chital oil diet elevated the plasma cholesterol level (53.3±2.9 to 62.3±7.6 mg/dL) while triacylglycerol and phospholipid contents remained unaltered. Both the dietary treatments decreased the levels of linoleic and arachidonic acids in liver but only under the hilsa oil diet did the eicosapentaenoic acid percentage increase markedly (0.8±0.06% to 5.5±0.06%) at the expense of arachidonic acid. This study strongly suggests that the hypolipidemic effect depends on the composition of the n−3 polyunsaturated fatty acids rather than on the total n−3 polyunsaturated fatty acid content of the dietary fish oil.     

Effect of low intake of n−3 fatty acids during development on brain phospholipid fatty acid composition and exploratory behavior in rats

The effect of dietary restriction of n−3 fatty acids during development on brain phospholipid fatty acid composition and exploratory behavior has been studied in male Sprague Dawley rats. Female rats were fed semipurified diets containing either 5.5% safflower oil or 6% soybean oil for 6 wk prior to mating and throughout gestation and lactation. Control rats were maintained on laboratory chow. The male pups were weaned to the diets of the dams except for one group which was switched from safflower to soybean oil at weaning. Behavioral studies and brain phospholipid analyses were conducted at 16–18 wk of age. Rats fed safflower oil showed significantly lower levels of 22∶6n−3 in phospholipids of synaptic membranes and myelin than rats fed soybean oil or chow. The decrease in 22∶6n−3 was compensated for by an increase in 22∶5n−6, the total content of polyunsaturated fatty acids remaining approximately constant. The brain phospholipid fatty acid composition of rats switched from safflower to soybean oil at weaning was similar to that of rats fed soybean oil throughout the experiment. There was no difference in spontaneous locomotor activity among the different dietary groups. However, rats raised on safflower oil displayed a significantly lower exploratory activity (horizontal movements and rearings) in a novel environment than rats fed soybean oil or chow. In contrast to the brain phospholipid fatty acid composition, there was no recovery of exploratory behavior in rats raised on safflower oil and switched to soybean oil at weaning suggesting a specific requirement of n−3 fatty acids during development.