Effect of cholesterol feeding and sex difference on the tissue n-6 and n-3 fatty acid levels in fat-deficient rats treated with linoleate or linolenate

Weanling rats of both sexes fed on a fat-free diet for 8 weeks were given 5 i.p. Injections every 48 hr of 60 mg/100 g body weight of pure ethyl linoleate (LA) or linolenate (LN) with or without 1% dietary cholesterol supplementation. Phospholipid fatty acid compositions in plasma and liver were examined. LA administration increased n-6 fatty acids while LN treatment increased n-3 fatty acids. Cholesterol feeding significantly reduced 20: 4n-6 in LA treated animals and 20: 5n-3 and 22: 6n-3 in LN treated animals. The reductions in males were significantly greater than in females suggesting that the sex difference modulates the cholesterol-induced reduction of n-6 and n-3 fatty acids.     

Influences of biotin deficiency and dietary trans-fatty acids on tissue lipids in chickens

1. The combined effects of feeding hydrogenated fats and varying the levels of biotin and linoleate (18:2 omega 6) on polyunsaturated fatty acids were studied in the chicken. 2. Biotin deficiency signs were not exacerbated by feeding hydrogenated fats or by diets low in linoleate for 21 d. 3. Biotin deficiency resulted in proportionately higher levels of 18:2 omega 6 and gamma-linolenate (18:3 omega 6) in liver triglycerides, and lower levels of dihomo-gamma-linolenate (20:3 omega 6) in liver and heart phospholipids irrespective of the 18:2 omega 6 level in the diet. 4. Biotin deficiency did not alter arachidonate (20:4 omega 6) levels in tissue lipids at 21 d. 5. Feeding high levels of trans-18:1 isomers with adequate biotin led to reduced 20:3 omega 6 and 20:4 omega 6 levels in liver and heart phospholipids with compensatory increases in omega 3 fatty acids. 6. The trans-isomers of 18:1 were incorporated into several tissues of the chick. Incorporation was dependent on the levels fed. Very small amounts were incorporated into brain compared with other tissues when dietary trans-isomer levels were high, but were similar when dietary trans-isomer levels were low. The trans-18:1 isomers appear to be preferentially incorporated into phospholipids as opposed to triglycerides in heart and liver.     

Effects of different quantities of fat on serum and liver lipids, phospholipid class distribution and fatty acid composition in alcohol-treated rats

The present study investigated the quantitative effect of dietary fats and ingestion of alcohol on serum and liver lipids, fatty acid bound to phospholipids and their class distribution of male Wistar rats. The rats in C (control) and A (alcohol) groups were fed a standard laboratory diet, HFC (high fat-control) and HFA (high fat-alcohol) groups were fed a high fat diet (standard diet supplemented with 20 g%w/w, sunflower oil: lard mixture 1: 1) for 6 wk. Alcohol-treated rats consumed alcohol at the rate of 9 g/kgbw/d (15-20% energy). Liver phospholipid (PL) content was decreased, and phospholipid/cholesterol liver molar ratio increased in the alcohol treated rats. The proportion of serum sphingophospholipid (Sph) was significantly lower and proportion of phosphatidylcholin (PC) significantly higher in serum PL in alcohol-treated rats. Phospholipid class distribution was unaffected by alcohol feeding in liver. Significantly lower levels of 16:1n-7 and higher levels of 20:5n-3 and 22:4n-6 in the serum PL were observed in the alcohol-treated rats. The groups on the HF diet increased levels of 20:4n-6, 22:4n-6 and total n-6, polyunsaturated fatty acid (PUFA) and decreased levels of 18:1n-9 and total monounsaturated fatty acids (MUFA)in both liver and serum PL, but n-3 fatty acid increased in serum PL and decreased in liver PL compared to groups on the standard diet. Alcohol fat interaction was evident in MUFA and PUFA/SFA in serum PL and n-6, MUFA, PUFA and polyunsaturated/saturated fatty acid ratios (PUFA/SFA) in liver PL. This study showed that the high fat intake in alcohol-treated rats increased levels of 20:4n-6, 22:4n-6 and 20:4/18:2 ratio, and decreased level of 18:1n-9 in liver and serum phospholipids.     

Low n-6:n-3 fatty acid ratio,with fish- or flaxseed oil,in a high fat diet improves plasma lipids and beneficially alters tissue fatty acid composition in mice

BACKGROUND: Health benefits from low n-6:n-3 fatty acid (FA) ratio on cardiovascular risk have been shown. However, the impact of the source of n-3 FAs has not been fully investigated. AIM: Our purpose was to investigate cardiovascular benefits of oils with a low ratio of n-6:n-3 FAs, but different sources of n-3 FAs in C57BL/6 mice. METHODS: Twenty-one mice were divided into 3 groups (n=7) and fed a diet supplemented with either a fish or flaxseed oil-based 'designer oils' with an approximate n-6:n-3 FA ratio of 2/1 or with a safflower-oil-based diet with a ratio of 25/1, for 16 weeks. Plasma lipids and fatty acid profile of the liver tissue were characterized. RESULTS: Compared to baseline, plasma triacylglycerol levels declined (>50%) in all groups by week 4. Plasma cholesterol levels were reduced in both fish and flax groups by 27% and 36%, respectively, as compared to controls at endpoint. The levels of EPA and DHA in liver phospholipids were significantly increased in both fish and flax groups as compared to the control group, with more profound increases in the fish group. Arachidonic acid levels were similarly decreased in the liver tissues from both fish and flax groups as compared to controls. CONCLUSIONS: Our data suggest that health benefits may be achieved by lowering dietary n-6:n-3 FA even in a high fat diet medium.     

Arachidonic acid concentrations in plasma and liver phospholipid and cholesterol esters of piglets raised on formulas with different linoleic and linolenic acid contents.

The influence of sow milk or infant formulas containing 18:2n-6 and 18:3n-3 (% fatty acids) at 30/1, 16/1, 35/4, or 16/4 on plasma and liver phospholipid (PL) and cholesterol ester (CE) arachidonic acid (20:4n-6) was studied in piglets fed from birth for 15 d. Piglets fed the 35/4, 16/1, and 16/4 formulas had a significantly lower percentage of plasma 20:4n-6 in PL than did piglets fed sow milk or the 30/1 formula. The lowest plasma PL 20:4n-6 was in the 16/4 group, the only group in which liver PL 20:4n-6 was significantly reduced. This suggests competitive inhibition of synthesis or acylation of 20:4n-6 when formula with a high content of 18:3n-3 is fed in conjunction with a low content of 18:2n-6. The percentage of plasma CE 20:4n-6 was not altered by formula feeding. In contrast, the liver CE 20:4n-6 was significantly lower in all formula-fed animals than it was in sow-milk-fed animals. These studies confirm that 20:4n-6 metabolism is altered in artificially fed neonates. Liver and plasma cholesterol concentrations were also significantly lower in all formula-fed than in milk-fed piglets. The potential relationship of the decrease in cholesterol to n-6 fatty acids in CE is unknown.     

Changes in serum lipoprotein lipids and their fatty acid compositions and lipid peroxidation in growing rats fed soybean protein versus casein with or without cholesterol

OBJECTIVE: We compared the effects of diets based on soybean protein and casein supplemented or not supplemented with 0.1% cholesterol on plasma lipoprotein lipid amounts and their fatty acid compositions, lecithin:cholesterol acyl-transferase activity, and lipid peroxidation. METHODS: The composition and concentration of lipid and apolipoprotein in different lipoprotein classes, plasma LCAT activity, and lipid peroxidation were determined in rats fed 20% highly purified soybean protein or casein with or without 0.1% cholesterol for 2 mo. RESULTS: Soybean protein and casein diets with or without cholesterol had similar plasma total cholesterol concentrations. Soybean protein consumption diminished very low-density lipoprotein particle number, as measured by diminished contents of very low-density lipoprotein triacylglycerol, phospholipid, and apolipoprotein-B100. Lecithin:cholesterol acyl-transferase activity was not significantly modified by either protein. The soybean protein diet decreased the linoleate desaturation index (20:4[omega-6]/18:2[omega-6]) in liver and high-density lipoprotein fraction 2-3-phospholipids but enhanced red blood cell resistance against free radical attack. Addition of cholesterol to both protein diets decreased concentrations of high-density lipoprotein fraction 2-3 cholesterol. Lecithin:cholesterol acyl-transferase activity tended to be greater after cholesterol feeding, likely due to the enhanced high-density lipoprotein fraction 2-3 apolipoprotein-AI, a cofactor activator for lecithin:cholesterol acyl-transferase. Regardless of dietary protein source, cholesterol supplementation decreased the linoleate desaturation index in liver and plasma lipoprotein lipids and red blood cell resistance to free radical attack. CONCLUSIONS: Our results suggest that the dietary protein origin affects lipid peroxidation and polyunsaturated fatty acid biosynthesis and distribution among liver and different lipoprotein lipid classes, but plays only a minor role in the regulation of plasma and lipoprotein cholesterol concentrations. Providing dietary cholesterol (0.1%) with casein or soybean protein attenuates the effects of these proteins, with the exception of plasma cholesterol.     

Effects of high vitamin a intake on plasma and liver phospholipid and triglyceride fatty acid compositions in hamsters

The fatty acid compositions of plasma and liver phospholipids and triglycerides were studied in hamsters fed for 4 weeks diets containing 0, 40 or 200 mg per kg diet of retinyl palmitate (vitamin A). No major differences were found between animals fed 0 and 40 mg/kg diet of vitamin A. However, significant increases in the levels of 20:3 (n-6) and 18:1 (n-9), and a concomitant decrease in those of 16:0 were found in hamsters fed 200 mg/kg vitamin A. High vitamin A intake also decreased the levels of 22:6 (n-3) in plasma and liver phospholipids. The levels of 20:4 (n-6) in both plasma and liver phospholipids were not affected but were decreased in plasma and liver triglycerides in animals fed various levels of vitamin A.     

Effect of altered dietary n-6-to-n-3 fatty acid ratio on erythrocyte lipid composition and membrane-bound enzymes

Three experimental diets with varied n-6-to-n-3 fatty acid ratios (120, 40 and 8) were prepared by a suitable blending of safflower oil containing 72.5% linoleic (18:2 n-6) acid and non-detectable levels of alpha-linolenic (18:3 n-3) acid, and soybean oil having 56.1% linoleic (18:2 n-6) acid and 7.9% alpha-linolenic (18:3 n-3) acid. These diets were fed to weanling female Wistar/NIN (inbred) rats for 16 wk to assess the impact of altered dietary n-6-to-n-3 fatty acid ratio on erythrocyte membrane (EMS) cholesterol, phospholipids, fatty acid composition and activities of membrane-bound enzymes such as Na+,K+-ATPase, Ca2+, Mg2+-ATPase and acetylcholinesterase. Activities of total and ouabain-sensitive-ATPases were significantly higher in the erythrocyte membranes of rats fed diets with a n-6-to-n-3 fatty acid ratio of 40 compared to other groups, whereas the erythrocyte membrane-bound acetylcholinesterase was significantly different among the three groups. The highest and lowest activities for this enzyme were observed in the dietary groups with n-6-to-n-3 fatty acid ratios of 8 and 40 respectively. However, the EMS of rats fed diets with a n-6-to-n-3 fatty acid ratio of 40 alone had significantly higher Ca2+,Mg2+-ATPase compared to those of other two groups. Significant increases were observed in absolute amounts of cholesterol, phospholipids and molar ratio of cholesterol to phospholipids in the EMS of rats fed a diet with a very high 18:2 n-6-to-18:3 n-3 fatty acid ratio (120) as compared to those from the dietary group with 18:2 n-6-to-18:3 n-3 fatty acid ratio (40), which had the lowest levels of cholesterol, phospholipids and cholesterol-to-phospholipid molar ratio. On the other hand, the EMS from rats fed a diet with a very low n-6-to-n-3 fatty acid ratio (8) had significantly lower cholesterol and higher proportions of stearic (18:0), oleic (18:1 n-9), eicosapentaenoic (20:5 n-3), and docosahexaenoic acids, and a higher ratio of docosahexaenoic (22:6 n-3) acid-to-a-linoleic (18:3 n-3) acid compared to the EMS from a very high n-6-to-n-3 fatty acid ratio of 120. Although these changes in EM fatty acid profiles were expected of the respective dietary regimens, the observed changes in the activities of membrane-bound enzymes could have resulted from their interaction with membrane cholesterol, phospholipids and fatty acyl chains.     

Response of tissue phospholipid fatty acid composition to dietary (n-6) and replacement with marine (n-3) and saturated fatty acids in the rat

Nine groups of weanling male rats were maintained for ten weeks on a fat-free semi-synthetic diet supplemented with 10% by weight of oil, composed wholly of gamma-linolenic acid-rich evening primrose oil, or replaced partly or completely (25%, 50%, 75%, and 100%) by marine or hydrogenated coconut oils. Plasma phospholipid content and phospholipid fatty acid composition of plasma, red blood cells, liver, kidney, and heart were determined. Replacement of marine oil as 2.5% of the diet caused a decrease of plasma phospholipid concentration to 60%, with no furthur decrease at higher proportions. Except in the heart, marine oil in combination with evening primrose oil caused an increase in 20:3(n-6) concentration, and a decrease in 20:4(n-6) levels in all tissues examined. The ratio 20:3(n-6)/20:4(n-6) increased with increasing marine oil supplementation to the diet, but not when marine oil was the sole source of dietary fatty acids (10%). Replacement of hydrogenated coconut oil did not affect 20:3(n-6) concentrations. A decrease in 20:4(n-6) was observed when hydrogenated coconut oil was supplemented to the diet at 10%, causing a state of EFA deficiency as shown by the elevation of 20:3(n-9). There was an increase in 20:5(n-3) and 22:6(n-3) with increased marine oil intake. The ratio 20:3(n-6)/20:4(n-6) correlated significantly with 20:5(n-3), but not with 22:6(n-3), in all tissues except the heart, suggesting an inhibitory effect of 20:5(n-3) on delta-5-desaturase enzyme.     

Influences of postnatal age and dietary nucleotides on plasma fatty acids in the weanling rat.

Dietary nucleotides seem to play a number of physiologic roles during early life. They are improved in the maintenance of the immune system, intestinal maturation, and lipid metabolism. Nucleotides affect the conversion of essential fatty acids into their long-chain polyunsaturated (PUFA) derivatives in both preterm and at-term newborn infants. This work examines the effect of postnatal age and dietary nucleotides on the fatty acid composition of total plasma lipids and lipid fractions in the rat. Weanling rats (21 days old) were divided into three groups. The first group was killed, and the other two groups were fed a standard semipurified diet, and the same diet supplemented with 250 mg each of CMP, UMP, AMP, GMP, and IMP per 100 g of diet for 4 weeks. Advancing postnatal age led to an increase of total plasma fatty acids, especially saturated, and PUFA of the n-6 series, whereas PUFA of the n-3 series decreased. The fatty acid profile of plasma phospholipids (PL) exhibited minor changes, although there was a tendency to show lower levels of saturates and PUFA of the n-3 series and increased levels of PUFA of the n-6 series. Cholesteryl esters showed a response similar to that of PL, although the increase in arachidonic acid (20:4n-6) was significant. For triglycerides, linoleic acid (18:2n-6) and monounsaturates increased their levels, whereas saturates decreased. Dietary nucleotides mediated a significant increase in total plasma fatty acids, namely monounsaturated fatty acids and PUFA of both n-6 and n-3 series as compared with the control group. The relative fatty acid composition of PL and cholesteryl esters was mostly unaffected.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of dietary fat content and composition during pregnancy on fetal hepatic HMG CoA reductase activities and lipids in rats

The effects of diets containing 20% (wt/wt) safflower, olive or palm oil or 5% (wt/wt) safflower oil when fed throughout gestation on hepatic 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase activity and on plasma and liver lipids were studied in fetal rats at d 21 of gestation. Hepatic total and active HMG CoA reductase activity, plasma free cholesterol and liver triglyceride and phospholipid 18:2(n-6) levels were higher in fetuses of rats fed 20% than in those of rats fed 5% safflower oil. Fetuses of rats fed olive oil had higher active HMG CoA reductase levels than fetuses of rats fed 20% safflower or palm oil; their total reductase activity was similar to that of the safflower oil group and higher than that for the palm oil group. Fetal liver and plasma cholesterol and triglyceride, as well as liver phospholipid concentrations, were not altered by the type of oil fed. The diets containing safflower oil resulted in higher 18:2(n-6) and lower 18:1 levels in fetal liver phospholipid and triglycerides than did the diets containing palm or olive oil. These studies demonstrate that fetal liver HMG CoA reductase activity is influenced by the maternal diet fat content and composition although the effect of specific fatty acids is unknown.     

Both (n-3) and (n-6) fatty acids stimulate wound healing in the rat intestinal epithelial cell line, IEC-6.

The control of proliferation and epithelial restitution are processes that are poorly understood. The effects of (n-3), (n-6) and trans fatty acids on proliferation of subconfluent IEC-6 cultures and restitution of wounded IEC-6 monolayers were investigated. Incorporation of supplemented fatty acids into cellular phospholipid was also assessed. Sulforhodamine B protein dye binding assay was utilized to assess the proliferative effects of fatty acids on growth of IEC-6 cultures. Incorporation of supplemental fatty acids into cellular phospholipid was examined by thin-layer chromatography combined with gas chromatography. The modulation of epithelial restitution was examined by razor blade wounding confluent IEC-6 monolayers grown in media supplemented with various fatty acids. Inhibition of eicosanoid synthesis by indomethacin during the wounding assay was also assessed. Both (n-3) and (n-6) fatty acids significantly inhibited growth of this intestinal epithelial cell model at concentrations above 125 micromol/L. The trans fatty acid, linoelaidate 18:2(n-6)trans, inhibited growth of IEC-6 cells at concentrations above 250 micromol/L. Another trans fatty acid, elaidate 18:1(n-9)trans, was well-tolerated at concentrations as high as 500 micromol/L. Eicosapentanoic 20:5(n-3), linoleic 18:2(n-6), alpha-linolenic 18:3(n-3), gamma-linolenic 18:3(n-6) and arachidonic 20:4(n-6) acids all significantly enhanced cellular migration in the IEC-6 model of wound healing. Eicosapentanoate, linoleate, alpha-linolenate, gamma-linolenate and arachidonate are all capable of improving reconstitution of epithelial integrity following mucosal injury. Inhibition of eicosanoid synthesis reduced the enhancement of restitution by n-6 fatty acids back to control levels.     

Macadamia nut consumption lowers plasma total and LDL cholesterol levels in hypercholesterolemic men

This study was conducted to assess the cholesterol-lowering potential of macadamia nuts. Seventeen hypercholesterolemic men (mean age 54 y) were given macadamia nuts (40-90 g/d), equivalent to 15% energy intake, for 4 wk. Plasma total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides and homocysteine concentrations and the fatty acid composition of plasma lipids were determined before and after treatment. Plasma MUFA 16:1(n-7), 18:1(n-7) and 20:1(n-9) were elevated after intervention with macadamia nuts. Plasma (n-6) and (n-3) PUFA concentrations were unaffected by macadamia nut consumption. Plasma total cholesterol and LDL cholesterol concentrations decreased by 3.0 and 5.3%, respectively, and HDL cholesterol levels increased by 7.9% in hypercholesterolemic men after macadamia nut consumption. Plasma triglyceride and homocysteine concentrations were not affected by treatment. Macadamia nut consumption was associated with a significant increase in the relative intake of MUFA and a reduced relative intake of saturated fatty acids and PUFA. This study demonstrates that macadamia nut consumption as part of a healthy diet favorably modifies the plasma lipid profile in hypercholesterolemic men despite their diet being high in fat.     

Dietary eritadenine and ethanolamine depress fatty acid desaturase activities by increasing liver microsomal phosphatidylethanolamine in rats

The effects of eritadenine, a constituent of the Lentinus edodes mushroom, and ethanolamine, the base constituent of phosphatidylethanolamine (PE), on fatty acid desaturase activities and lipid profiles were investigated comparatively in rats. Rats were fed a control diet or a diet supplemented with either eritadenine (0.05 g/kg) or ethanolamine (8 g/kg) for 14 d. Eritadenine and ethanolamine had marked hypocholesterolemic effects. The concentration of liver microsomal PE was significantly increased and the ratio of phosphatidylcholine (PC) to PE was significantly decreased by both eritadenine and ethanolamine. These changes in phospholipid profile were also observed in the mitochondria and plasma membranes in the liver. The activities of the Delta5-, Delta6- and Delta9-desaturases in liver microsomes were significantly decreased by eritadenine and ethanolamine; there was a significant correlation between the activity of Delta5- or Delta6-desaturase and the proportion of PE in the total phospholipids or the PC/PE ratio. Reflecting decreased Delta5- and Delta6-desaturase activities, the 20:4(n-6)/18:2(n-6) ratio was significantly decreased by eritadenine and ethanolamine in PC of the liver microsomes, mitochondria and plasma membranes. Although the 20:4(n-6)/18:2(n-6) ratio of liver microsomal PE was also significantly decreased by eritadenine and ethanolamine, the fatty acid composition of phosphatidylinositol and phosphatidylserine was less affected by these compounds. Eritadenine and ethanolamine increased the proportion of 16:0-18:2 and decreased the proportion of 18:0-20:4 in liver PC. The results suggest that dietary eritadenine and ethanolamine might lead to decreases in desaturase activities and changes in fatty acid and molecular species composition of PC through an increase in liver microsomal PE.     

Dose-response relationships between dietary (n-3) fatty acids and plasma and tissue lipids, steroid excretion and urinary malondialdehyde in rats.

For a 28-d experimental period, rats were fed a nonpurified, cereal-based diet containing 9.1% supplemental beef tallow or fish oil or one of the following beef tallow:fish oil blends: 95:5; 90:10; 80:20 and 50:50. All diets provided between 21.3 and 22.7 g linoleic acid/kg. Higher fish oil intake was paralleled by elevated incorporation of long-chain (n-3) fatty acids in plasma total lipid, mainly at the expense of arachidonic acid. Significant inverse relationships were found between plasma total (n-3) fatty acid concentration and plasma triglyceride, cholesterol or free fatty acid concentrations. Fish oil intake did not lead to a shift of triglycerides or cholesterol from the plasma to the tissues (liver, heart, kidneys). Reduced plasma cholesterol concentrations in the fish oil-fed rats could not be explained by higher fecal excretion of neutral sterols and bile acids. In vivo lipid peroxidation, assessed by urinary malondialdehyde excretion, was enhanced when diets containing greater than 1.8% fish oil were fed.     

Docosahexaenoic and arachidonic acid prevent a decrease in dopaminergic and serotoninergic neurotransmitters in frontal cortex caused by a linoleic and alpha-linolenic acid deficient diet in formula-fed piglets.

This study examined the effects of diets deficient (D) in linoleic [18:2(n-6)] and linolenic acid [18:3(n-3)] at 0.8 and 0.05% energy, respectively, or adequate (C) in 18:2(n-6) and 18:3(n-3) at 8.3 and 0.8% energy, respectively, without (-) or with (+) 0.2% energy arachidonic [20:4(n-6)] and 0.16% energy docosahexaenoic [22:6(n-3)] acid in piglets fed from birth to 18 d. Frontal cortex dopaminergic and serotoninergic neurotransmitters and phospholipid fatty acids were measured. Piglets fed the D- diet had significantly lower frontal cortex dopamine, 3,4-dihydroxyphenylacetic (DOPAC), homovanillic acid (HVA), serotonin and 5-hydroxyindoleacetic acid (5-HIAA) concentrations than did piglets fed the C- diets. Frontal cortex dopamine, norepinephrine, DOPAC, HVA, serotonin and 5-HIAA were higher in piglets fed the D+ compared to those fed the D- diet (P < 0.05) and not different between piglets fed the D+ and those fed the C- diets or the C- and C+ diets. Piglets fed the D- diet had lower frontal cortex phosphatidylcholine (PC) and phosphatidylinositol (PI) 20:4(n-6) and PC and phosphatidylethanolamine (PE) 22:6(n-3) than did piglets fed the C- diet (P < 0.05). Piglets fed the D+ diet had higher frontal cortex PC and PI 20:4(n-6) and PC, PE, PS and PI 22:6(n-3) than did piglets fed the D- diet. These studies show that dietary essential fatty acid deficiency fed for 18 d from birth affects frontal cortex neurotransmitters in rapidly growing piglets and that these changes are specifically due to 20:4(n-6) and/or 22:6(n-3).     

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.     

A mixed Australian fish diet and fish-oil supplementation: impact on the plasma lipid profile of healthy men

Twelve healthy men were fed in turn three diets for 6 wk each in a 3 x 3 randomized block design: a control diet (essentially fish free), a fish diet (200 g lean Australian fish flesh/d), and the same fish-based meal but supplemented with 5 g fish oil/d. Dietary eicosapentaenoic acid [EPA, 20: 5n-3 (omega-3)] was strongly associated with erythrocyte membrane EPA (r = 0.908 at 6 wk), strengthening its value as a measure of compliance in fish and fish-oil feeding trials. On the fish diet, subjects had increased incorporation of n-3 polyunsaturated fatty acids (PUFAs) at the expense of n-6 PUFAs in their erythrocyte membranes. When the fish-based diet was supplemented with fish oil (5 g/d), there was a significant lowering of plasma triacylglycerol (-0.16 +/- 0.24 mmol/L; mean +/- SD). No change in plasma total cholesterol was detected although the fish + oil diet produced a reduction in very-low-density-lipoprotein cholesterol (-0.24 +/- 0.26 mmol/L).     

Influence of the sex-linked dwarfing gene (dw) on the lipid composition of plasma, egg yolk and abdominal fat pad in White Leghorn laying hens: effect of dietary fat

The levels and fatty acid composition of lipids were determined in very low density lipoproteins (VLDL, d less than 1.006), yolk and abdominal adipose tissue of normal (Dw) and sex-linked dwarf (dw) White Leghorn laying hens. Effects of adding 4% tallow to the diet were also examined. In 40-wk-old hens, neither plasma lipids (triglycerides, phospholipids and cholesterol), VLDL levels, nor the chemical composition of VLDL was altered by the dw gene or dietary fat. Dwarfism reduced egg and yolk weights. Though the yolk lipid content was similar in normal and dwarf hens, yolk from dwarfs had slightly more phospholipids and less triglycerides than yolk from normal hens. Higher linoleic acid [18:2(n-6)] and lower oleic acid [18:1(n-9)] levels were observed in triglycerides of VLDL, yolk and adipose tissue from dwarf hens. In addition, the dietary fatty acid pattern had a greater influence on the fatty acid composition of the yolk lipid major precursors (VLDL triglycerides) in dwarf laying hens than in normal hens. These results suggest that the dwarfing gene might reduce the hepatic de novo fatty acid synthesis and/or dwarf hens might incorporate more dietary lipids into yolk than do normal hens.