Effect of fish oil and safflower oil in common Japanese diet on human plasma fatty acid composition

The influence of fish oil and safflower oil contained in the common Japanese diet as the main dietary polyunsaturated fatty acid source on plasma fatty acids in ten female student volunteers (21-22 years old) was investigated. The subjects were divided into two groups and fed the experimental diets for five days. The total daily fat intake in the fish diet and safflower oil diet was 54.4 g and 56.2 g, respectively, and the fat derived from fish and safflower oil was 16 g and 23 g, respectively. The proportion of linoleic acid was reduced in the plasma of subjects fed the fish diet and increased in the plasma of subjects fed the safflower oil diet. The plasma levels of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) were significantly elevated in the fish diet group. The ratio of EPA/arachidonic acid (AA) was higher, and those of n-6/n-3 and n-9/n-3 were lower in the plasma of subjects fed the fish diet when compared to the results obtained from plasma of subjects fed the safflower oil diet. From these results, it seems likely that fish oil in the common Japanese diet is a favorable source of plasma EPA and DHA even in such short term supplementation and with such a small amount of daily consumption.     

Influence of high-fat diet from differential dietary sources on bone mineral density, bone strength, and bone fatty acid composition in rats

Previous studies have suggested that high-fat diets adversely affect bone development. However, these studies included other dietary manipulations, including low calcium, folic acid, and fibre, and (or) high sucrose or cholesterol, and did not directly compare several common sources of dietary fat. Thus, the overall objective of this study was to investigate the effect of high-fat diets that differ in fat quality, representing diets high in saturated fatty acids (SFA), n-3 polyunsaturated fatty acids (PUFA), or n-6 PUFA, on femur bone mineral density (BMD), strength, and fatty acid composition. Forty-day-old male Sprague-Dawley rats were maintained for 65?days on high-fat diets (20% by weight), containing coconut oil (SFA; n = 10), flaxseed oil (n-3 PUFA; n = 10), or safflower oil (n-6 PUFA; n = 11). Chow-fed rats (n = 10), at 105?days of age, were included to represent animals on a control diet. Rats fed high-fat diets had higher body weights than the chow-fed rats (p?< 0.001). Among all high-fat groups, there were no differences in femur BMD (p?> 0.05) or biomechanical strength properties (p?> 0.05). Femurs of groups fed either the high n-3 or high n-6 PUFA diets were stronger (as measured by peak load) than those of the chow-fed group, after adjustment for significant differences in body weight (p = 0.001). As expected, the femur fatty acid profile reflected the fatty acid composition of the diet consumed. These results suggest that high-fat diets, containing high levels of PUFA in the form of flaxseed or safflower oil, have a positive effect on bone strength when fed to male rats 6 to 15?weeks of age.     

Effect of dietary saturated fatty acids on intracellular free fatty acids and kinetic properties of hormone-sensitive lipase of rat adipocytes

Experiments were conducted to examine the effects of dietary saturated fatty acids on the intracellular free fatty acid concentration and composition and on the kinetic parameters of hormone-sensitive lipase of rat adipocytes. Animals were fed for 4 wk 14% coconut oil, beef fat or safflower oil and 2% corn oil in a purified diet. Adipocytes of animals fed the coconut oil diet contained higher basal level of intracellular free fatty acids than those of animals fed other beef fat or safflower oil diets. Norepinephrine (10(-5) M) stimulated the basal intracellular free fatty acid concentration by 2.3-3.4-fold in adipocytes from animals fed saturated fatty acids, compared with 6.4-fold in those of animals fed the safflower oil diet. The concentrations of intracellular free fatty acids in adipocytes of experimental animals after stimulation with 10(-5) M norepinephrine, however, were not significantly different. The intracellular free fatty acid pool of adipocytes of animals fed the saturated fatty acids had more palmitic acid and less linoleic acid than those of safflower oil-fed animals. The results indicate that type of dietary fat had no effect on kinetic properties of hormone-sensitive lipase.     

Influence of Dietary Fats Upon Systolic Blood Pressure in the Rat

Studies were performed to determine whether feeding diets with differing fatty acid content and composition had an influence on systolic blood pressure in the rat. Weanling male rats were fed standard laboratory chow (2.9% fat in total), or synthetic diets (10% fat in total) containing fish oil, butter, coconut oil or corn oil, for 5 weeks. Coconut oil and butter diets were rich in saturated fatty acids, whilst fish oil and corn oil were rich in the n-3 and n-6 unsaturated fatty acids respectively. Systolic blood pressure was measured using an indirect tail-cuff method at the end of the feeding period, and compared to a group of weanling rats.

Feeding the different diets did not alter the growth of the rats, so all animals were of similar weights at the time of blood pressure determination. Control (chow fed) animals, at nine weeks of age, had higher systolic blood pressures than the weanling, baseline control group. Fish oil fed rats had similar pressures to the chow fed rats. Corn oil fed rats had significantly lower systolic pressures than the controls. The rats fed the diets rich in saturated fatty acids (butter and coconut oil) had significantly higher blood pressures than all other groups. Systolic blood pressure was found to be significantly related to the dietary intakes of saturated and unsaturated fatty acids. The dietary intake of linoleic acid was significantly higher in corn oil fed rats than in other groups. Systolic blood pressure was inversely related to linoleic acid intake. Feeding a diet rich in saturated fatty acids significantly increases blood pressure in the rat. A high intake of n-6 fatty acids, and in particular linoleic acid, appears to have a hypotensive effect. Prenatal exposure of the rats to a maternal low protein diet, abolished the hypertensive effects of the coconut oil diet and the hypotensive effect of the corn oil diet upon young adult females. The intrauterine environment may, therefore, be an important determinant of the effects of these fatty acids on blood pressure in later life.     

Health benefits of dietary fat reduction by a novel fat replacer: Mimix

The primary goals of this study were to identify any health benefits of the replacement of dietary fat with a novel fat replacer, Mimix, and to assure that the consumption of this fat replacer did not convey any deleterious health effects. Male, weanling, Fischer 344 rats were fed one of six diets containing between 5 and 20% w/w as fat for 8 weeks. These diets included two high fat diets (safflower oil or lard), a low fat diet and three diets where 15% of the fat in the high fat diets was replaced with various amounts of Mimix. When animals were fed a diet rich in saturated fat they consumed significantly more energy than other diet groups. When 15% saturated fat (lard) was replaced with safflower oil animals adjusted their food intake so that no difference in energy intake was observed between the high safflower diet and the low fat and Mimix diets. When the various Mimix fat replacements were compared to animals fed a high fat lard diet there was incomplete compensation of energy intake. Animals fed the high fat lard diet also had higher glucose and total serum cholesterol than their low fat and fat replacement counterparts. Feeding a high fat safflower oil diet to rats resulted in a significantly lower total serum cholesterol and serum triglyceride than all other diets. Replacement of dietary fat with Mimix demonstrated no deleterious effects on the heart, liver and intestinal tract that were all of normal weight, morphology and colour compared to other diet groups. Body composition analysis demonstrated that animals fed high fat diets had higher body fat mass at the expense of lean body mass. This was most obvious for animals fed high fat lard diets who had heavier epididymal fat pads. These data demonstrate that the replacement of dietary fat with the novel fat replacer Mimix can convey a number of health benefits in the absence of any deleterious effects.     

Health benefits of dietary fat reduction by a novel fat replacer: Mimix

The primary goals of this study were to identify any health benefits of the replacement of dietary fat with a novel fat replacer, Mimix, and to assure that the consumption of this fat replacer did not convey any deleterious health effects. Male, weanling, Fischer 344 rats were fed one of six diets containing between 5 and 20% w/w as fat for 8 weeks. These diets included two high fat diets (safflower oil or lard), a low fat diet and three diets where 15% of the fat in the high fat diets was replaced with various amounts of Mimix. When animals were fed a diet rich in saturated fat they consumed significantly more energy than other diet groups. When 15% saturated fat (lard) was replaced with safflower oil animals adjusted their food intake so that no difference in energy intake was observed between the high safflower diet and the low fat and Mimix diets. When the various Mimix fat replacements were compared to animals fed a high fat lard diet there was incomplete compensation of energy intake. Animals fed the high fat lard diet also had higher glucose and total serum cholesterol than their low fat and fat replacement counterparts. Feeding a high fat safflower oil diet to rats resulted in a significantly lower total serum cholesterol and serum triglyceride than all other diets. Replacement of dietary fat with Mimix demonstrated no deleterious effects on the heart, liver and intestinal tract that were all of normal weight, morphology and colour compared to other diet groups. Body composition analysis demonstrated that animals fed high fat diets had higher body fat mass at the expense of lean body mass. This was most obvious for animals fed high fat lard diets who had heavier epididymal fat pads. These data demonstrate that the replacement of dietary fat with the novel fat replacer Mimix can convey a number of health benefits in the absence of any deleterious effects.     

Effects of dietary fish oil on fatty acids and eicosanoids in metastasizing human breast cancer cells

We examined the relationships between the suppressive effects of dietary fish oil on growth and metastasis of MDA-MB-435 human breast cancer cells in female nude mice and the primary tumor phospholipid fatty acid concentrations, phospholipase A2 activity, and eicosanoid levels. Mice (n = 120) were fed a 23% (wt/wt) corn oil (CO) linoleic acid (LA)-rich diet for seven days before and after 10(6) tumor cells were injected into a mammary fat pad, and then the mice receive one of three isocaloric diets containing 23% total fat but different proportions of CO and menhaden oil (MO) (18% CO-5% MO, 11.5% CO-11.5% MO, 5% CO-18% MO) or a 23% fat diet containing 18% deodorized fish oil supplemented with tocopherol and tert-butylhydroquinone antioxidants (FAO). Primary tumor growth rate was significantly greater in mice fed the 18% CO diet than in the three diets containing higher levels of fish oil (all p < 0.05). The 18% MO diet, but not the 11.5% MO or the 18% FAO diet, suppressed the development of lung metastases compared with the 18% CO diet. Increasing the proportion of MO relative to CO in the diets produced corresponding increases in the primary tumor phospholipid eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) concentrations and reductions in LA and arachidonic acid. There was a significant positive correlation between the LA concentration in these tumors and the extent of lung metastasis (r = 0.504). Tumor phospholipase A2 activity was unaffected by dietary MO intake. Prostaglandin E2 concentration was inversely correlated with phospholipid EPA (r = -0.484) and DHA (r = -0.439), but there was no relationship with lung metastasis. Tumor leukotriene B4 and 5-hydroxyeicosatetraenoic acid levels were not reduced by dietary MO. The 18% FAO- and the 18% MO-fed mice showed similar relationships for the phospholipid fatty acids and prostaglandin E2, despite the lack of effect on metastasis. The strong correlation between phospholipid LA levels and metastasis and the lack of an association with tumor eicosanoids suggest that the 18% MO diet inhibited metastasis because dietary LA was replaced by other fatty acids.     

Effects of dietary fish oil or pectin on blood pressure and lipid metabolism in the DOCA-salt hypertensive rat

This study investigated the effects of diets containing fish oil or pectin on blood pressure and lipid metabolism in the deoxycorticosterone acetate (DOCA)-salt hypertensive rat. Three groups (8 rats/group) of unilaterally nephrectomized rats were fed for 21 d one of three purified diets: a) 8% fish oil + 2% safflower oil + 5% alpha cellulose (fish oil diet), b) 10% safflower oil + 5% pectin (pectin diet), or c) 10% safflower oil + 5% alpha cellulose (control diet). Each of the diets contained 6% NaCl and all rats received DOCA (30 mg/kg body wt, subcutaneously) twice weekly. Systolic blood pressure of rats fed fish oil was significantly lower (P less than 0.05) than that of rats fed the control diet; there was no significant difference between the pectin and control groups. Plasma renin activity and net sodium and potassium balances were similar among the three groups. Plasma total cholesterol, LDL cholesterol and HDL cholesterol were significantly lower (P less than 0.05) in the group fed the fish oil diet than in the group fed the control diet. Total, LDL and HDL cholesterol did not differ between rats fed the pectin and rats fed the control diet. Plasma triglyceride concentration did not differ among the three groups. Thus, dietary fish oil attenuated the development of DOCA-salt hypertension, unrelated to alterations of net sodium balance. Fish oil feeding also lowered total, LDL and HDL cholesterol, but did not alter the HDL/LDL ratio. In contrast, dietary pectin exerted no effect on blood pressure or lipid metabolism.     

The eicosapentaenoic to docosahexaenoic acid ratio of diets affects the pathogenesis of arthritis in Lew/SSN rats

Dietary-induced changes in tissue levels of polyunsaturated fatty acids modify inflammatory reactions through changes in the synthesis of lipid and peptide mediators of inflammation. Four semipurified 20% fat diets, based on beef tallow (BT), safflower oil (SFO), docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) were provided. The DHA and EPA ratios of the (n-3) fatty acid-based diets were 1.1 and 3.4, respectively. The effect of prefeeding diets differing in EPA to DHA ratios prior to the induction of streptococcal cell wall (SCW) arthritis in female Lew/SSN rats was examined. Weanling rats were fed diets for 5 wk before arthritis induction and 5 wk post-arthritis induction. Footpad thickness, hock circumference, plasma and macrophage fatty acids and histological assessment were compared. There were no differences in food intake and final body weights among the groups. Footpad inflammation, reported as percentage change (adjusted for growth) was greatest for rats fed the BT-based diet, intermediate in those fed the SFO-based diet and least for the rats fed the EPA- and DHA-based diets (P < 0.05). Macrophage phospholipids revealed cellular incorporation of EPA and DHA from the fish-oil based diets which modified lipid and peptide mediators of inflammation. Histological sections of rat hocks ranked by severity of arthritis-related changes suggested that the SFO- and EPA-based diets were more successful in ameliorating the destructive arthritic phase in hock joints than the BT- and DHA-based diets (P = 0.09) in this model of arthritis. The course of SCW-induced arthritis can be altered by diet-induced changes in macrophage fatty acid composition. The EPA-based diet is more effective in suppression of inflammation than the DHA-based diet.     

Dietary fatty acids temporarily alter liver very long-chain fatty acid composition in mice.

To determine the influence of dietary fatty acids on tissue very long-chain fatty acid (VLFA) composition, mice were fed four diets containing 15 g fat/100 g diet derived largely from either safflower oil, peanut oil, olive oil or glycerol trioleate oil. The diets varied widely in the composition of VLFA and other fatty acids. Digestibility of total dietary VLFA ranged from 84.6% in mice fed the glycerol trioleate diet to 96.7% in those fed the safflower oil diet. After 3 mo, the saturated VLFA composition of liver total lipids and sphingomyelin was lower in animals fed the glycerol trioleate oil diet than in mice fed most other diets. Although the saturated VLFA content of the peanut oil diet was more than 15-fold greater than that of the other diets, animals fed the peanut oil diet showed little or no selective increase in liver saturated VLFA. The VLFA composition of brain was comparable in all dietary groups. After 8 mo of feeding, the liver saturated VLFA composition tended to increase and differences between groups disappeared. Liver peroxisomal beta-oxidation of lignocerate (24:0) was similar among all dietary groups. These results demonstrate that dietary fatty acids shorter than VLFA temporarily influence the saturated VLFA composition of liver.     

Quantitative and qualitative changes in phospholipid in the intestine of the gerbil and the development of lipodystrophy.

Female gerbils fed a diet containing 20% coconut oil develop an intestinal lipodystrophy that is not seen in animals fed a diet containing 20% safflower oil or a diet of 20% coconut oil supplemented with 0.1% inositol. The coconut oil diets contained 1.5% safflower oil to prevent essential fatty acid deficiency. The level of inositol in the intestinal tissue of animals fed the coconut oil diet not supplemented with inositol has been shown to be decreased. Phospholipid analyses of the intestinal tissue were undertaken to determine if this decrease in total inositol was reflected in a decrease in phosphatidylinositol or resulted in an altered phospholipid pattern. No difference in the phosphatidylinositol level was seen between animals fed 20% coconut oil with and without inositol supplementation (microgram P/gut section), although animals fed coconut oil diets had lower levels of phosphatidylinositol than animals fed safflower oil diets. Fatty acid analyses of total phospholipid and phosphatidylinositol in gut tissue revealed that animals which deveoped the lesion had an ultered phosphatidylinositol fraction with a depressed level of arachidonic acid and an elevated level of oleic acid. This suggests that the development of the intestinal lipodystrophy may be correlated with qualitative rather than quantitative changes in phosphatidylinositol.     

The cholesterolaemic effects of dietary fats in cholesteryl ester transfer protein transgenic mice.

In order to investigate the role of cholesteryl ester transfer protein (CETP) in the cholesterolaemic response to dietary fats, we analysed plasma lipid profiles of CETP-transgenic and control C57BL/6 mice fed standard chow (AIN-93G; AIN), a low-fat diet, and diets high in butter (saturated fatty acids; SFA), high-oleic acid safflower oil (monounsaturated fatty acids; MUFA), and safflower oil (polyunsaturated fatty acids; PUFA) for 5 weeks. Each group contained four or five mice. There were significant diet and dietxgenotype effects on plasma total cholesterol (TC; and respectively), liver TC ( and respectively), and esterified cholesterol (EC; and respectively); diet effects on plasma triacylglycerol liver free cholesterol and body weight a genotype effect on body-weight gain and a dietxgenotype effect on energy intake In transgenic mice the SFA diet caused significantly higher plasma TC than the PUFA diet In control mice MUFA and PUFA diets, but not the SFA diet, caused significantly higher plasma TC than the low-fat and AIN diets Transgenic mice fed PUFA had lower plasma TC while transgenic mice fed MUFA had lower LDL+VLDL-cholesterol than controls in the same dietary groups. Transgenic mice fed MUFA and PUFA diets also had significantly higher liver TC and respectively) and EC and respectively) than controls fed the same diets. In the present study we showed that: (1) CETP transgenic mice had a cholesterolaemic response to dietary fats similar to that in human subjects; (2) CETP transgenic mice fed PUFA showed significantly lower plasma TC, while those fed MUFA had lower LDL+VLDL-cholesterol than controls; (3) hepatic accumulation of cholesterol, possibly resulting from the combination of the enhanced cholesteryl ester transfer to apolipoprotein B-containing lipoproteins and increased hepatic uptake of cholesterol, may contribute to the cholesterol-lowering effect of MUFA and PUFA in CETP-transgenic mice; (4) CETP may play a role in appetite and/or energy regulation.     

Fat and endocrine-responsive cancer in animals

Studies using the N-nitrosomethylurea mammary tumor model indicate that the tumor-promoting effect of dietary fat is dependent on both qualitative and quantitative factors. Rats were fed diets containing either safflower, corn, or olive oil at either 23 (HF) or 5% (LF) in the diet (w/w). Coconut oil was fed to one group at 23% (w/w). It was found that animals fed HF diets rich in linoleic acid, such as safflower and corn oil, exhibited increased incidence and decreased latent period compared with either their LF counterparts or animals fed HF diets rich in oleic acid (olive oil) or medium-chain saturated fatty acids (coconut oil). Analysis of tumor lipid fatty acid content indicated that tumor-neutral lipids reflected the diet whereas tumor phospholipids did not. Moreover, tumor prostaglandins (PGE2) were high in the two high-incidence groups (HF safflower and corn) and low in the two low-incidence groups (HF olive and coconut). These results indicate that HF intake is a necessary, but not a sufficient, condition for mammary tumor promotion, and that the proportion of essential polyunsaturates vis a vis monounsaturates and saturates is a critical determinant of the fat effect. In addition, our studies suggest that alterations in the metabolism of linoleic acid to (prosta . . .) prostaglandins may underlie the fat effect. Dose-response studies in the same model, using four different levels of corn oil, suggest that instead of a linear relationship with respect to tumor incidence, there appears to be a threshold lying between 20 and 33% fat as calories, above which tumor promotion is manifested and below which it is not.     

A highly saturated fat-rich diet is more obesogenic than diets with lower saturated fat content

The present study tested the hypothesis that a saturated fatty acid (SFA)–rich diet is more obesogenic than diets with lower SFA content. In 8 female Sprague-Dawley rats fed a low-SFA canola or a moderate-SFA lard-rich diets at 67% of energy for 26 days, body weight gain, final body weight, obesity index, and food and energy intake were comparable. Twenty-nine rats were fed canola or high-SFA butter-rich diets (67% of energy) or chow for 50 days; then high-fat feeding was followed by ad libitum low-fat feeding (27% of energy) for 28 days and by a food-restricted low-fat diet for 32 days. High-fat feeding resulted in a greater body weight gain (P < .04), final body weight (P < .04), and energy intake (P < .008) in butter-fed rats than in canola- and chow-fed controls, after 26 or 50 days. Ad libitum canola and butter low-fat diets or chow feeding resulted in similar weight change, whereas food-restricted low-fat diets led to comparable weight loss and final weight. Canola-fed animals adjusted their intake based on diet energy density, whereas lard and butter-fed animals failed to do so. Abdominal fat (P = .012) and plasma leptin (P = .005) were higher in chow-fed controls than in canola-fed rats, but comparable with those of butter-fed rats. Prone and resistant phenotypes were detected with high-fat feeding. In conclusion, only feeding the high-SFA butter-rich diet led to obesity development and failure to adjust intake based on the energy density and preserving body fat even after weight loss. The high availability of SFA-rich foods in today's obesogenic environment could contribute to develop and maintain obesity.     

Effect of the fat/carbohydrate ratio in the diet on obesity and oral glucose tolerance in C57BL/6J mice

To study whether consumed dietary fat has a linear relationship or a threshold with glycemic controls, female C57BL/6J mice were fed different levels of a safflower oil (10, 20, 30, 40, 50, and 60% of total energy) diet ad libitum for 15 wk. Food intake, body weight, parametrial white adipose tissue (WAT) and liver weight were measured, and oral glucose tolerance tests were conducted. Although there was no significant difference in average energy intake, graded increments of safflower oil resulted in graded deterioration of glucose tolerance during 5 and 12-wk feeding, and deterioration of glucose tolerance was more manifested after 12-wk feeding as compared to 5-wk feeding. After 12-wk feeding, a significant deterioration of glucose tolerance was observed in diets of more than 40% fat. Graded increments of body weight and WAT weight were observed, and their weight increases were manifested in diets of more than 30% fat. These data indicated that the amount of dietary fat had an almost linear relationship with glucose tolerance, and significant differences were observed in mice fed diets more of than 40% fat.     

Hepatic fatty acids and acyl desaturases in rats: effects of dietary carbohydrate and essential fatty acids

For a 9-week period, six groups of weanling male rats were fed either a fat-free diet or a diet containing 10% hydrogenated coconut oil (HCO) or 10% safflower oil (SAF), respectively. Each of these diets contained either glucose or sucrose as the only carbohydrate. In the fat-free diets, the carbohydrate level was 67.3% and in the fat-supplemented diets 44.8%. Including HCO in the fat-free diet did not significantly alter hepatic 5-, 6-, and 9-desaturase activity, whereas addition of SAF significantly depressed all these activities. As compared to glucose, sucrose induced higher 9-desaturase activity in the rats on the fat-free diets. Adding HCO or SAF to the diet, simultaneously with lowering the carbohydrate level, diminished the stimulatory effect of dietary sucrose versus glucose on 9-desaturase activity. Levels of 20:4n6 and 20:3n9 in the fatty acid profiles of the liver microsomes were not influenced by dietary carbohydrate source, neither were the activities of the 5- and 6-desaturases, providing indirect evidence that dietary sucrose, as compared to glucose, did not differently affect biosynthesis of 20:4n6 and 20:3n9.     

Docosahexaenoic acid is superior to eicosapentaenoic acid as the essential fatty acid for growth of grouper, Epinephelus malabaricus.

Juvenile grouper (Epinephelus malabaricus) were fed seven experimental diets, one control diet and one reference diet for 12 wk to determine the dietary requirement of grouper for docosahexaenoic (DHA) and eicosapentaenoic (EPA) acids. Each of the seven diets contained 1 g/100 g DHA and EPA in various combinations and 9 g/100 g tristearin. The control diet contained 1 g/100 g trilinolenin and trilinolein (3:1, wt/wt), and no supplemental EPA or DHA. The reference diet contained only natural oils from a mixture of cod liver oil, linseed oil and safflower oil at a ratio of 2:1:1 (wt/wt/wt). Significant differences (P < 0.05) in growth were observed among the dietary treatments but not in survival rate or relative liver weight. Only the diet with the highest DHA/EPA ratio (3:1) promoted significantly greater growth than the control diet. Purified EPA and DHA did not perform better in promoting growth than did the impure EPA and DHA oils. Enhanced growth was observed when the dietary DHA/EPA ratio was greater than 1, indicating that DHA was superior to EPA in promoting fish growth. Neutral lipid (NL) was the predominant lipid fraction (>70%) in both liver and muscle. Tissue NL/polar lipid did not differ among groups except the reference diet group that had a higher ratio (P < 0.05). DHA and EPA levels in the grouper tissues, especially muscle, were highly reflective of dietary levels of DHA and EPA, indicating that direct incorporation was likely. In addition, the 20:1(n-9), concentration in NL fractions seems to be an appropriate indicator of dietary essential fatty acid deficiency in grouper.     

Will dietary omega-3 fatty acids change the composition of human milk?

The most abundant long-chain polyunsaturated fatty acid in brain and retinal lipids is docosahexaenoic acid (DHA, C22:6 omega 3). It becomes incorporated into nerve tissues mostly in utero and during the 1st yr of life. DHA is derived in humans either performed in the diet or by hepatic synthesis from dietary linolenic acid (C18:3 omega 3). Since human milk contains DHA, this study was designed to see if increased dietary DHA would be reflected in a higher DHA content in human milk. Eight lactating women were given supplements of a fish oil concentrate rich in omega-3 fatty acids, including DHA (11% of fatty acids). Six women took 5 g/day of fish oil for 28 days; five women consumed 10 g/day for 14 days; and one woman consumed 47 g/day for 8 days. Each intake level of fish oil produced significant dose-dependent increases in the DHA content of milk and plasma. Base-line DHA levels in milk were 0.1 +/- 0.06% of total fatty acids. Five g/day of fish oil raised the levels to 0.5 +/- 0.1% (p less than 0.001); 10 g/day raised DHA levels to 0.8 +/- 0.1% (p less than 0.001); and 47 g/day produced DHA levels of 4.8%. The results of this study indicated that relatively low intakes of dietary DHA significantly elevated milk DHA content. This would clearly elevate the infant's DHA intake and might have implications for brain and retinal development.     

Enrichment of (n-3) fatty acids of suckling rats by maternal dietary menhaden oil

The study was undertaken to determine whether the content of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in neonatal rats can be increased through milk provided by lactating mothers fed a diet containing 20% menhaden oil (experimental group), in comparison with a group fed a 20% corn oil diet (control group). The test diets were isocaloric and provided 41% of total energy as fat. Coinciding with 3-9% higher maternal body weight gain throughout the lactation period with the menhaden oil diet, the suckling rats in the experimental group at the ages of 3-9 d gained 5-10% more weight than did their control counterparts. When compared with corn oil, maternal dietary menhaden oil induced not only a higher weight percentage but also higher concentrations (microgram/mL) of EPA, DHA and total (n-3) fatty acids in milk, plasma, platelets and erythrocytes of neonates. These changes were accompanied by lower arachidonic and linoleic acid levels. EPA and DHA were detected in all three blood components of the control group, whose corn oil diet contained linolenic acid but not longer chain (n-3) fatty acids. This finding, together with the higher DHA to EPA ratios found in the three blood components than in the milk of the experimental group, suggests that neonatal rats possess the enzymes necessary for producing DHA from EPA and linolenate by desaturation and elongation mechanisms.     

Effect of different dietary triglycerides on liver fatty acids and prostaglandin synthesis by mouse peritoneal cells.

The effect of dietary triglycerides varying in fatty acid composition on the tissue fatty acids and prostaglandin synthesis was studied in mice. The dietary fats were medium-chain triglycerides (rich in C8:0 and C10:0), structured lipids (rich in 12:0), high oleic sunflower oil (rich in 18:1), corn oil (rich in n-6 polyunsaturated fatty acids), and menhaden oil (rich in n-3 polyunsaturated fatty acids) fed at 5% by weight in refined diets. The medium chain fatty acids C8 to C12 from medium-chain triglycerides and structured lipids did not accumulate in liver phospholipids. However, long-chain fatty acids from the dietary fats were incorporated into liver lipids, with n-3 polyunsaturated fatty acids replacing arachidonic acid. The synthesis of 6-keto-prostaglandin F1 alpha and prostaglandin E2 by peritoneal cells in response to intraperitoneal injection of zymosan decreased as the arachidonic acid levels were decreased. When the same dietary fats were added to the refined, fat-free diets, at 7.5 wt% levels, together with 2.5 wt% of safflower oil to provide essential fatty acids, only the long-chain fatty acids from the dietary fats were incorporated into the liver lipids. The arachidonic acid in liver lipids was enhanced after supplementation of diets with safflower oil. However, the reduction in prostaglandin synthesis by peritoneal cells in response to intraperitoneal injection of zymosan was similar to that observed when 5% fat was fed. The data suggest that dietary fats of defined composition, with or without added essential fatty acids, may be useful as alternate fat sources in parenteral nutrition in reducing inflammatory responses mediated via prostaglandins.