Reduction of essential fatty acid deficiency in rats fed a low iron fat free diet

Young male rats were fed ad libitum for 8 weeks a low iron fat-free (FF-Fe) diet or a fat-free diet supplemented with iron (FF+Fe). The relative levels of 16∶1 to 16∶0 and 18∶1 to 18∶0 in the total fatty acids of liver and other tissues (plasma, erythrocytes and intestinal mucosa) were considerably decreased because of a lack of dietary iron. In rats fed the FF-Fe diet, the levels of essential fatty acids (18∶2ω6+20∶4ω6) in tissues were 2-to 3-fold greater than in the corresponding tissues of rats fed the FF+Fe diet. Eicosatrienoic acid (20∶3ω9) levels in tissue lipids from rats fed the FF+Fe diet were high (8–16%), whereas they were low (2–5%) in the case of animals fed the FF-Fe diet. The proportion of 20∶4 in total fatty acids of tissues was 2-to 3-fold greater in rats fed the FF-Fe diet than when they were fed the FF+Fe diet. Therefore, the relative levels of 20∶3ω9/20∶4ω6 varied from 1-2.9 in tissue lipids of rats fed the FF+Fe diet, while it varied only from 0.2–0.3 in animals fed the FF-Fe diet. These results suggest that a lack of dietary iron may reduce the synthesis of 16∶1, 18∶1, 20∶3 and 20∶4 and the metabolism of 20∶4.     

The effect of long-chain monoenes on prostaglandin E2 synthesis by rat skin

In order to ascertain whether the dermal lesions observed in male rats fed rapeseed oils are due to impaired prostaglandin biosynthesis, endogenous levels of prostaglandin E₂ (PGE₂) in skin and the capacity of this tissue to synthesize PGE₂ from arachidonic acid was investigated. Male Sprague-Dawley rats were fed from weaning for 8 weeks either a standard rat diet (chow) or semisynthetic diets containing 20% by weight of the following fat sources: corn oil; commercial lard; commercial lard to which was added 5.4% free erucic acid; rendered pig fat; or the following rapeseed oils:Brassica napus var. Zephyr;B. campestris var. Span;B. campestris var. Arlo (15%) and var. Echo (85%) designated HEAR (high erucic acid rapeseed). The long-chain monoene content (18∶1, 20∶1, and 22∶1) of the diets fed ranged from 30 to 71 mole % and that of skin from 27 to 74 mole %. A significant (P<0.01) correlation was found between the level of 18∶2n−6 in the diet and the endogenous PGE₂ levels in skin and the capacity of this tissue to synthesize PGE₂. No relationship was found between these two PGE₂ parameters and the level of erucic acid in the diet. The rate of turnover of PGE₂ appeared to be lower in rats fed rapeseed oil as evidenced by the relatively high endogenous PGE₂ levels when these oils were fed (96 to 105 μg/g). On the other hand, the lowest capacity for PGE₂ synthesis was found with skin from rats fed Zephyr rapeseed oil, rats which also had the most severe incidence of hair loss and dermal lesions. Significant (P<0.01) negative correlations were observed between the level of monoenes and specifically the level of oleic (18∶1n−9) acid in the diets and PGE₂ synthesis capacity of skin, possibly confirming the known inhibitory effect of 18∶1n−9 on the prostaglandin synthesizing enzyme system. Contribution No. 687, Animal Research Institute.     

Rat testicular lipids and dietary isomeric fatty acids in essential fatty acid deficiency

Weanling rats were fed essential fatty acid-deficient diets, either completely fat-free, or with partially hydrogenated fish oil (PHFO, 28 wt %), or with fractions derived from PHFO containing primarily positional isomers oftrans-eicosenoate (20∶1, 3 wt %) ortrans-docosenoate (22∶1, 3 wt %). Control animals were fed a peanut oil-containing diet (28 wt %). After 5 or 15 weeks on the diet, the content of neutral and phosphorus-containing lipids in the testes was determined. The fatty acid distribution in major lipid classes was analyzed for animals fed the diets for 15 weeks. The testicular stage of maturation or degeneration was assessed by histology. The group fed PHFO exhibited signs of complete testicular degeneration, or lack of maturation, already after 5 weeks, whereas the animals on the diets with the very long chain monoenoic acids suffered severe degenerations only after 15 weeks. In the PHFO-fed rats, a sharp decline in the concentration of testicular triacylglycerols was observed. In all of the essential fatty acid-deficient groups, an increase in testicular sphingomyelin was observed. Cholesterol levels were fairly similar among all dietary groups. The total testicular fatty acids of the PHFO-fed animals contained somewhat more eicosadienoic acid than found in the other groups, and somewhat less (n−9)-acids. In all EFA-deficient groups, (n−6)-acids were lowered, in particular in triacylglycerols and phosphatidyl cholines. The PHFO group did not show a lower (n−6)-concentration than the other deficient groups, in spite of the more severe symptoms of deficiency. There was no evidence of a major accumulation of long chain isomeric fatty acids in the degenerated testes of the PHFO-, 20∶1, and 22∶1-fed groups.     

Slow recovery of the fatty acid composition of sciatic nerve in rats fed a diet initially low in n−3 fatty acids

The sciatic nerve of rats fed sunflower oil (6 mg 18∶3n−3/100 g of diet) presented dramatic alterations in the long chain polyunsaturated fatty acids in comparison with those fed soy oil (130 mg 18∶3n−3/100 g of diet). In both 15-day-old and 60-day-old animals fed sunflower oil, 22∶6n−3 (cervonic acid) was fourfold less, 22∶5n−6 was 10-fold greater; adrenic acid (22∶4n−6) was slightly greater and arachidonic acid (20∶4n−6) was close to that in rats fed soy oil. The percentage distribution of total polyunsaturated fatty acids as well as the individual saturated and monounsaturated fatty acids were the same in both groups. When the sunflower oil-fed animals were switched to a soy oil-containing diet for either 15 or 60 days, the percentage distribution of 22∶6n−3 increased slowly to reach the control value 2.5 months later. Conversely 22∶5n−6 decreased slowly. The decay of 22∶5n−6 was more rapid than the increase of 22∶6n−3.     

The effect of dietary fatty acid balance on myocardial lesions in male rats

Three hundred (experiment I) and 350 (experiment II) weanling, 3-week-old male Sprague-Dawley rats weighing between 40–50 g were randomly assigned two per cage and 50 per dietary treatment to study the effect of dietary fatty acid balance on myocardial lesions. The following oils were tested: Experiment I.Brassica napus var. Tower rapeseed oil [Tower RSO, 1974 cultivar and 1975 cultivar, each containing 0.3% erucic (22∶1) acid];B. napus var. Zephyr RSO containing 0.9% 22∶1; corn oil; olive oil; and soybean oil. Experiment II.B. napus var. Tower RSO (1974 cultivar), olive oil, soybean oil, and the following oils to which was added the indicated level of free 22∶1; Tower +0.5% 22∶1; Tower +5.6% 22∶1; olive oil +4.4% 22∶1; soybean oil +5.7% 22∶1. In each case the oils were incorporated in a semisynthetic diet at a level of 20% by weight. Heart and heart lipid weights of rats fed the different oils did not differ statistically from each other. Fatty acid analyses of heart lipids revealed that the fatty acid composition of the cardiac lipids reflected that of the diet fed. In experiment I, there was a definite but significantly lower incidence (P<0.01) and severity (P<0.01) of heart lesions in rats fed control oils (corn, olive, soybean) than in rats fed rapeseed oils. Also, in experiment II, a definite but lower incidence and severity of heart lesions occurred in rats fed control oils (soybean, olive) compared to rats fed Tower RSO or this oil with added free 22∶1. Adding 22∶1 to an oil naturally high in 18∶3 (soybean) did not alter the incidence of heart lesions, whereas adding 22∶1 to an oil naturally high in 18∶1 (olive) increased significantly (P<0.01) both the incidence and severity of heart lesions. Thus, it appears that the background incidence of heart lesions that are found in the rat in any case, and which are increased by rapeseed oil feeding, is caused by the imbalanced fatty acid composition of the oil for the growing rat, i.e. high monoenes (18∶1, 20∶1, and 22∶1) and high 18∶3 and is not only due to the presence of excess 18∶3. Contribution No. 706, Animal Research Institute.     

Diet-induced alterations in the discoid shape and phospholipid fatty acid compositions of rat erythrocytes

For eight weeks young male rats were fed diets rich in 18∶2 (stock diet, or 10% corn oil, CO) or those devoid of 18∶2 (fat free, FF, or 10% hydrogenated coconut oil, HCNO). The CO and HCNO diets were fed in the absence or presence of eicosa-5,8,11,14-tetraynoic acid (TYA). When 18∶2 was excluded, an increase in the level of 16∶1, 18∶1 and 20∶3 and a decrease in 18∶2 was observed in the fatty acids of red cells. On feeding TYA, an increase in 18∶2 and in the case of the HCNO+TYA diet, a decrease of 12∶0 and 14∶0 was also observed. In all cases the levels of 20∶4 in erythrocyte fatty acids were similar. Saturated fatty acids were predominant in phosphatidyl choline (PC), lysophosphatidylcholine, (LPC) and sphingomyelin whereas unsaturated acids were predominant in phosphatidyl ethanolamine (PE), (PS), and phosphatidyl inositol (PI). Acids containing three or more double bonds comprised about 90% of the total acids in PI. In all the phospholipids, the characteristic changes in the composition of fatty acids were observed due to the exclusion of 18∶2 from the diet. However, changes due to the feeding of TYA were found only in PC and LPC. In rats fed the 18∶2-rich diet, about 60% of the red cells were discocytes. In those fed the 18∶2-free diet, the level of discocytes decreased to about 23%, and the levels of echinocytes II and III increased. The exclusion of 18∶2 for even a few days decreased the proportion of discocytes. The loss of discoid shape was reversed in a few days by feeding an 18∶2-rich diet. Fatty acid analysis of erythrocytes of rats of the various dietary manipulations showed that the change in the proportion of discocytes followed the change in the level of 18∶2.     

Cholesteryl ester hydrolase activity in adrenal homogenates from normal and essential fatty acid-deficient female rats

Cholesteryl ester hydrolase was assayed in adrenal homogenates from mature female rats fed a control (corn oil-containing) or essential fatty acid (EFA)-deficient diet. Cholesteryl ester of 16∶0, 18∶0, 18∶1, 18∶2(n−6), 20∶4(n−6) and 22∶4(n−6) were used as substrates. In control rats, the unsaturated esters were hydrolyzed more rapidly than the saturated esters and cholesteryl arachidonate was the preferred substrate of the six investigated; cholesteryl oleate elicited the highest activity in the deficient group. Polyunsaturated esters were hydrolyzed at a significantly lower rate by homogenates from EFA-deficient rats than by those from control animals. The esters of 18∶1, 18∶2(n−6) and 20∶4(n−6) were hydrolyzed more extenstively in relation to their concentrations in adrenal tissue than were cholesteryl esters of 16∶0, 18∶0 and 22∶4(n−6). This difference was more pronounced in control than in EFA-deficient rats. No simple relationship of adrenal cholesteryl ester hydrolase activity to ester fatty acid structure or to nutritional essentiality was evident.     

Myocardial changes in newborn piglets fed sow milk or milk replacer diets containing different levels of erucic acid

This study was undertaken to determine whether the neonate was more susceptible to the effects of dietary erucic acid (22∶1n−9) than the adult. Newborn piglets were used to assess the safety of different levels of 22∶1n−9 on lipid and histological changes in the heart. Newborn piglets showed no myocardial lipidosis as assessed by oil red 0 staining, but lipidosis appeared with consumption of sow milk and disappeared by seven days of age. Milk replacer diets containing soybean oil, or rapeseed oil mixtures with up to 5% 22∶1n−9 in the oil, or 1.25% in the diet, gave trace myocardial lipidosis. Rapeseed oil mixtures with 7 to 42.9% 22∶1n−9 showed definite myocardial lipidosis in newborn piglets, which correlated to dietary 22∶1n−9, showing a maximum after one week on diet. The severity of the lipidosis was greater than observed previously with weaned pigs. There were no significant differences among diets in cardiac lipid classes except for triacylglycerol (TAG), which increased in piglets fed a repeseed oil with 42.9% 22∶1n−9. TAG showed the highest incorporation of 22∶1n−9, the concentration of 22∶1n−9 in TAG was similar to that present in the dietary oil. Among the cardiac phospholipids, sphingomyelin and phosphatidylserine had the highest, and diphosphatidylglycerol (DPG) the lowest level of 22∶1n−9. The low content of 22∶1n−9 in DPG of newborn piglets is not observed in weaned pigs and rats fed high erucic acid rapeseed oil. The relative concentration of saturated fatty acids was lowered in all cardiac phospholipids of piglets fed rapeseed oils, possibly due to the low content of saturated fatty acids in rapeseed oils. The results suggest that piglets fed up to 750 mg 22∶1n−9/kg body weight/day showed no adverse nutritional or cardiac effects.     

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.     

Effects of essential fatty acid deficiency on prostaglandin synthesis and fatty acid composition in rat renal medulla

Studies are reported on the capacity of isolated rat renal papilla (inner medulla) to synthesize and release prostaglandin (PG) E from endogenous and exogenous precursor(s) during development of an essential fatty acid (EFA) deficiency in the rat. Weanling (21-day-old) male Sprague-Dawley rats were fed a fat-free diet supplemented with either 5% hydrogenated coconut oil (HCO) or 5% safflower oil (SO). At approximately 3, 6 and 7 weeks (6, 9 and 10 weeks of age), groups of animals fed each diet were killed for studies of PGE synthesis in the renal papillae. Differences in the fatty acid composition of the papillae lipids of the animals of each group were also determined. The in vitro production of PGE from endogenous precursor(s) was significantly reduced in the papillae from the 6-week-old rats fed the HCO diet compared to the control (SO) rats, and appeared to be near maximally depressed in the 10-week-old animals compared to that of animals fed an EFA deficient diet for over a year in an accessory experiment. Analyses of the fatty acids of the papillae lipids of the HCO groups showed that the levels of 18∶2 and 20∶4 were markedly reduced, and those of 16∶1, 18∶1 and 20∶3 were elevated compared to the controls even in the 6-week-old animals, typical of an EFA deficiency. The papillae lipids of the animals fed the HCO diet were also depleted of their stores of 22∶4ω6. A fatty acid believed to be derived by chain elongation of 20∶3ω9, 22∶3, was found in large concentrations in the papillae triglycerides of the EFA deficient rats. Incubations of exogenous arachidonic acid (20∶4) in homogenates and tissue slices of the papillae of the HCO dietary groups showed that the PG synthetase was not impaired by an EFA deficiency. The rate of PGE synthesis in the papillae of the EFA deficient animals was generally enhanced when exogenous 20∶4 was added, indicating that the concentration of available precursor(s) is a primary factor in the control of PGE synthesis in the papilla of the rat.     

Effects of dietary primrose oil on mammary tumorigenesis induced by 7,12-dimethylbenz(a) anthracene

The mammary tumor-promoting effect of a high-fat diet containing 20% evening primrose oil (PO) was compared to that of a 20% corn oil (CO) diet. Mammary tumors were induced in female Sprague-Dawley rats using 10 mg (Study 1) and 5 mg (Study 2) 7,12-dimethylbenz(a)anthracene (DMBA). The 10 mg dose of DMBA gave a total mammary tumor incidence of 47% in rats fed the PO diet and 80% for those fed the CO diet. When only adenocarcinomas were counted, the malignant mammary tumor incidences were 41% in rats fed the PO diet and 73% in rats fed the CO diet. In a second study using 5 mg DMBA to induce mammary tumors, total tumor incidences were 50% for PO-fed rats and 63% for those receiving a CO diet. Again, when only adenocarcinomas were counted, tumor incidences were 27% for PO- and 63% for CO-dieted rats. Analysis of plasma fatty acid profiles indicated that animals fed a 20% PO diet showed significant increases in 18∶3 and 20∶4 fatty acids and significant decreases in 16∶0 and 18∶1 compared to animals fed a 20% CO diet. These results indicate that the mammary tumor promoting effect of a diet containing 20% fat can be diminished by substituting PO for CO. Moreover, the promoting effect on mammary cancer by a high-fat diet could be depressed by feeding a source of γ-linolenic acid (GLA).     

Dietary arachidonic acid reduces fatty liver,increases diet consumption and weight gain in ethanol-fed rats

We fed young male Sprague-Dawley rats for 4 wk ad libitum liquid diets containing 34% of the calories as ethanol and 35% as fat with (AA+) and without (AA−) arachidonic acid (20∶4). Additional rats in the control groups were fed similar diets made isocaloric with dextrose with (CA+) and without (CA−) 20∶4. The liver triglyceride (TG) content of rats in the AA+ group was reduced ca. 3-fold over that of rats in the AA-group. The diet consumption and body wts of rats in the AA+ group were significantly greater than those of rats fed alcohol without the 20∶4 supplement (AA−). Also livers from rats in the AA+ group were as large as those from rats in control groups (CA+, CA−) and ca. twice as large as those from rats in the AA-group. The fatty acid composition of liver TG in rats fed the alcohol diet was similar to that of dietary fat. Levels of 20∶4 and docosatetraenoic acid (22∶4) in liver TG fatty acids from rats fed diets without arachidonate (AA−, CA−) were low (trace to 1.6%). After ingestion of arachidonic acid, 20∶4 increased to ca. 10% and 22∶4 to ca. 5%. The content of liver phospholipids was higher in livers of rats fed ethanol (AA−) than in those of controls (CA−). Presented at the ISF/AOCS World Congress, April 27-May 1, 1980, New York City.     

Effects of coconut oil on heart lipids and on fatty acid utilization in rapeseed oil

Male adult Sprague-Dawley rats were fed diets containing 15% by weight of sunflower oil, coconut oil, rapeseed oil or combinations of these oils for 5 or 60 days. The digestibility of erucic acid (22∶1), lauric acid (12∶0) and linoleic acid (18∶2) was measured and found to be decreased for erucic acid at both time intervals, and for lauric acid after 60 days when coconut oil and rapeseed oil were blended. The cardiac lipodosis was proportional to the content of erucic acid in the diet. At 60 days, the high level of 22∶6 in the cardiac phospholipids of rats fed rapeseed oil was reduced by the addition of sunflower oil but not by coconut oil. Thus, the blending of rapeseed oil with coconut oil apparently is less desirable than that of rapeseed oil and sunflower oil.     

Reduction in medium chain acids and monoenoic acids in livers and plasma of rats fed eicosa-5,8,11,14-tetraynoic acid

Male Sprague-Dawley rats were fed for 8 weeks a corn oil (CO) diet or a hydrogenated coconut oil (HCNO) diet. These diets were fed in the absence or presence of eicosa-5,8,11,14-tetraynoic acid (TYA). The inclusion of TYA in the HCNO diet reduced the levels of 12∶0 and 14∶0 in the total fatty acids of livers and plasma. With either diet, the presence of TYA caused an alteration in the fatty acid composition of these tissues so as to reduce the values of the ratios: 16∶1/16∶0, 18∶1/18∶0, and 20∶4/18∶2. These results suggest that dietary TYA can influence the hepatic metabolism of medium chain fatty acids and that it may inhibit the desaturase enzyme involved in the synthesis of not only 20∶4 but also of monoenoic fatty acids.     

Effect of marine oil and rapessee oil on composition of fatty acids in lipoprotein triacylglycerols from rat blood plasma and liver perfusate

The fatty acid patterns of triacylglycerols (TG) from very low density lipoprotein (VLDL) in blood plasma and liver-perfusate from rats fed partially hydrogenated marine oil or rapeseed oil were determined. In the plasma from rats fed rapeseed oil for three days and three weeks, there was a small but significant decrease in the percentage of 22∶1 fatty acid from 17.2 to 11.2% with length of feeding. In liver-perfusate, the comparable decrease with dietary rapeseed oil was from 18.5 to 5.2%, and with dietary marine oil from 13.4 to 8.0%. In contrast to the liver-perfusate, the remaining liver had only a very low 22∶1 composition (ca 2%) independent of feeding period or diet. The results indicated that the liver exported the very long chain fatty acids and that an adaptation took place after three days feeding with rapeseed oil or marine oil. This adaptation in the liver could possibly explain why TG accumulation in hearts, which appears after three days' feeding with rapeseed oil or marine oil, disappears after an extended feeding period.     

Myocardial alterations resulting from feeding partially hydrogenated marine oils and peanut oil to rats

Myocardial alterations were observed in 5 groups of rats fed diets containing 20% fat for 16 weeks. The incidence was comparable to that from other studies and uniform at 6/20 in hearts from rats fed: partially hydrogenated herring oil to give dietary levels of either 16.7% or 4.6% 22∶1; partially hydrogenated redfish/flatfish oil to give 4.5% 22∶1 in the dietary fat; and peanut oil (of unknown origin) containing 0.1% 22∶1. The incidence was 9/20 in the hearts of rats fed an unrefined and unprocessed redfish oil at a dietary level of 16.0% 22∶1 in fatty acids.     

The effect of clofibrate on heart and plasma lipids in rats fed a diet containing rapeseed oil

The effect of clofibrate on heart and plasma lipids in rats fed a diet containing 30% of the calories as peanut oil (PO) or rapeseed oil (RSO) (42.7% erucic acid and 0.5% eicosenoic acid) was studied. A decrease of erucic acid content to one-third and concomitant increase in the content of 18∶1, 16∶1 and 16∶0 fatty acids in plasma triacylglycerols were observed after administration of clofibrate to rats fed the RSO-diet. It is suggested that these changes reflect the increased capacity of the liver to chainshorten very long chain length fatty acids. The extent of lipidosis in the heart of rats fed the RSO-diet was decreased by 50% by clofibrate. However, the concentration of erucic acid in heart triacylglycerols decreased much less (30%) than the concentration of all other fatty acids (50–65%). It is concluded that the clofibrate administration increased the oxidative capacity of the heart mitochondria and that the heart cell does not have an efficient system to handle very long chain length monounsaturated fatty acids as does the liver.     

The prevention of alcoholic fatty liver using dietary supplements: Dihydroxyacetone,pyruvate and riboflavin compared to arachidonic acid in pair-fed rats

Male Sprague-Dawley rats were fed for 30 days a high-fat liquid ethanol diet with dihydroxyacetone, pyruvate and riboflavin added as supplements (AMA-). Plasma triglyceride (TG) levels were 6-fold greater in these rats than in those fed and alcohol with without the supplements (AA-). The liver TG content in rats fed the AMA-diet was similar to that of rats fed a control diet (CA-) in which alcohol was replaced with isocaloric amounts of dextrose. Livers of rats fed the AA- diet had 3 times more TG than controls. Alcohol ingestion also enhanced the hepatic content of cholesteryl esters (CE) and phospholipids (PL). These lipids were reduced to levels found in livers of rats fed the control diet (CA-) when dihydroxyacetone, pyruvate and riboflavin were included in the alcohol diet. The fatty acid compositions of TG, CE and PL from livers of rats fed the AMA-diet were similar to those of corresponding lipids from rats fed the control diet (CA-) but differed from compositions when fed the alcohol diet (AA-). Regardless of the diet fed, TG had the same fatty acid composition in plasma and liver. The same was true of PL fatty acid composition. However, the fatty acid composition of CE differed between liver and plasma. The major fatty acid in liver CE was 18∶1 whereas in plasma it was arachidonic acid (20∶4). Reduced fatty liver was observed in an earlier study when rats were fed ad libitum an ethanol diet containing 20∶4. In the present study, we pair-fed the same diet and fatty liver was not reduced. Dihydroxyacetone, pyruvate and riboflavin did not prevent alcohol-induced fatty liver when 20∶4 was included in the AMA-diet. Our results confirm that dietary dihydroxyacetone, pyruvate and riboflavin prevent alcohol-induced fatty liver, and show that this effect may result from increased mobilization of fat from liver.     

Increased hepatic β-oxidation of docosahexaenoic acid, elongation of eicosapentaenoic acid, and acylation of lysophosphatidate in rats fed a docosahexaenoic acid-enriched diet

Rats were fed a diet supplemented with corn oil (n-3 deficient), soy oil, or a mixture containing 8% 22∶6n-3 ethyl ester for 6 wk. The hepatic capacities for the β-oxidation and synthesis of 22∶6n-3, in addition to the acylation of lysophosphatidate, were tested in vitro. In rats that were fed a 22∶6n-3-enriched diet, both the β-oxidation of 22∶6n-3 and elongation of 20∶5n-3 were enhanced compared to those in rats fed the other diets. Acylation of lysophosphatidate was also enhanced in rats fed a 22∶6n-3-enriched diet, while the rate of dephosphorylation of phosphatidate was not changed. The amount of 22∶6n-3 in the liver was much less than that consumed in a docosahexaenoic acid-enriched diet. These results suggest that a significant amount of dietary 22∶6n-3 was degraded via β-oxidation, and that a portion of the retroconverted 20∶5n-3 was recycled for the synthesis of 22∶6n-3. The recycling of 20∶5n-3 might contribute to the low level of 22∶6n-3 in rats fed an n-3-deficient diet.     

Modulation of prostaglandin synthesis in rat peritoneal macrophages with ω-3 fatty acids

In view of the findings that ω3 fatty acids inhibit the synthesis of prostaglandins (PG) from arachidonic acid (20∶4ω6) and that among immunologically active cells, the macrophage, is a major producer of PG, we undertook a study of the effect of dietary α-linolenic acid (18∶3ω3) on PG synthesis in the macrophage. Rats were fed purified diets containing either 10% corn oil (CO) or linseed oil (LO), providing either a low (1/32) or high (3.5/1) ratio of 18∶3ω3 to 18∶2ω6, respectively, for 6 weeks. Fatty acid analysis of macrophage phospholipids showed that there was an appreciable increase in the percentage of ω3 fatty acids and a decrease in the ω6 fatty acids in macrophages from rats fed the LO diet. The changes in fatty acid composition were associated with a significant decrease in the synthesis of prostaglandin E (PGE) by macrophages from rats fed the LO diet. Macrophages from rats fed the 2 dietary, oils did not differ in their ability to degrade PG, thus the difference in PG production appeared to be a consequence of decreased synthesis only. The dietarily induced changes in PGE synthesis were readily overcome in vitro by culturing macrophages with complexes of fat-free bovine serum albumin and either 20∶4ω6 or 20∶5ω3. Part of a dissertation submitted by Linda J. Magrum in partial fulfillment of the requirements for the Ph.D. degree in Nutritional Sciences. Honored Student Presentation at the AOCS 74th Annual Meeting, Chicago, 1983.