Fatty acid pattern of tissue phospholipids in copper and iron deficiencies

Because copper and iron have been reported to be essential cofactors in Δ9 desaturation of fatty acids, the effects of different dietary intakes of copper and iron on tissue fatty acids were studied. Male Long-Evans rats (ten per group) were fed diets containing adequate, deficient or excess copper or iron. On day 42 of the dietary regimen, the animals were killed and tissues and blood were removed for analysis of metals and fatty acids of phospholipids. Compared with the copper-adequate rats, the copper-deficient rats showed increased 18∶0 in liver and decreased 16∶1ω7 in liver, heart and serum. There were no differences for 16∶0 or 18∶1ω9. Intake of excess copper did not cause an increase in products of Δ9 desaturation. Comparisons between iron-deficient and iron-adequate rats showed that iron deficiency increased 18∶2ω6 in liver and serum and decreased 20∶4ω6 in serum only. Relative percentages of 16∶0, 18∶0, 16∶1ω7 and 18∶1ω9 in liver and serum phospholipids were similar for both groups. Intake of excess iron caused a decrease in 18∶2ω6; and 16∶0 and 18∶1ω9 were higher in the liver of the iron-excess group than the iron-deficient group. This study did not support the requirement for copper or iron in the Δ9 desaturation of fatty acids as expressed in phospholipids of liver, heart and serum.     

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.     

Effect of dietary linolenic acid and docosahexaenoic acid on growth and fatty acid composition of rainbow trout (Salmo gairdneri)

Methyl linolenate 18∶3ω3 and docosahexaenoate 22∶6ω3 were incorporated in semipurified diets at several levels and fed to trout previously maintained on a fat-free diet. After 14 weeks, the weight gain and feed conversion of the fish on each diet were determined. The fatty acid composition of the lipid from each group of fish was analyzed by gas liquid chromatography. Both 18∶3ω3 and 22∶6ω3 fed at the 1% level supported maximum growth of the fish. The control group, which were fed no ω3 fatty acids, exhibited a shock syndrome, poor appetite and a very slow growth rate. Tissue fatty acid analysis revealed eicosatrienoic acid 20∶3ω9 accumulated in the phospholipid fraction of this group. The 20∶3ω9 level was lowered when either 18∶3ω3 or 22∶6ω3 was included in the diet. Analysis showed that the dietary 18∶3ω3 was rapidly converted by the fish into 22∶6ω3 with a high concentration in the phospholipid. However 22∶6ω3 fed to the fish remained unchanged and little or no retroconversion of this fatty acid was observed. Presented in part at the AOCS Meeting, Atlantic City, October 1971. Technical paper no. 3247, Oregon Agricultural Experiment Station.     

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.     

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.     

Dietary saturated fat level alters the competition between α-linolenic and linoleic acid

Male weanling rats were fed semi-synthetic diets high in saturated fat (beef tallow) vs high in linoleic acid (safflower oil) with or without high levels of α-linolenic acid (linseed oil) for a period of 28 days. The effect of feeding these diets on cholesterol content and fatty acid composition of serum and liver lipids was examined. Feeding linseed oil with beef tallow or safflower oil had no significant effect on serum levels of cholesterol. Serum cholesterol concentration was higher in animals fed the safflower oil diet than in animals fed the beef tallow diet without linseed oil. Feeding linseed oil lowered the cholesterol content in liver tissue for all dietary treatments tested. Consumption of linseed oil reduced the arachidonic acid content with concomitant increase in linoleic acid in serum and liver lipid fractions only when fed in combination with beef tallow, but not when fed with safflower oil. Similarly, ω3 fatty acids (18∶3ω3, 20∶5ω3, 22∶5ω3, 22∶6ω3) replaced ω6 fatty acids (20∶4ω6, 22∶4ω6) in serum and liver lipid fractions to a greater extent when linseed oil was fed with beef tallow than with safflower oil. The results suggest that the dietary ratio of linoleic acid to saturated fatty acids or of 18∶3ω3 to 18∶2ω6 may be important to determine the cholesterol and arachidonic acid lowering effect of dietary α-linolenic acid.     

Effect of different acids with Δ9,12-dienoic structures on Δ9 desaturation activity in rat liver microsomes

The effect of oral administration, for 24 or 48 hr, of different octadeca fatty acids containing a 9,12-dienoic structure on the fatty acid composition and Δ9 desaturation activity of liver microsomes of rat fed a fat-free diet was studied. The ethyl esters of linoelaidic and γ-linolenic acids, the methyl ester of linoleic acid and free columbinic acid were administered to rats maintained on a fat-free diet. The supplementation of the fat-free diet with linoelaidate produced no relevant changes in the fatty acid composition pattern of liver microsomes and did not modify the percentage of conversion of palmitic to palmitoleic acid. The addition of linoleate or γ-linolenate to the fat-free diet returned liver microsome Δ9 desaturation activity toward the control and partially restored the liver microsome fatty acid spectrum found in the fat-free diet. Columbinic acid (5-trans-9-cis,12-cis-18∶3), which cannot be transformed into arachidonic acid, also decreased the Δ9 desaturation activity enhanced by the fat-free diet and evoked changes in the microsomal fatty acid composition similar to those produced by the ω6 fatty acids. These results suggest that the modulation of Δ9 desaturase activity evoked by dietary administration of unsaturated acids of ω6 series would depend on thecis double bond configuration of these acids.     

A relationship between essential fatty acid and vitamin E deficiency

To test whether vitamin E deficiency might influence the course of essential fatty acid (EFA) deficiency, Long Evans rats were fed diets containing a marginal amount (1.5% of calories) of 18∶2ω6 or 18∶3ω3 fatty acid with complete absence of the other and with or without vitamin E. Vitamin E contents decreased continuously in serum and liver in all rats fed the E-free diets but in the brains of only the rats fed the marginal 18∶3ω3, E-free diet. It is considered that the vitamin E is cooxidized in the liver with 22∶6ω3, since this fatty acid is very low in livers of the rats fed the marginal 18∶2ω6 diet but much higher in livers of the rats fed the marginal 18∶3ω3 diet. Brain 22∶6ω3 values are comparable for both groups. The source of 22∶6ω3 is evidently in the mother's milk, since following weaning there is a precipitous drop in 22∶6ω3 in serum, liver and carcass of rats on the 18∶2ω6-containing diet. No significant signs of EFA deficiency were seen in the E-deficient rats. Operated for the U.S. Department of Energy by the University of California under contract no. DE-AC03-76-SF00012.     

An interaction of DDT in the metabolism of essential fatty acids

The growth of female rats was depressed further by the incorporation of DDT into a ration deficient in essential fatty acids (EFA). With female rats fed a ration supplemented with EFA, DDT produced a slight stimulation in growth. DDT also produced an increase in the 20∶3ω9/20∶4ω6 ratio in liver lipids of male rats fed a ration deficient in EFA. These data indicate an effect in EFA nutrition. Substantial changes in the fatty acid composition of liver lipids resulted from the feeding of DDT. The proportion of 16∶0 was decreased, while that of 18∶0 was increased. With rats on the supplemented rations an increase in the proportion of 20∶4ω6 was observed, while in the deficient rats a comparable increase was observed in the proportion of 20∶3ω9. These changes in fatty acid composition have been related to the proliferation of hepatic smooth endoplasmic reticulum induced by the DDT, and it is suggested that this effect could increase the demand for EFA by the liver, thus influencing EFA nutrition. Technical Paper No. 3156, Oregon Agricultural Experiment Station.     

Influence of dietary fat composition on intestinal absorption in the rat

Omega-3 fatty acids influence the function of the intestinal brush border membrane. For example, the omega-3 fatty acid eicosapentaenoic acid (20∶5ω3) has an antiabsorptive effect on jejunal uptake of glucose. This study was undertaken to determine whether the effect of feeding α-linolenic acid (18∶3ω3) or EPA plus docosahexaenoic acid (22∶6ω3) on intestinal absorption of nutrients was influenced by the major source of dietary lipid, hydrogenated beef tallow or safflower oil. Thein vitro intestinal uptake of glucose, fatty acids and cholesterol was examined in rats fed isocaloric diets for 2 weeks: beef tallow, beef tallow + linolenic acid, beef tallow + eicosapentaenoic acid/docosahexaenoic acid, safflower oil, safflower oil + linolenic acid, or safflower oil + eicosapentaenic acid/docosahexaenoic acid. Eicosapentaenoic acid/docosahexaenoic acid reduced jejunal uptake of 10 and 20 mM glucose only when fed with beef tallow, and not when fed with safflower oil. Linolenic acid had no effect on glucose uptake, regardless of whether it was fed with beef tallow or safflower oil. The jejunal uptake a long-chain fatty acids (18∶0, 18∶2ω6, 18∶3ω3, 20∶4ω6, 20∶5ω3 and 22∶6ω3) and cholesterol was lower in salfflower oil than with beef tallow. When eicosapentaenoic acid/docosahexaenoic acid was given with beef tallow (but not with safflower oil), there was lower uptake of 18∶0, 20∶5ω3 and cholesterol. The demonstration of the inhibitory effect of linolenic acid or eicosapentaenoic acid/docosahexaenoic acid on cholesterol uptake required the feeding of a saturated fatty acid diet (beef tallow). These changes in uptake were not explained by differences in the animals’ food intake, body weight gain or intestinal weight. Feeding safflower oil was associated with an approximately 25% increase in the jejunal and ileal mucosal surface area, but this increase was prevented by combining linolenic acid or eicosapentaenoic acid/docosahexaenoic acid with safflower oil. Different inhibitory patterns were observed when mixtures of fatty acids were present together in the incubation medium, rather than in the diet: for example, when 18∶0 was in the incubation medium with 20∶4ω6, the uptake of 20∶4ω6 was reduced, whereas the uptake was unaffected by 18∶2ω6 or 20∶5ω3. Thus, (1) the inhibitory effect of eicosapentaenoic acid/docosahexaenoic acid on jejunal uptake of glucose, fatty acids and cholesterol was influenced by the major dietary lipid, saturated (beef tallow) or polyunsaturated fatty acid (safflower oil); and (2) different omega-3 fatty acids (linolenic acid versus eicosapentaenoic acid/docosahexaenoic acid) have a variable influence on the intestinal absorption of nutrients.     

The effect of dietary fat level and quality on plasma lipoprotein lipids and plasma fatty acids in normocholesterolemic subjects

This study examined the effect on the plasma lipids and plasma phospholipid and cholesteryl ester fatty acids of changing from a typical western diet to a very low fat (VLF) vegetarian diet containing one egg/day. The effect of the addition of saturated, monounsaturated or polyunsaturated fat (PUFA) to the VLF diet was also examined. Three groups of 10 subjects (6 women, 4 men) were fed the VLF diet (10% energy as fat) for two weeks, and then in the next two weeks the dietary fat in each group was increased by 10% energy/week using butter, olive oil or safflower oil. The fat replaced dietary carbohydrate. The VLF diet reduced both the low density lipoprotein (LDL)-and high density lipoprotein (HDL)-cholesterol levels; addition of the monounsaturated fats and PUFA increased the HDL-cholesterol levels, whereas butter increased the cholesterol levels in both the LDL- and HDL-fractions. The VLF diet led to significant reductions in the proportion of linoleic acid (18∶2ω6) and eicosapentaenoic acid (20∶5ω3) and to increases in palmitoleic (16∶1), eicosatrienoic (20∶3ω6) and arachidonic acids (20∶4ω6) in both phospholipids and cholesteryl esters. Addition of butter reversed the changes seen on the VLF diet, with the exception of 16∶1, which remained elevated. Addition of olive oil resulted in a significant rise in the proportion of 18∶1 and significant decreases in all ω3 PUFA except 22∶6 compared with the usual diet. The addition of safflower oil resulted in significant increases in 18∶2 and 20∶4ω6 and significant decreases in 18∶1, 20∶5ω3 and 22∶5ω3. These results indicate that the reduction of saturated fat content of the diet (<6% dietary energy), either by reducing the total fat content of the diet or by exchanging saturated fat with unsaturated fat, reduced the total plasma cholesterol levels by approximately 12% in normocholesterolemic subjects. Although the VLF vegetarian diet reduced both LDL- and HDL-cholesterol levels, the long-term effects of VLF diets are unlikely to be deteterious since populations which habitually consume these diets have low rates of coronary heart disease. The addition of safflower oil or olive oil to a VLF diet produced favorable changes in the lipoprotein lipid profile compared with the addition of butter. The VLF diets and diets rich in butter, olive oil or safflower oil had different effects on the 20 carbon eicosanoid precursor fatty acids in the plasma. This suggests that advice on plasma lipid lowering should also take into account the effect of the diet on the fatty acid profile of the plasma lipids.     

Does a threshold for the effect of dietary omega-3 fatty acids on the fatty acid composition of nuclear envelope phospholipids exist?

Existence of a dietary maximal level or threshold for incorporation of ω3 fatty acids into membrane phospholipids is of interest as it may further define understanding of the dietary requirement for ω3 fatty acids. To test whether feeding increasing levels of dietary ω3 fatty acids continues to increase membrane ω3 fatty acid content, weanling rats were fed a nutritionally adequate semipurified diet which provided increasing amounts of C₂₀ and C₂₂ ω3 fatty acids, such as 20∶5ω3 and 22∶6ω3. Dietary 20∶5ω3 and 22∶6ω3 were provided by substituting a purified shark oil concentrate of high 22∶6ω3 content for safflower oil high in 18∶2ω6. After four weeks of feeding, nuclear envelopes from four animals in each diet group were prepared, lipid was extracted and phospholipids separated. Arachidonic acid content in membrane phosphatidylcholine, phosphatidylethanolamine, phosphatidylinositol and phosphatidylserine was significantly reduced by feeding increased dietary levels of ω3 fatty acids. Decline of 20∶4ω6 level in phospholipid tended to stabilize when the dietary content of total ω3 fatty acids reached 4–5% of total fatty acids. Above this level, dietary ω3 fatty acids did not result in a further decrease in membrane content of 20∶4nω6. Increase in membrane phospholipid content of 20∶5ω3 occurred as the dietary intake of ω3 fatty acids increased from 1.1% to 5% of total fatty acids. A dietary ω3 fatty acid level of 2.2–3% was sufficient to result in maximum incorporation of 22∶6ω3 into membrane phosphatidylcholine and phosphatidylethanolamine, but not into phosphatidylinositol or phosphatidylserine.     

Severe fatty liver in rats fed a fat-free ethanol diet,and its prevention by small amounts of dietary arachidonate

Rats were fed ethanol and a fat-free diet for 30 days to determine whether dietary fat is needed for the development of fatty liver. The severity of fatty liver was similar to that of rats fed an isocaloric diet with 35% fat. Small amounts (29 mg/day) of dietary arachidonic acid prevented alcoholic fatty liver. Rats fed either the alcohol (AF) or control (CF) fat-free diets developed essential fatty acid deficiency (EFAD) as measured by the triene/tetraene ratio of liver and plasma lipids. Rats fed arachidonic acid (AA, alcohol and CA, control diets) did not develop EFAD. Although EFAD alone did not cause the development of fatty liver, the combination of dietary ethanol and EFAD did. The ratios of 16∶1/16∶0 and 18∶1/18∶0 in liver lipids indicated that desaturase enzymes were less active and lipogenesis was reduced in rats fed the AA diet compared to those fed the AF diet. In contrast, stimulated lipogenesis appears to have been the cause of fatty liver in rats fed the AF diet. Presented at the XII International Congress of Nutrition, San Diego, CA, August 1981. Abbreviations: Diets are indicated as fat-free with ethanol (AF), fat-free without ethanol (CF), or similar diets with 0.9% of the calories as arachidonic acid with (AA) or without (CA) ethanol. The composition of these diets is discribed in the text and Table 1.     

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 dietary fat on diabetes-induced changes in liver microsomal fatty acid composition and glucose-6-phosphatase activity in rats

Experimental diabetes may manifest itself in a defect in liver microsomal fatty acid desaturation and increased activity of glucose-6-phosphatase (G-6-Pase). The present study was designed to determine whether these changes could be normalized by a change in the dietary fat consumed. Control and streptozotocin-induced diabetic rats were fed nutritionally adequate diets which varied in fatty acid composition. Fatty acid analysis of liver microsomal phospholipids revealed that non-diabetic control animals fed saturated fat (beef tallow) or a diet high in ω3 fatty acids (fish oil) exhibited a significantly higher level of 18∶2ω6 and a lower level of 20∶4ω6 in the phosphatidylcholine and phosphatidylethanolamine fractions compared with diabetic animals. Control and diabetic animals fed the high linoleic acid diet had similar levels of 18∶2ω6 in the microsomal phosphatidylcholine and phosphatidylserine fractions. Microsomal G-6-Pase activity was higher in diabetic than in control animals. Activity of G-6-Pase was lower in microsomes of control animals fed the soybean oil or the fish oil diet, but was not significantly reduced in diabetic animals fed high polyunsaturated fats. Blood glucose levels were similar in control groups fed the different diets, but the plasma hemoglobin A1c level was lower in diabetic animals fed the soybean oil diet. Cholesterol and triglyceride levels were lower in diabetic animals fed the fish oil-based diet. The results suggest that dietary fat manipulation has the potential to change at least some of the abnormalities in the microsomal membrane in experimental diabetes.     

Differential effects of dietary linoleic and α-linolenic acid on lipid metabolism in rat tissues

Comparative effects of feeding dietary linoleic (safflower oil) and α-linolenic (linseed oil) acids on the cholesterol content and fatty acid composition of plasma, liver, heart and epididymal fat pads of rats were examined. Animals fed hydrogenated beef tallow were used as isocaloric controls. Plasma cholesterol concentration was lower and the cholesterol level in liver increased in animals fed the safflower oil diet. Feeding the linseed oil diet was more effective in lowering plasma cholesterol content and did not result in cholesterol accumulation in the liver. The cholesterol concentration in heart and the epididymal fat pad was not affected by the type of dietary fatty acid fed. Arachidonic acid content of plasma lipids was significantly elevated in animals fed the safflower oil diet and remained unchanged by feeding the linseed oil diet, when compared with the isocaloric control animals fed hydrogenated beef tallow. Arachidonic acid content of liver and heart lipids was lower in animals fed diets containing safflower oil or linseed oil. Replacement of 50% of the safflower oil in the diet with linseed oil increased α-linolenic, docosapentaenoic and docosahexaenoic acids in plasma, liver, heart and epididymal fat pad lipids. These results suggest that dietary 18∶2ω6 shifts cholesterol from plasma to liver pools followed by redistribution of 20∶4ω6 from tissue to plasma pools. This redistribution pattern was not apparent when 18∶3ω3 was included in the diet.     

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

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

Dietary fats containing concentrates ofcis ortrans octadecenoates and the patterns of polyunsaturated fatty acids of liver phosphatidylcholine and phosphatidylethanolamine

The effects of the mixedcis- 18∶1 isomers and mixedtrans-18∶1 isomers present in partially hydrogenated soybean oil (PHSO) upon the patterns of polyunsaturated fatty acids (PUFA) in liver phosphatidylcholine (PC) and phosphatidylethanolamine (PE) were studied in rats fed concentrates ofcis- 18∶1 ortrans- 18∶1 isomers isolated as triacylglycerides from PHSO. Thecis- 18∶1 andtrans- 18∶1 concentrates were fed at levels equal to those present in PHSO fed at 17.9% of the diet. All diets contained the required amounts of both linoleic and linolenic acids. Thetrans- 18∶1 concentrate was found to suppress the levels of 20∶4ω6 and 20∶3ω9, and to increase the levels of 18∶2ω6 and 20∶5ω3 in PC and PE. Thecis- 18∶1 concentrate suppressed 20∶4ω6 in PC, 20∶5ω3 in PC and PE, and 18∶2ω6 was more effective than thetrans concentrate in suppressing 22∶6ω3. Thetrans- 18∶1 concentrate was more effective in suppressing 20∶4ω6. Thetrans-18∶ isomers appear to modify PUFA metabolism by inhibition of PUFA synthesis, whereas thecis- 18∶1isomers appear to compete with 2-position fatty acyl transfer and to inhibit ω3 PUFA acylation.     

Response of docosapentaenoic acids of rat heart phospholipids to dietary fat

Groups of male Holtzman strain rats were fed from weanling one of the following diets: 20% hydrogenated soybean fat (20% HF), and 20% HF plus 2%, 3% and 4% corn oil, respectively, for 20 weeks. The animals were killed, and the heart phospholipid fractions isolated by chromatographic procedures. The levels and distribution of the docosapolyenoic acids, especially 22∶5ω3, were compared among the animals fed the corn oil supplemented and nonsupplemented diets. Although dietary linolenate (18∶3ω3) level was very low in the nonsupplemented diet, 22∶5ω3 accounted for 8.4% of the total fatty acids of heart total phospholipids when this diet was fed-half the level of total eicosatetraenoic acids. The amounts of 22∶5ω3 were decreased by corn oil supplementation of the diet and got down to the “normal” range of 2.0–2.5% at corn oil supplementation levels greater than 2%. The docosapolyenoic acids were confined largely to the phosphatidylcholine and phosphatidylethanolamine classes of phospholipids. These findings are discussed from the standpoint of the structural role of the phospholipids in the heart subcellular fractions.     

Isolated brain capillary endothelia: Influence of various levels of essential fatty acids on the acyl group composition of glycerophospholipids

On day seven of gestation, Wistar rats were assigned to a high essential fatty acid (EFA), low EFA, or a fat free diet. The same diets were continued during lactation. On weaning, the offspring were fed the same diets as their mother. Rats were killed at 222 days, brain capillary endothelia isolated, and total lipids extracted from the purified capillaries. The composition of the constituent fatty acids of ethanolamine glycerophospholipid (EGP), choline glycerophospholipid (CGP), and the alk-1-eny EGP composition from each diet is reported. A decrease in dietary EFA led to reduced proportions of total saturated acyl groups in EGP with no change observed in the total saturated acyl groups from CGP, and an increase in monoenoic fatty acids, particularly 18∶1n−9 for each phospholipid class. The proportions of 20∶4n−6 in alk-1-enyl EGP were reduced in fat-free fed animals. In addition, the relationship between 20∶3n−9 and 20∶4n−6 fatty acids in brain capillary endothelia were markedly increased with a reduction in dietary fat. Low EFA and fat deficient animals showed a tendency to sequester 22∶6n−3.