Free fatty acid fractions from some vegetable oils exhibit reduced survival time-shortening activity in stroke-prone spontaneously hypertensive rats

Previously, we demonstrated that several vegetable oils that included low-erucic rapeseed oil markedly shortened the survival time (by ∼40%) of stroke-prone spontaneously hypertensive (SHRSP) rats as compared with perilla oil, soybean oil, and fish oil. We considered that a factor other than fatty acids is toxic to SHRSP rats, because the survival time-shortening activity could not be accounted for by the fatty acid compositions of these oils. In fact, a free fatty acid (FFA) fraction derived from lipase-treated rapeseed oil was found to be essentially devoid of such activity. A high-oleate safflower oil/safflower oil/perilla oil mixture exhibited a survival time-shortening activity comparable to that of rapeseed oil, but the activity of this mixed oil was also reduced by lipase treatment. A partially hydrogenated soybean oil shortened the survival time by ∼40%, but a FFA fraction derived from lipase-treated partially hydrogenated soybean oil shortened it by 13% compared with soybean oil. Fatty acid compositions of the rapeseed oil and a FFA fraction derived from lipase-treated rapeseed oil were similar, but those of hepatic phospholipids of rats fed the oil and FFA were slightly but significantly different. These results support the interpretation that the survival time-shortening activity exhibited by some vegetable oils is due to minor components other than fatty acids, and that an active component(s) were produced in or contaminated soybean oil during the partial hydrogenation processes.     

Unusual effects of some vegetable oils on the survival time of stroke-prone spontaneously hypertensive rats

Preliminary experiments have shown that a diet containing 10% rapeseed oil (low-erucic acid) markedly shortens the survival time of stroke-prone spontaneously hypertensive (SHRSP) rats under 1% NaCl loading as compared with diets containing perilla oil or soybean oil. High-oleate safflower oil and high-oleate sunflower oil were found to have survival time-shortening activities comparable to that of rapeseed oil; olive oil had slightly less activity. A mixture was made of soybean oil, perilla oil, and triolein partially purified from high-oleate sunflower oil to adjust the fatty acid composition to that of rapeseed oil. The survival time of this triolein/mixed oil group was between those of the rapessed oil and soybean oil groups. When 1% NaCl was replaced with tap water, the survival time was prolonged by ∼80%. Under these conditions, the rapeseed oil and evening primrose oil shortened the survival time by ∼40% as compared with n-3 fatty acid-rich perilla and fish oil; lard, soybean oil, and safflower oil with relatively high n-6/n-3 ratios shortened the survival time by roughly 10%. The observed unusual survival time-shortening activities of some vegetable oils (rapeseed, high-oleate safflower, high-oleate sunflower, olive, and evening primrose oil) may not be due to their unique fatty acid compositions, but these results suggest that these vegetable oils contain factor(s) which are detrimental to SHRSP rats.     

The effect of dietary partially hydrogenated marine oils on desaturation of fatty acids in rat liver microsomes

The influence of dietary partially hydrogenated marine oils on distribution of phospholipid fatty acids in rat liver microsomes was studied with particular reference to the metabolism of linoleic acid. Five groups of weanling rats were fed diets containing 20% (w/w) peanut oil (PO), partially hydrogenated peanut oil (HPO), partially hydrogenated Norwegian capelin oil (HCO), partially hydrogenated herring oil (HHO), and rapeseed oil (RSO) for 10 weeks. The partially hydrogenated oils were supplemented with linoleic acid corresponding to 4.6 cal % in the diets. Accumulation of linoleic acid and reduced amount of total linoleic acid metabolites were observed in liver microsomal phospholipids from rats fed partially hydrogenated oils as compared to PO feeding. The most striking effects on the distribution of ω6-polyunsaturated fatty acids was obtained after feeding HHO, a marine oil with a moderate content oftrans fatty acids in comparison with HPO but rich in isomers of eicosenoic and docosenoic acids. Liver microsomal Δ⁶-as well as Δ⁶-desaturase activities as measured in vitro were reduced in rats kept on HHO as compared to PO dietary treatment. The results obtained suggest that the dietary influence of partially hydrogenated marine oils on the metabolism of linoleic acid might be better related to the intake of isomeric eicosenoic and docosenoic acids than to the total intake oftrans fatty acids.     

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.     

Influence of partially hydrogenated vegetable and marine oils on lipid metabolism in rat liver and heart

Partially hydrogenated marine oils containing 18∶1-, 20∶1- and 22∶1-isomers and partially hydrogenated peanut oil containing 18∶1-isomers were fed as 24–28 wt % of the diet with or without supplement of linoleic acid. Reference groups were fed peanut, soybean, or rapeseed oils with low or high erucic acid content. Dietary monoene isomers reduced the conversion of linoleic acid into arachidonic acid and the deposition of the latter in liver and heart phosphatidylcholine. This effect was more pronounced for the partially hydrogenated marine oils than for the partially hydrogenated peanut oil. The content oftrans fatty acids in liver phospholipids was similar in groups fed partially hydrogenated fats. The distribution of various phospholipids in heart and liver was unaffected by the dietary fat. The decrease in deposition of arachidonic acid in rats fed partially hydrogenated marine oils was shown in vitro to be a consequence of lower Δ6-desaturase activity rather than an increase in the peroxisomal β-oxidation of arachidonic acid. The lower amounts of arachidonic acid deposited may be a result of competition in the Δ6-desaturation not only from the C22-and C20-monoenoic fatty acids originally present in the partially hydrogenated marine oil, but also from C18- and C16-monoenes produced by peroxisomal β-oxidation of the long-chain fatty acids. Part of this work was presented at the ISF-AOCS Congress, New York City, 1980.     

Influence of sources of dietary oils on the life span of stroke-prone spontaneously hypertensive rats

In recent studies, the life span of stroke-prone spontaneously hypertensive (SHRSP) rats was altered by a variety of dietary fats. It was relatively shorter in rats fed canola oil as the sole source of fat. The present study was performed to find out whether the fatty acid profile and the high content of sulfur compounds in canola oil could modulate the life span of SHRSP rats. SHRSP rats (47 d old, n=23/group) were matched by body weight and systolic blood pressure and fed semipurified diets containing 10% canola oil, high-palmitic canola oil, low-sulfur canola oil, soybean oil, high-oleic safflower oil, a fat blend that mimicked the fatty acid composition of canola oil, or a fat blend high in saturated fatty acids. A 1% sodium chloride solution was used as drinking water to induce hypertension. After consuming the diets for 37 d, five rats from each dietary group were killed for collection of blood and tissue samples for biochemical analysis. The 18 remaining animals from each group were used for determining their life span. The mean survival time of SHRSP rats fed canola oil (87.4±4.0 d) was not significantly different (P>0.05) from those fed low-sulfur canola oil (89.7±8.5 d), suggesting that content of sulfur in canola oil has no effect on the life span of SHRSP rats. The SHRSP rats fed the noncanola oil-based diets lived longer (mean survival time difference was 6–13 d, P<0.05) than those fed canola and low-sulfur canola oils. No marked differences in the survival times were observed among the noncanola oil-based groups. The fatty acid composition of the dietary oils and of red blood cells and liver of SHRSP rats killed after 37 d of treatment showed no relationship with the survival times. These results suggest that the fatty acid profile of vegetable oils plays no important role on the life span of SHRSP rat. However, phytosterols in the dietary oils and in liver and brain were inversely correlated with the mean survival times, indicating that the differential effects of vegetable oils might be ascribed, at least partly, to their different phytosterol contents.     

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.     

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.     

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

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

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.     

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.     

Effects of diets high in saturated fat and cholesterol on the lipid composition of canine platelets

The phospholipid composition of platelets from dogs on various experimental diets was determined. Thyroidectomized foxhounds were fed a control diet or the control diet supplemented with (1) beef tallow, (2) beef tallow and cholesterol, or (3) beef tallow, cholesterol, and safflower oil for 23 weeks prior to isolation of platelets. Platelets from animals fed the control diet contained 36.7% phosphatidylcholine (PC), 22.8% phosphatidylethanolamine (PE), 18.4% sphingomyelin (Sph), 11.8% phosphatidylserine (PS), 6.3% phosphatidylinositol (PI), and 2.2% lysophosphatidylcholine. The PE was 77.6% in the plasmalogen form. No highly significant changes in the phospholipid class composition resulted from the experimental diets. Cholesterol supplementation of the diets, however, caused consistent alterations in the fatty acid compositions of the platelet phospholipids including increases in the percentages of 18∶1ω9 (oleic acid), 18∶2ω6 (linoleic acid), and 20∶3ω6 (homo-gamma linolenic acid) and a decrease in the percentage of 20∶4ω6 (arachidonic acid). Addition of safflower oil to the tallow-cholesterol diet partially reversed these effects. These cholesterol-induced alterations in fatty acid composition could be due to exchange with plasma lipids, de novo synthesis, or altered platelet metabolism. The mechanism remains to be determined. Der. Nelson’s current affiliation is the Lipid Metabolism Branch, Division of Heart and Vascular Diseases, National Heart, Lung, and Blood Institute.     

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.     

The circadian cycles of plasma corticosterone and adrenal cholesteryl esters in the normal and EFA-deficient female rat

In female rats subjected to a 12 hr light-12 hr darkness schedule and fed a semipurified diet containing 10% corn oil, plasma corticosterone concentration showed a monophasic circadian cycle with minimum and maximum concentrations at the start of the light and dark periods, respectively. Adrenal total cholesteryl ester concentration was inversely related to plasma corticosterone, as were those of several of the individual esters; changes in cholesteryl ester concentration appeared to follow rather than precede changes in plasma corticosterone. There was preferential depletion of the cholesteryl esters of 18∶1, 18∶2ω6, and 20∶4ω6 during glucocorticoid secretion. [Abbreviations: EFA, essential fatty acid (s);X:YωZ, fatty acid with X carbon atoms and Y olefinic bonds with the terminal double bond Z carbon atoms from the methyl group.] In female rats fed hydrogenated coconut oil (EFA-deficient), a monophasic cycle for plasma corticosterone was also observed, but the peak was much broader than that recorded for rats fed corn oil, although minima and maxima occurred at similar times for the two groups. No significant cycle of adrenal total cholesteryl esters was evident in the deficient rats, but the 20∶3ω9 and 22∶3ω9 esters did decrease significantly during the period of high plasma corticosterone concentration. Preferential net decreases in adrenal cholesteryl esters during corticosteroidogenesis were more apparent in normal than in EFA-deficient rats.     

Incorporation ofcis- andtrans-octadecenoic acids into the membranes of rat liver mitochondria

The incorporation of dietary isomeric fatty acids into the membranes of liver mitochondria was investigated. Three groups of rats were fed diets containing 3% sunflower seed oil plus 15%, 20%, or 25% partially hydrogenated arachis oil. A fourth group was fed 25% partially hydrogenated arachis oil, but no sunflower seed oil. All diets were given for 3, 6, or 10 weeks. After 10 weeks, the content oftrans fatty acids in the lipids of the mitochondrial membranes was 15–19% of the total fatty acids. The composition of thetrans- and thecis-octadecenoic acids in the lipids of the mitochondrial membranes was similar for all groups supplemented with sunflower seed oil (SO), irrespective of time and dietary level of partially hydrogenated arachis oil (HAO). Thecis 18∶1 (n−8), which was a major isomer of the partially hydrogenated arachis oil, was almost excluded from the mitochondrial fatty acids. Likewise, the content oftrans 18∶1 (n−8) was considerably lower in the mitochondrial lipids than in the diet. On the contrary, the content oftrans 18∶1 (n−6) was higher in the mitochondrial lipids than in the diet. In the group fed without sunflower seed oil, isomers of linoleic acid and arachidonic acid were observed in the lipids of mitochondrial membranes. Presented in part at the ISF Congress, Marseille, September 1976.     

Effects of different dietary intake of essential fatty acids on C20∶3ω6 and C20∶4ω6 serum levels in human adults

Four diets which differed in fatty acid composition were provided for five months each to a group of 24 healthy nun volunteers. The diets contained 54% carbohydrates, 16% proteins and 30% lipids. One-third of the lipid part remained unchanged during the whole study, and two-thirds were modified during each period. For this latter portion, one of the following dietary fats was used: sunflower oil, peanut oil, low erucic acid rapeseed (LEAR) oil or milk fats. This procedure allowed an evaluation of the effects of various amounts of dietary linoleic acid (C18∶2ω6) and alpha-linolenic acid (C18∶3ω3) on the serum level of their metabolites. A diet providing a large amount of linoleic acid (14% of the total caloric intake) resulted in low levels of dihomo-gamma-linolenic acid (C20∶3ω6) and arachidonic acid (C20∶4ω6) in serum phospholipids and cholesteryl esters. A diet providing a small amount of linoleic acid (0.6% to 1.3% of the total caloric intake) induced high levels of ω6 fatty acid derivatives. Intermediate serum levels of C20∶3ω6 and C20∶4ω6 were found with a linoleic acid supply of about 6.5% of the total caloric intake. Serum levels of ω6 metabolites were not different after two diets providing a similar supply of C18∶2ω6 (4.5% to 6.5% of the total caloric intake), although in one of them the supply of C18∶3ω3 was higher (1.5% for LEAR oil versus 0.13% for peanut oil). Under our experimental conditions (healthy human adults fed on a normo-caloric diet with 30% lipids), we tried to determine PUFA (linoleic and linolenic acid) allowances which should be recommended for adults. The aim of the study was to obtain a hypocholesterolemic or normocholesterolemic effect while keeping normal 20∶3ω6 and 20∶4ω6 serum levels which would evidence a normal linoleic acid metabolism. The amounts recommended are: linoleic acid 5 to 6% of the total calories; alpha-linolenic acid 0.5 to 1% of the total calories.     

Essential fatty acid-deficient rats: II. On the fatty acid composition of partially hydrogenated arachis,soybean and herring oils and of normal,refined arachis oil

The fatty acid composition of partially hydrogenated arachis (HAO), partially hydrogenated soybean (HSO) and partially hydrogenated herring (HHO) oils and of a normal, refined arachis oil (AO) was studied in detail by means of direct gas liquid chromatography, ultraviolet and infrared spectrophotometry and by thin layer chromatography fractionation on silver nitrate-silica gel plates followed by gas liquid chromatography. It was shown that the partially hydrogenated oils all contained fatty acids withtrans double bonds. In the plant oils, thetrans acids were present mainly as elaidic acid. The HHO showed an almost equal distribution betweentrans 18∶1 ω9,trans 20∶1 ω>9 andtrans 22∶1 ω>9. Sometrans configuration was also found in the C₂₀-and C₂₂-dienes and trienes of the HHO. In all the oils, conjugated fatty acids were present in minor amounts only (<0.5%). Special attention was given to the ω-acids known to be of specific nutritional value. The HSO contained about 32% linoleic acid, whereas the content ofcis, trans+trans, cis andtrans, trans octadecadienoic isomers was 1.7% and 0.5%, respectively. The amount of linoleic acid in the HSO was even higher than that of AO (29%). The HAO contained only 0.8% 18∶2 ω6 (linoleic acid). Further, two 18∶2 fatty acids with ω>6, acis, cis and atrans, trans isomer, were present in small amounts. The HHO contained 0.5% 18∶2 ω6 (linoleic acid). Isomers of 18∶2 ω>6 were also found in the HHO. They may be hydrogenation products of higher unsaturated C₁₈-acids orginally present. All the C₂₀- and C₂₂-dienes and trienes were shown to have an ω-chain greater than 6. Fatty acids with ω6-structure were not formed during partial hydrogenation of the oils studied.     

Maternal diet and brain fatty acids in young rats

In order to determine to what extent maternal diet influenced the brain lipids of young rats, female rats were maintained on diets differing in fatty acid composition. Fatty acid determinations on the total brain lipids of the young from these dams indicated that the maternal dietary lipids influence the polyunsaturated fatty acid composition of these animals. A maternal diet with a high linoleic-linolenic acid ratio (corn oil) resulted in lower levels of 22∶6ω3 and higher levels of 22∶5ω6 than one with a low linoleic-linolenic acid ratio (grain). Transfer of young rats at birth to a foster mother, which was fed a diet differing from that of the natural dam, resulted in brain polyunsaturated fatty acid patterns at weaning similar to those of the natural young, and suckling, of the foster mother, thus indicating that the maternal diet in the immediate postnatal period can modify the brain lipids of young rats prior to weaning. The brain lipids of young rats from dams which were fed corn oil exhibited a marked tendency to incorporate 22∶6ω3 in the immediate postnatal period in spite of a relatively high linoleic-linolenic acid ratio in the milk.     

Comparative study of the blood pressure effects of four different vegetable fats on young,spontaneously hypertensive rats

Following the suckling period, four groups of male four-week-old spontaneously hypertensive rats (SHR) were fed semisynthetic diets with 14% (by weight) of either sunflower seed oil [46% 18∶2(n−6); linoleic acid (LA)-rich], linseed oil [62.5% 18∶3(n−3)+12.9% 18∶2(n−6); α-linolenic acid (LNA)-rich], evening primrose oil [9.2% 18∶3(n−6)+71% 18∶2(n−6); γ-linolenic acid (LNA)-rich] or hydrogenated palm kernel fat [1.5% 18∶2(n−6); polyunsaturated fatty acid (PUFA)-deficient], respectively, up to an age of 18 wk. All diets enriched with PUFA provoked an attenuation of hypertension development. The effect was lowest in the LA-rich group and highest in the γ-LNA-rich group. Differences in fatty acid composition of renal phospholipids between groups reflect the fatty acids present in the respective dietary fats. Renomedullary production of PGF_2α was significantly reduced in α-LNA-rich and slightly diminished in γ-LNA-rich fed rats. Aortic formation of 6-keto-PGF_1α and TXB₂ was increased in animals fed the γ-LNA-rich diet. Thus, the attenuation of hypertension development cannot be explained only by changes in prostanoid formation. Other mechanisms possibly involved should be pursued.     

Effect of high fat corn oil,olive oil and fish oil on phospholipid fatty acid composition in male F344 rats

Epidemiological and laboratory animal model studies have provided evidence that the effect of dietary fat on colon tumorigenesis depends on the amount of fat and its composition. Because of the importance of the composition of dietary fat and of tissue membrane fatty acid composition in tumor promotion, experiments were designed to investigate the relative effects of high fat diets rich in ω3, ω6 and ω9 fatty acids and colon carcinogen on the phospholipid fatty acid composition of liver, colon, small intestine, erythrocytes and blood plasma. At 6 wk of age, groups of animals were fed diets containing 5% corn oil (LFCO), 23.5% corn oil (HFCO), 23.5% olive oil (HFOO), and 20.5% fish oil plus 3% corn oil (HFFO). Two weeks later all the animals except the vehicle-treated animals received azoxymethanes.c. once weekly for 2 wk at a dose rate of 15 mg/kg body weight. Animals were sacrificed 5 d later and liver, colon, small intestine and erythrocytes and blood plasma were analyzed for phospholipid fatty acids. The results indicate that the phospholipid fatty acid composition of liver, colon and small intestine of HFCO diet fed animals, were not significantly different from those fed the LFCO diet. The levels of palmitoleic acid and linoleic acid were increased in erythrocytes and blood plasma of the animals fed the HFCO diet compared to those fed the LFCO diet. Feeding the HFCO diet significantly increased the oleic acid content and decreased the linoleic acid and arachidonic acid levels in various organs when compared to the HFCO diet. Animals fed the HFFO diet showed a marked increase in eicosapentaenoic acid and docosahexaenoic acid and a decrease in linoleic acid and arachidonic acid levels as compared to those fed the HFCO diet. The results also indicate that carcinogen treatment had only a minimal effect on the phospholipid fatty acid composition.