The effects of partially hydrogenated marine oils on the mitochondrial function and membrane phospholipid fatty acids in rat heart

The influence of dietary partially hydrogenated marine oils containing docosenoic acid on rat heart mitochondrial membrane phospholipid fatty acid composition was studied with particular reference to cardiolipin and oxidative phosphorylation. Five groups of male 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. All the cardiac phospholipids investigated were influenced by the experimental diets. An increased amount of arachidonic acid observed in phosphatidylethanolamine (PE) after feeding partially hydrogenated oils suggests a changed regulation of the arachidonic acid metabolism in comparison with PO treatment. 22∶1 originating from the dietary oils was incorporated only to a small extent into phosphatidylcholine (PC) and PE. A selective incorporation of 18∶1 isomers into the 1- and 2-positions of PC and PE with respect to geometry and position of the double bond was observed. Large amounts of 18∶1trans were incorporated into the 1-position of PC and PE, irrespective of the amount of 18∶2 supplemented to the diets, replacing a considerable proportion of stearic acid in this position. After feeding HHO and RSO, the content of 22∶1 in mitochondrial cardiolipin of rat heart was found to be 3% (mainly cetoleic acid) and 10% (mainly erucic acid), respectively, indicating a high affinity forcis isomers of 22∶1, but also a considerable resistance against incorporation oftrans isomers was observed. The ability of rat cardiac mitochondria to oxidize palmitoylcarnitine and to synthesize ATP was depressed after feeding HHO and RSO. Dietarycis isomers of 22∶1 seem to have a specific ability to interfere with cardiac ATP synthesis and also to alter the fatty acid composition of cardiolipin of rat heart.     

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.     

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.     

Comparison of lipid status in the hearts of piglets and rats on short term feeding of marine oils and rapeseed oils

A series of 4 experiments with piglets and one experiment with rats has been conducted to establish the cardiac lipid status of weanling (3 weeks old) male animals fed fats with different contents of docosenoic fatty acids. Experimental fats were rapeseed oil (RSO) (48.0% 22∶1), refined fish oil (RFO) (14.6% 22∶1), partially hydrogenated fish oil (PHFO) (14.3% 22∶1) and lard (0% 22∶1) combined with sunflower seed oil (SFO) in different proportions in diets with 21% total fat. Lipidosis could not be detected in piglets as increased heart weights, by chemical assay for myocardial contents of triglycerides, or by accumulation of docosenoic fatty acids or nonesterified fatty acids (NEFA). In rats, diets with RSO at a level of 16% increased myocardial triglyceride and docosenoic fatty acid contents about 7 times while the effect on cardiac NEFA was inconsistent. Histological examinations of the hearts revealed stainable intracellular fat droplets in some piglets fed 16% RSO for 8 to 13 days, but not after 2,4 and 6 and 16, 19 and 22 days of feeding. After 10 days of feeding, mild to moderate histological lipidosis was found in piglets fed diets containing 2% or more of 22∶1 fatty acids, with no significant difference between RSO, RFO and PHFO in this respect. The same diets in rats gave about 5 times more histological lipidosis than in piglets. This is attributed to a difference in species response, the rat reacting in a more pronounced manner than the piglet. The cardiac lipidosis no-effect level in piglets corresponded to a daily intake of docosenoic fatty acids of 0.4 g per kg body weight. Mild lipidosis was also found in a few animals on docosenoic acid-free diets.     

The effect of dietary erucic acid on cardiac triglycerides and free fatty acid levels in rats

Male Sprague-Dawley rats, 3 weeks of age, were fed semisynthetic diets containing test oils at 20% by weight for 3 days, 1 week, and 16 weeks. The test oils contained up to 22.3% erucic acid. Growth retardation was evident in rats fed rapeseed oil high in erucic acid, and soybean oil and Tower rapeseed oil diets containing about 5% erucic acid. Cardiac triglyceride accumulation was found in rats fed diets containing about 5% erucic acid but not in rats fed Tower rapeseed oil which contains 0.2% of this acid. The cardiac free fatty acid levels were low, 50–100 μg/g of wet heart tissue, and were not affected by feeding diets containing about 5% erucic acid. Feeding a diet containing a high erucic acid rapeseed oil did result in higher free fatty acid levels but only at 3 days and 1 week; the level at 16 weeks was similar to the other oils. The fatty acid analysis of cardiac triglycerides and free fatty acids showed high percentages of erucic acid at 3 days and 1 week; at 16 weeks these levels had declined significantly. The results indicate that the accumulated erucic and eicosenoic acids, at 3 days and 1 week, accounted for the increase in cardiac free fatty acids when rats were fed the high erucic acid rapeseed oil. There appears to be no evidence that the early cardiac triglyceride or free fatty acid accumulation is related to the formation of the long term myocardial lesions. Contribution No. 739 Animal Research Institute.     

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.     

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.     

Cardiopathogenicity of soybean oil and tower rapessed oil triglycerides when fed to male rats

The triglycerides of soybean oil were purified by molecular distillation and those of Tower rapeseed oil by molecular distillation and adsorption chromatography. The original oils and the purified triglycerides were incorporated in semisynthetic diets at 20% by weight and fed for 16 weeks to weanling male Sprague-Dawley rats to compare the nutritional and pathological effects of the oils and their triglyceride fractions on rats. The study was carried out at two independent laboratories. No significant differences were observed between the results of the two establishments. The incidence of myocardial lesions was significantly higher in rats fed Tower rapeseed oil than in those fed soybean oil. Purification of the triglycerides by molecular distillation and adsorption chromatography appeared to have no major effect on the incidence of myocardial lesions. This supports our previous findings that the cardiopathogenicity of the test oils to rats resides in the triglycerides of these oils. Contribution No. 832 from Animal Research Institute and No. I-78 from Engineering and Statistical Research Institute.     

The effects of original and randomized rapeseed oils containing high or very low levels of erucic acid on cardiac lipids and myocardial lesions in rats

The nutritional status of the very lowerucate rapeseed oil,Brassica napus var. ‘Tower,’ was compared with that of the high-erucate oil,Brassica napus var. ‘Target’, as well as with corn oil. The effect of randomization on the nutritional qualities of rapeseed oil was investigated as well. The feeding of diets containing the original and randomized ‘Tower” oil or the original ‘Target’ oil, at the 20% level by weight, gave growth rates which were not significantly different from that for corn oil. However, the randomized ‘Target’ oil gave growth rates which were significantly less than all other groups. The growth results could not be explained simply on the basis of food consumption. The level of triglycerides in the hearts of rats fed the very low-erucate oils was not significantly different from the corn oil group. Triglyceride concentrations in the hearts of animals given the high-erucate oils were 7–12 times greater than all other groups. The level of total fatty acids in tissue phospholipids was the same regardless of dietary treatment. Fatty acid compositions of the tissue lipids were the same in animals fed either the original or randomized rapeseed oils. A much higher incidence of focal myocardial necrosis was found in animals receiving high-erucate rapeseed oil relative to animals given the corn oil. The incidence in rats fed diets containing very low-erucate rapeseed oil was intermediate between these latter two extremes.     

The nutritive value of refined rapeseed oils: A review

Recent findings on the nutritive value of rapeseed oil (RSO) with high erucic acid content have been compared to those of canbra oil (CO), an oil extracted from newly bred Canadian rapeseed with no erucic acid. Erucic acid in diets retards animal growth even if food consumption is not altered. Growth performances of CO are as good as olive or peanut oil. The unbalanced ratio of palmitic acid to monoethylenic acids of CO does not affect rat growth rate. Because of its glyceride structure and high content of erucic acid, RSO has a lower digestibility (81%) than CO (96%) in the rat. Unabsorbed erucic acid is not preferentially excreted as calcium soaps. Interesterification of RSO which converts 31.7% of the erucic chains to the 2 position improves digestibility of erucic acid. 2-Monoerucin is more efficiently absorbed than the free acid. In vivo metabolic conversion of erucic to oleic acid has been proved in the rat. β-oxidation of injected 14-¹⁴C labeled erucic acid proceeded at the same rate as oleic acid but the over-all yield of the reaction was lower. Fatty acid composition of tissues in animals fed RSO or CO is influenced on one hand by erucic and gadoleic (C_20∶1) acids of RSO, and on the other hand by the unbalanced ratio of palmitic-monoethylenic acids and the linolenic acid content of both oils. Nonnegligible amounts of erucic acid are deposited in the body fats of rats, chickens, turkeys, lambs and found in the milk of female rats fed RSO. Almost no erucic acid is incorporated in liver and testicles in the rat and it is not recovered in chicken egg yolk. The effect of RSO on rat reproduction has been re-examined. Dietary lipid and vitamin levels are of great importance in the results obtained. RSO induces myocarditis in several animal species. Similar lesions, although less frequent and severe, have been observed also with CO in the rat. Some authors have reported that erucic acid of RSO was responsible for the effect on heart muscle. Common fatty acid patterns to both RSO and CO have to be further investigated to explain the persisting effect of CO. One of 9 papers presented at the Symposium, “Cruciferous Oil-seeds,” ISF-AOCS World Congress, Chicago, September 1970.     

Changes in fatty acid composition of cardiac mitochondrial phospholipids in rats fed rapeseed oil

Male Wistar rats were fed rapeseed oil containing high or low levels or erucic acid for 20 weeks, and changes in the fatty acid composition of cardiac mitochondrial phospholipids were studied. Treatment with rapeseed oil containing 46.2% erucic acid showed incorporation of 22∶1 (5.6%) into isolated cardiolipin from heart mitochondria. After high or low (3.7%) erucic rapeseed oil feeding, linoleic acid was slightly incorporated into cardiolipin. Moreover, both of these rapeseed oils induced a significant increase of linoleate-arachidonate ratio in phosphatidylethanolamine and phosphatidylcholine. This ratio was also significantly increased in fatty acids esterified to the β-position of these phospholipids. On the basis of such results, we have to consider the role of linolenic acid which is present at a high level in the different rapeseed oils used, as a possible inhibitor of heart microsomal enzymes involved in linoleate arachidonate conversion. Such alterations might account for mitochondrial fragility and myocardial lesions obtained in long term rapeseed oil feeding experiments. ERA-CNRS n^o 070497     

Changes in rat heart phospholipid composition after rapeseed oil feeding

The influence of long duration rapeseed oil feeding with high or low levels of erucic acid has been investigated on rat heart phospholipids. The rats treated for 20 wk with rapeseed oil containing 46.2% erucic acid showed a twofold increase in the sphingomyelin content of the heart. Treatment with primor rapeseed oil (3.7% erucic acid) for 20 wk did not modify phospholipid composition of rat heart. The fatty acid patterns of phosphatidylethanolamine and phosphatidylcholine were slightly influenced by the high erucic rapeseed oil; eicosenoic acid was incorporated preferentially into position one, but erucic acid showed a random distribution in both. After high erucic rapeseed oil feeding, 22∶1 was incorporated into cardiolipin (5.6%) and sphingomyelin (10.5%). The incorporation of 22∶1 into sphingomyelin was associated with an increase of the percentage of 24∶1 (14.6%) and a decrease of saturated long chain fatty acid (22∶0, 24∶0) percentages. Primor rapeseed oil caused a slight increase of 24∶1 and a decrease of 22∶0 and 24∶0 in rat heart sphingomyelin. As cardiolipin is localized in the inner membrane of mitochondria and sphingomyelin in plasma and microsomal membranes, the acyl-moiety alterations of both phospholipids might be correlated to the pathological lesions of rat heart after a long duration of rapeseed oil feeding.     

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.     

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.     

Cardiopathogenicity of rapeseed oils and oil blends differing in erucic,linoleic, and linolenic acid content

Male Wistar rats were fed semipurified diets containing 20% fat for 25 weeks. Ten different oils or oil blends were employed, including rapeseed oils, simulated rapeseed-type oils, and modified rapeseed-type oils. Safflower, soybean, and hydrogenated coconut oils served as control oils. Histopathological examination of the cardiac tissue was conducted at the end of the study and an incidence-severity rating assigned to the lesions induced by each fat. Oils containing high levels of erucic acid (26–30%) induced the most severe cardiac necrosis, irrespective of the source of erucic acid (rapeseed oil or nasturtium oil). Increasing the linoleic: linolenic acid ratio of the high erucic oils to that of soybean oil failed to reduce necrosis, but the absence of linolenic acid from a high erucic acid oil blend resulted in a markedly reduced lesion incidence-severity rating, comparable to those obtained for low erucic acid rapessed oil and soybean oil which were similar. Lowest lesion incidence was obtained with safflower oil and hydrogenated coconut oil. We have postulated that linolenic acid plays a role in the etiology of cardiac necrosis observed when rats are fed diets containing low erucic acid rapeseed oils.     

Exacerbation of heart and liver lesions in rats by feeding of various mildly oxidized fats

Groups of 40 male Charles River rats were fed diets containing cottonseed oil, olive oil, corn oil, soybean oil, coconut oil, chicken fat, beef fat, butter oil, lard and saturated medium chain triglycerides. The fats were fed fresh and after 40 hr aeration at 60 C, which hardly changed peroxide values. In addition, fresh and aerated soybean oil and lard were fed to W/Fu rats. Body weights and life span were significantly influenced by the kind of fat fed, but not by aeration. Many hearts exhibited unspecific focal myocarditis and focal fibrosis. The latter was graded in a blind test, which revealed highly significant differences in the incidence of severe lesions; those fed corn oil had the most, followed by cottonseed oil, soybean oil, olive oil, beef fat, saturated medium chain triglycerides, butter, chicken fat and lard, in that order. Feeding of aerated fat resulted in an increased incidence with six of the eight fats. The W/Fu rats had lower incidences, but those fed soybean oil had more than those fed lard, and aeration led to a higher incidence. Some heart sections stained with Light Green SF Yellowish revealed areas of muscle fibrils that did not accept the stain, probably as a consequence of cellular damage. Higher incidences of this lesion were associated with the same fats as was severe fibrosis, and feeding of aerated fats led to higher incidences. Many livers revealed marked proliferation of bile ducts. The groups fed cottonseed, soybean, olive and corn oils had higher incidences of severe lesions, and feeding of the oxidized oils led to still higher incidences. None of the results appeared to be associated with the fatty acid composition of the fats, which suggested that these long term effects may have been due to minor constituents in the individual fats. One of seven papers presented in the symposium “Biological Significance of Autoxidized and Polymerized Oils,” JOCS-AOCS Joint Meeting, Los Angeles, April 1972.     

Metabolism of erucic acid in perfused rat liver: Increased chain shortening after feeding partially hydrogenated marine oil and rapeseed oil

The metabolism of [14-¹⁴C] erucic acid was studied in perfused livers from rats fed on diets containing partially hydrogenated marine oil or rapeseed oil for three days or three weeks. Control rats were given groundnut oil. Chain-shortening of erucic acid, mainly to 18∶1, was found in all dietary groups. In the marine oil and rapeseed oil groups, the percentage of chain-shortened fatty acids in very low density lipoproteins-triacylglycerols (VLDL-TG) exported from the liver increased after prolonged feeding. A similar increase was found in liver TG only with partially hydrogenated marine oil. This oil, rich intrans fatty acids, thus seemed to be more effective in promoting chain-shortening. The fatty acid composition of the secreted and stored TG differed both with respect to total fatty acids and radioactively labeled fatty acids, indicating that at least 2 different pools of TG exist in the liver. The lack of lipidosis in livers from rats fed dietary oils rich in 22∶1 fatty acids is discussed in relation to these findings. In conclusion, a discussion is presented expressing the view that the reversal of the acute lipidosis in the hearts of rats fed rapeseed oil or partially hydrogenated marine oils is, to a large extent, derived from the increased chain-shortening capacity of erucic acid in liver.     

Ratios of polyunsaturated fatty acids to α-tocopherol in tissues of rats fed corn or soybean oils

This study was part of a larger experiment designed to assess the vitamin E adequacy of corn and soybean oils in relation to their polyunsaturated fatty acids (PUFA). Young male rats were fed a semipurified diet containing 20% corn or soybean oil and adequate selenium. After 8 and 12 weeks, animals were sacrificed, and 7 tissues analyzed for α- and γ-tocopherols and for fatty acids. Calculations were made of the molar ratios of total polyunsaturated fatty acids/α-tocopherol, and also of all polyunsaturated fatty acids, except linoleate, designated polyunsaturated fatty acids>18∶2, to α-tocopherol. It is proposed that the latter ratio may have more significance, physiologically, than when linoleic acid also is considered. Tissues from rats fed corn oil had slightly more favorable (lower) ratios than did tissues from rats fed soybean oil. In both groups, the molar polyunsaturated fatty acids>18∶2/α-tocopherol ratio was lowest for heart and lung, intermediate for muscle and testis, and highest for liver, kidney, and adipose tissue. Since both corn and soybean oils provide adequate vitamin E as determined by several biochemical and physiological parameters, adequate molar ratios of polyunsaturated fatty acids>18∶2/α-tocopherol were: lung, 400; heart and leg muscles, 700; testis, 1100; liver and kidney, 1500–2000; and adipose tissue, 2000.     

Low erucic acid canola oil does not induce heart triglyceride accumulation in neonatal pigs fed formula

Canola oil is not approved for use in infant formula largely because of concerns over possible accumulation of triglyceride in heart as a result of the small amounts of erucic acid (22∶1n−9) in the oil. Therefore, the concentration and composition of heart triglyceride were determined in piglets fed from birth for 10 (n=4–6) or 18 (n=6) d with formula containing about 50% energy fat as 100% canola oil (0.5% 22∶1n−9) or 100% soybean oil, or 26% canola oil or soy oil (blend) with palm, high-oleic sunflower and coconut oil, providing amounts of 16∶0 and 18∶1 closer to milk, or a mix of soy, high-oleic sunflower and flaxseed oils with C₁₆ and C₁₈ fatty acids similar to canola oil but without 22∶1. Biochemical analysis found no differences in heart triglyceride concentrations among the groups at 10 or 18 d. Assessment of heart triglycerides using Oil Red O staining in select treatments confirmed no differences between 10-d-old piglets fed formula with 100% canola oil (n=4), 100% soy oil (n=4), or the soy oil blend (n=2). Levels of 22∶1n−9 in heart triglyceride and phospholipid, however, were higher (P<0.01) in piglets fed 100% canola oil or the canola oil blend, with higher levels found in triglycerides compared with phospholipids. The modest accumulation of 22∶1n−9 associated with feeding canola oil was not associated with biochemical evidence of heart triglyceride accumulation at 10 and 18 d.     

Einfluß der Hydrierung auf Haltbarkeit und ernährungsphysiologische Eigenschaften von Qualitätsrapsölen

Effect of Hydrogenation on Stability and Nutritional Properties of Low-Erucic Rapeseed Oils Low-erucic rapeseed oils, Lesira and Erglu, were converted to more stable edible oils by selective hydrogenation of the linolenic acid moieties while retaining most of the linoleic acid groups. Feeding Lesira oil, hydrogenated Lesira oil, soybean oil and hydrogenated soybean oil to rats did not result in any appreciable differences in growth rates, whereas feeding conventional rapeseed oil caused extensive depression of growth. Among all the groups of animals the group fed conventional rapeseed oil showed the highest weights of heart and liver. The fatty acid patterns of depot and organ lipids did not show any major difference between the groups fed hydrogenated fats and those fed the corresponding unhydrogenated oils. The fatty acid composition of the organ lipids did not reveal deficiency in essential fatty acids. In the groups fed Lesira oil and hydrogenated Lesira oil half of the animals investigated exhibited myocardial lesions of light degree, probably due to the relatively high residual level of long-chain monoenoic fatty acids, whereas in the groups fed soybean oil and hydrogenated soybean oil only one-eighth of the rats examined exhibited such effects. The occurrence and severity of these myocardial lesions are known to be much higher in rats fed conventional rapeseed oils.