Cardiac lipids in rats and gerbils fed oils containing C 22 fatty acids.
TL;DR: Oil fromLimnanthes douglasii and hydrogenated herring oil also increased the amount of cardiac fatty acids in gerbils, and a high intake of docosenoic acid was common to the animals displaying the cardiac alterations.
Abstract: Docosenoic acid from rapeseed oil or herring oil in the diet of the young rat promoted an accumulation of cardiac lipid. The triglyceride fraction accounted for most of the deposited fat and contained a high concentration of the docosenoic acid. Liquid rapeseed oil, partially hydrogenated rapeseed oil or partially hydrogenated herring oil increased the amount of cardiac fatty acids at 1 week and led to the development of degenerative lesions at 16 weeks. Whale or seal oils low in C22 fatty acids produced little effect on the amount of lipids in the heart of rats or gerbils. The latter species receiving 20% rapeseed oil in the diet showed a peak in cardiac lipid deposition at 4 days with similar levels of total fatty acids to that of rats, but with a lower concentration of erucic acid. Oil fromLimnanthes douglasii and hydrogenated herring oil also increased the amount of cardiac fatty acids in gerbils. A high intake of docosenoic acid was common to the animals displaying the cardiac alterations.
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TL;DR: Peroxisomal beta-oxidation in rat liver is characterized by a high extent of induction following exposure of rats to a variety of amphipathic compounds possessing a carboxylic-, or sulphonic acid group, and recent findings of the involvement of a member of the steroid hormone receptor superfamily during induction suggest that induction of peroxisome beta-Oxidation represents another regulatory phenomenon controlled by nuclear receptor proteins.
269 citations
TL;DR: A role is proposed for peroxisomal beta-oxidation in relation to the metabolism of fatty acids that are poorly oxidized by mitochondrial beta-Oxidation, and, in general, as regards oxidation of fatty amino acids during periods of sustained high hepatic influx of fatty fatty acids.
Abstract: 1. Rat liver peroxisomal fractions were isolated in iso-osmotic Percoll gradients by using vertical-rotor centrifugation. The fractions obtained with rats given various dietary treatments were characterized. 2. The effect on peroxisomal beta-oxidation of feeding 15% by wt. of dietary fat for 3 weeks was investigated. High-fat diets caused induction of peroxisomal beta-oxidation, but diets rich in very-long-chain mono-unsaturated fatty acids produced a more marked induction. 3. Peroxisomal beta-oxidation induced by diets rich in very-long-chain mono-unsaturated fatty acids can oxidize such acids. Trans-isomers of mono-unsaturated fatty acids are oxidized at rates that are faster than, or similar to, those obtained with corresponding cis-isomers. 4. Rates of oxidation of [14-14C]erucic acid by isolated rat hepatocytes isolated from rats fed on high-fat diets increased with the time on those diets in a fashion very similar to that previously reported for peroxisomal beta-oxidation [see Neat, Thomassen & Osmundsen (1980) Biochem, J. 186, 369-371]. 5. Total liver capacities for peroxisomal beta-oxidation (expressed as acetyl groups produced per min) were estimated to range from 10 to 30% of mitochondrial capacities, depending on dietary treatment and fatty acid substrate. A role is proposed for peroxisomal beta-oxidation in relation to the metabolism of fatty acids that are poorly oxidized by mitochondrial beta-oxidation, and, in general, as regards oxidation of fatty acids during periods of sustained high hepatic influx of fatty acids.
153 citations
TL;DR: In this paper, a tolerable daily intake (TDI) of 7 mg/kg body weight (bw) per day for erucic acid was established, based on a no observed adverse effect level of 0.7 g/kg bw per day.
Abstract: Erucic acid is the trivial name of the fatty acid cis-13-docosenoic acid and occurs at high concentrations mainly in the seeds of species of the Brassicaceae (e.g. rape seed or mustard seed). The European Commission requested EFSA to deliver a scientific opinion on the risks for animal and human health related to the presence of erucic acid in feed and food. For most humans, the main contributor to dietary exposure to erucic acid was the food group ‘Fine bakery wares’. In ‘Infants’, ‘Food for infants and small children’ was the main contributor to exposure. The heart is the principal target organ for toxic effects after exposure. Myocardial lipidosis was identified as the critical effect for chronic exposure to erucic acid. This effect is reversible and transient during prolonged exposure. A tolerable daily intake (TDI) of 7 mg/kg body weight (bw) per day for erucic acid was established, based on a no observed adverse effect level of 0.7 g/kg bw per day for lipidosis in young rats and newborn piglets. Mean chronic exposure of the different groups of the population did not exceed the TDI. The 95th percentile dietary exposure level was highest in infants and other children, ranging from 1.3 to 7.4 mg/kg bw per day; the higher level being at the level of the TDI. This may indicate a risk for young individuals with high erucic acid exposure. In pigs, levels of erucic acid are unlikely to represent a health concern. However, for poultry, the small margin between the lowest observed adverse effect level (LOAEL) and the estimated exposure may indicate a health risk where maximum inclusion rates are applied. Due to the absence of adequate data, the risk for ruminants, horses, fish and rabbits could not be assessed.
129 citations
TL;DR: The finding that oxidation of erucoyl carnitine by rat liver mitochondrial from clofibrate-treated rats was not markedly different from the rate obtained with control mitochondria, while oxidation of [14-'4C]erucate by hepatocytes isolated from cl ofibrates treated rats was markedly increased suggested that a nonmitochondrial process might be significant for cellular oxidation of C,,,-fatty acids.
Abstract: Rats fed on diets containing appreciable amounts of rapeseed oil or partially hydrogenated marine oil have been shown to develop transient muscular lipidosis, usually most marked in heart muscle.',' The lipidosis usually decreases after 3 to 4 days of dietary treatment, although a mild lipidosis often has been observed for an extended period following the initial acute lipidosis. With rapeseed oil diets necrotic scars have also been observed following long-term dietary treatment? The transient nature of the lipidosis suggests that metabolic adaptation occurred, facilitating recovery from a state where muscle tissues were faced with lipids that their metabolism were less able to handle. A number of rapeseed oils, like partially hydrogenated marine oil, contain a high proportion of C,,,-fatty acids. In rapeseed oil this is erucic acid (cis-C,,,,w 9). Partially hydrogenated marine oil also contain cetoleic acid (cis-C,, lw 11) together with a series of cis and trans positional isomers formed during the hydrogenation process?' These are fatty acids which are known to be poorly oxidized by mitochondrial /%oxidation.' Partially hydrogenated marine oil, in addition, contains appreciable amounts trans-fatty acids possessing 16-20 carbon atoms.' Most trans-fatty acids are poorly oxidized by mitochondrial P-~xida t ion .~ As there is no evidence of cardiac lipidosis resulting from similar treatments with dietary oils not containing these types of fatty acids [e.g. soya-bean oil), it seems plausible to link lipidosis with intake of very long chain fatty acids and their metabolism. It has been shown that perfused livers from rats fed on diets containing partially hydrogenated marine oil or rapeseed oil contain an increased portion of C,, and C,, fatty acids, and also showed increased ability to metabolize added labeled erucic A similar observation was also made with hepatocytes isolated from rats fed on a diet containing partially hydrogenated marine O ~ I . ~ . ' ~ Clofibrate treatment is known to cause peroxisomal proliferation.\" and to cause induction of peroxisomal @-oxidation. The finding that oxidation of erucoyl carnitine by rat liver mitochondrial from clofibrate-treated rats was not markedly different from the rate obtained with control mitochondria, while oxidation of [14-'4C]erucate by hepatocytes isolated from clofibrate-treated rats was markedly increased,\" suggested that a nonmitochondrial process might be significant for cellular oxidation of C,, ,-fatty acids. The striking parallel between effects due to partially hydrogenated marine oil diet and clofibrate treatment suggested that peroxisomal fatty acid metabolism could be involved.
104 citations
TL;DR: The high levels of free fatty acid and diglyceride reported in the cardiac lipids of rats fed rapeseed oil suggest that extensive autolysis occurs during homogenization with a rotating blade-type homogenizer.
101 citations
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162 citations
TL;DR: It was shown that the fatty infiltration of the heart and skeletal muscles occurs after 1 day of RSO feeding and becomes most severe after 3–6 days, and erucic acid appears to be the constituent in RSO responsible for its pathological effects.
Abstract: The pathological effects of dietary rapeseed oil (RSO) in rats have been investigated. Rats given 60 cal% RSO for 2 weeks showed fatty accumulation in the heart, skeletal muscles and adrenals. In another experiment, 60 cal% RSO was given for 2, 4, 8 and 16 weeks. The fatty infiltration of the skeletal muscles, adrenals and hearts regressed with the increase in the dietary period, but in the heart, necrotic foci, aggregations of mono-nuclear cells, and an increase in the connective tissue elements ensued. From a 2-week dose-response study, 20 cal% RSO was established as the minimum level causing the fatty accumulation. Similar lesions were produced by feeding RSO or glyceryl trierucate on an isocaloric erucic acid basis. Erucic acid thus appears to be the constituent in RSO responsible for its pathological effects. It was shown that the fatty infiltration of the heart and skeletal muscles occurs after 1 day of RSO feeding and becomes most severe after 3–6 days. The myocardial fatty infiltration in rats given RSO for 3 days markedly decreased after the feeding of this oil had been discontinued. It is suggested that the fatty infiltration of the heart and skeletal muscles by RSO reflects a slower oxidation of fatty acids in these organs.
140 citations
TL;DR: In this paper, the composition of the cardiac fatty acids and the histopathology in rats receiving oil as 40% of calories were studied after 3, 7, 14 and 28 days.
97 citations
TL;DR: The pigs appeared to be in general more sensitive than rats to the high fat content of the diet, for all the examined pigs showed histological evidence of thyroid hyperfunction, interstitial myocarditis, and inflammatory reaction in the gastric mucosa.
Abstract: Rats were fed diets in which rapeseed oil provided 0, 15, 30, 50 or 70 per cent of the calories. The controls were rats whose diet contained 30 or 70 cal. per cent of soybean oil. The diet containing 50 and especially that containing 70 per cent of rapeseed oil clearly retarded the growth of the animals. These groups also showed interstitial inflammatory changes in the myocardium. Similar changes were not found when 30 cal. per cent or less rapeseed oil was given. The histological changes were evidently produced by the rapeseed oil, since soybean oil even at the level of 70 cal. per cent produced no changes.
90 citations
TL;DR: Seed oils from five species ofCuphea show three distinct patterns of fatty acid composition as mentioned in this paper : C. hookeriana and C. painteri oils contain ca. 70% caprylic acid, C. ignea and c.llavea oils have over 80% capric acid, andC. carthagenensis oil contains 57% lauric and 18% ca.
Abstract: Seed oils from five species ofCuphea show three distinct patterns of fatty acid composition.C. hookeriana andC. painteri oils contain ca. 70% caprylic acid,C. ignea and C.llavea oils have over 80% capric acid, andC. carthagenensis oil contains 57% lauric and 18% capric acids.
65 citations