Metabolic aspects of peroxisomal β-oxidation

Metabolism of very long-chain monounsaturated fatty acids (22:1) and the adaptation to their presence in the diet.

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.

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Effects of high-fat diets on hepatic fatty acid oxidation in the rat. Isolation of rat liver peroxisomes by vertical-rotor centrifugation by using a self-generated, iso-osmotic, Percoll gradient.

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.

https://efsa.onlinelibrary.wiley.com/doi/pdf/10.2903/j.efsa.2016.4593

Erucic acid in feed and food

Differential mobilization of fatty acids from adipose tissue

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.

Cardiac lipids in rats and gerbils fed oils containing C 22 fatty acids.

Synthesized oils containing a high proportion of oleic, eicosenoic or docosenoic acid were fed to weanling rats as 20% w/w of the diet. After 1 week, a high intake of eicosenoate produced cardiac fat droplets detected histologically, whereas erucate (22∶1 Δ 13) or cetoleate (22∶1 Δ 11) caused an appreciably greater accumulation of cardiac lipid characterized by the dietary fatty acids.

J. L. Beare-Rogers

Papers

Cardiac lipids in rats and gerbils fed oils containing C 22 fatty acids.

Accumulation of cardiac fatty acids in rats fed synthesized oils containing C22 fatty acids.