Alpha linolenic acid (ALA) from Rosa canina, sacha inchi and chia oils may increase ALA accretion and its conversion into n 3 LCPUFA in diverse tissues of the rat

January 1, 2014 Human Health and Nutrition Data 0 Comments

Alpha linolenic acid (ALA) from Rosa canina, sacha inchi and chia oils may increase ALA accretion and its conversion into n 3 LCPUFA in diverse tissues of the rat

Year: 2014
Authors: Valenzuela, R. Barrera, C.R. Astorga, M.G. Sanhueza, J. Valenzuela, A.
Publication Name: Food Funct
Publication Details: Volume 5; Issue 7; Pages 1564 to 1572

Abstract:

Alpha linolenic acid (ALA) is an essential n 3 PUFA, its n 3 LCPUFA derivatives EPA and DHA, which have diverse beneficial effects, are scarce in the human diet. In recent years nontraditional vegetable oils rich in ALA (up to 45 per cent) have been developed as new alternatives to increase ALA consumption. This work evaluated the accretion of ALA, EPA and DHA into the phospholipids extracted from erythrocytes, liver, kidney, small intestine, heart, quadriceps and the brain in rats fed sunflower (SFO), canola (CO), Rosa canina (RCO), sacha inchi (Plukenetia volubilis, SIO) and chia (Salvia hispanica, ChO) oils. Five experimental groups (n of 12 per group) were fed for 21 days with SFO (1 per cent ALA), CO (10 per cent ALA), RCO (33 per cent  ALA), SIO (49 per cent ALA), and ChO (64 per cent ALA). SIO and ChO allowed higher ALA accretion in all tissues, except the brain, and a reduction in the content of arachidonic acid in all tissues except the brain. EPA was increased in erythrocytes, liver, kidney, small intestine, heart and quadriceps, but not in the brain. DHA was increased in the liver, small intestine and brain tissues. Our results demonstrate that ALA, when provided in significant amounts, can be converted into n 3 LCPUFA, mostly DHA in the liver and brain. It is suggested that oils rich in ALA, such as SIO and ChO are good sources for obtaining higher tissue levels of ALA, also allowing its selective conversion into n 3 LCPUFA in some tissues of the rat. (Authors abstract)
The low consumption of n 3 LCPUFA creates concern because these fatty acids have been extensively associated with benefits for the cardiovascular and nervous system health.  Consumption of EPA and DHA in the near future will be more restricted because of the declining availability of fatty fish, which are the main source of these fatty acids.   Traditionally, the Western diet is characterized by a high consumption of n 6 PUFAs (LA plus AA), which is associated with increased risk of chronic disease, particularly cardiovascular disease and non-alcoholic fatty liver disease, as well as neurological diseases.  At present a group of oils that contain high concentrations of ALA are commercially available. These oils are extracted from seeds harvested in Central and South America and may contain up to 30 to 60 per cent of ALA. Nontraditional oils extracted from ancestrally consumed seeds such as Rosa canina, native to Chile; sacha inchi (Plukenetia volubilis), of Peruvian origin; and chia (Salvia hispanica), native to Mexico and Central America (Honduras, Guatemala, El Salvador) are now commercially produced. In this study, the effect of consuming Rosa canina oil, sacha inchi oil and chia oil in the accretion of ALA, EPA and DHA into the phospholipids of diverse tissues of rats that received these oils as the exclusive dietary fat was investigated. The metabolic effects of these three oils were compared to the effects of two commonly consumed oils, such as sunflower oil (Helianthus annuus) and canola oil (Brassica campestris), which provide a very low amount of ALA (sunflower oil 1 per cent) and a low amount of ALA (canola oil 10 per cent).
ALA accretion into erythrocyte phospholipids reflects a direct relationship to dietary ALA, because the accretion of the fatty acid into membrane phospholipids was increased with the amount of ALA provided by the different oils assayed (SFO, CO, RSO, SIO and ChO). No significant differences were observed for SIO and ChO despite the higher amount of ALA provided by these oils, particularly by ChO, which may suggest a maximum capacity of erythrocytes to incorporate ALA into the membrane phospholipids.   Accretion of AA and EPA in erythrocyte phospholipids was increased with the supply of LA and ALA in the diets. This effect was not observed for DHA, which remained unchanged despite the amount of ALA provided by the diets. The differences in the supply of LA and ALA of the diets and the differential accretion of n 6 and n 3 fatty acids into membrane phospholipids was also reflected by changes in the n 6 per n 3 ratios. The high accretion of EPA observed for SIO and ChO in erythrocytes, which is not seen in DHA accretion, can be interpreted as erythrocytes not being selective targets for accretion of this n 3 LCPUFA. A similar result was obtained for plasma  and observed that increasing amounts of dietary ALA do not modify the amount of DHA in plasma phospholipids.  Hepatic phospholipid fatty acid composition also showed a good association with dietary ALA and the hepatic accretion of EPA. DHA was also increased, although no significant differences were observed for SIO and ChO.   This may suggest the existence of a metabolic regulation in the hepatic bioconversion of ALA into DHA, possibly due to inhibition, by excess ALA, of the enzymatic machinery that carries out conversion of ALA, first to EPA and then to DHA, and or to negative feedback exerted by DHA to its formation from EPA.   Brain tissue showed a particular fatty acid composition compared to the other tissues previously evaluated, because very low levels of LA, ALA and EPA and high levels of AA and DHA were observed. However, the high levels of DHA, normally found in this tissue, were significantly increased after RCO, SIO and ChO were compared to SFO, which is the diet that provided the lowest supply of ALA (0.1 g ALA per 100 g diet). With the exception of brain, all other tissues showed higher ALA and EPA levels, in line with the amount of ALA supplied by the different diets. It has been demonstrated that excess ALA not converted into n 3 LCPUFA is beta oxidized.   With the exception of the brain, ALA was observed in all other tissues. The results demonstrate that when high dietary levels of ALA are provided, enhancement of its transformation into EPA and DHA in some tissues of the rat occurs. However, the possible modification of the activity and or expression of tissue desaturase and elongase enzymes,  which are responsible for the conversion of ALA into EPA and DHA in the liver and almost exclusively into DHA in the brain,  remain to be studied. It has been demonstrated that tissue conversion of ALA into EPA and DHA is generally low in many tissues with the exception of brain, because despite the low conversion of ALA into DHA, the tissue allows an adequate accretion of the n 3 LCPUFA.  The rat is considered to be an efficient converter of ALA into n 3 LCPUFA compared to humans, therefore, results of ALA supplementation in humans may eventually turn out to be different to those obtained in rats.  Current evidence indicates that in humans, n 3 LCPUFA status can be improved by increasing their intake or decreasing LA intake, and a combination of the two is likely to be most effective. (Editors comments)



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