Lower Efficacy in the Utilization of Dietary ALA as Compared to Preformed EPA + DHA on Long Chain n-3 PUFA Levels in Rats

January 1, 2010 Human Health and Nutrition Data 0 Comments

Lower Efficacy in the Utilization of Dietary ALA as Compared to Preformed EPA + DHA on Long Chain n-3 PUFA Levels in Rats

Year: 2010
Authors: Talahalli, R.R. Vallikannan, B. Sambaiah, K. Lokesh, B. R.
Publication Name: Lipids
Publication Details: Volume 45; Pages 799 – 808.


We made a comparative analysis of the uptake, tissue deposition and conversion of dietary a-linolenic acid (ALA) to its long chain metabolites eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) with preformed EPA+DHA. Diets containing linseed oil [with ALA at 2.5 (4 g/kg diet), 5 (8 g/kg diet), 10 (16 g/kg diet), 25% (40 g/kg diet)] or fish oil [with EPA+DHA at 1 (1.65 g/kg diet), 2.5 (4.12 g/kg diet), 5% (8.25 g/kg diet)] or ground nut oil without n-3 polyunsaturated fatty acids (n-3 PUFA) were fed to rats for 60  days. ALA and EPA+DHA in serum, liver, heart and brain increased with increments in the dietary ALA level. When preformed EPA+DHA were fed, the tissue EPA+DHA increased significantly compared to those given ALA. Normalized values from dietary n-3 PUFA to tissue EPA+DHA indicated that 100 mg of dietary ALA lead to accumulation of EPA+DHA at 2.04, 0.70, 1.91 and 1.64% of total fatty acids respectively in liver, heart, brain and serum. Similarly 100 mg of preformed dietary EPA+DHA resulted in 25.4, 23.8, 15.9 and14.9% of total fatty acids in liver, heart, brain and serum, respectively. To maintain a given level of EPA+DHA, the dietary ALA required is 12.5, 33.5, 8.3 and 9.1 times higher than the dietary EPA+DHA for liver, heart, brain and serum, respectively. Hence the efficacy of precursor ALA is lower compared to preformed EPA+DHA in elevating serum and tissue long chain n-3 PUFA levels. (Author`s abstract)
ALA plays a major role in vegetarians for the maintenance of EPA and DHA supply to the body. The bioavailability of an individual fatty acid is influenced by the presence of other fatty acids and studies have focused on apparent differences in the deposition of linoleic acid (LNA, 18:2n-6) and ALA in tissue lipids. Some research has shown that, despite adequate ALA intake, n-6 PUFA deficiency decreased the accumulation of ALA and total n-3 PUFA. Thus n-6 PUFA affected the homeostasis of ALA. Humans show differences in LNA and ALA accumulation. The levels of the long chain n-3 PUFA in serum and tissue are dependent on intake of either their precursors or preformed product. If an increased level of ALA is to be promoted for maintaining a given level of long chain n-3 PUFA, it is necessary to consider to what extent dietary ALA is absorbed, stored and converted into long chain metabolites. In the present investigation, with an increase in the dietary ALA levels, there was a corresponding increase in the levels of ALA with a small but significant increase in the accumulation of EPA+DHA in the serum and liver. EPA+DHA also increased from 1 to 5% of total fatty acids in serum lipids. This indicated that though higher amounts of ALA are fed to rats, only a small proportion of ALA and its long chain metabolites are accumulating in serum lipids.The competition of LNA for delta-6 desaturase may reduce conversion of ALA to long chain n-3 PUFA. The background diet is another factor which can modulate the conversion process. It has been reported that conversion of ALA to EPA was highest in rats receiving saturated fats but lowest in PUFA fed rats. In addition, the ability of ALA conversion to long chain n-3 PUFA particularly DHA varied depending on the animal models used. ALA can also undergo metabolism in a recycling pathway. Unlike ALA, long chain fatty acids like DHA seem to undergo less beta-oxidation and carbon recycling. The ratio of n-6 to n-3 fatty acids is crucial for the conversion of ALA to long chain n-3 PUFA as n-6 fatty acid (LNA) can compete with delta-6 desaturase which acts on both n-6 and n-3 fatty acids. The changes in the n-3 PUFA levels in different tissues in response to dietary lipids were not uniform. The DHA content in heart did not change appreciably up to 10.0% ALA in the diet. Even at 25.0%, the ALA level in the diet there had only a 54% increase in DHA content above that found in the control group. The heart tissue readily takes the n-3 fatty acids, particularly DHA. In the brain, feeding incremental amounts of ALA in the diets progressively increased DHA levels by 13-49% when ALA levels were increased from 2.5 to 25% in the diet. Even limited production/accumulation of EPA and DPA from dietary ALA may be physiologically relevant as they may provide a circulating reservoir for DHA synthesis in tissues. Feeding incremental amounts of ALA from 2.5 to 25.0% in the diet resulted in the accumulation of ALA from 1.9 to 12.1% in the adipose tissue. Adipose tissue represents one of the important storage tissues for ALA that can be made available to the body when needed. The data suggest that effects of LNA, ALA, ARA and DHA on tissue fatty acid composition may be an indicator for differential handling of essential fatty acids by the body. The authors suggest that there is a need to define a physiological end point while fixing the requirements for ALA rather than the conventional criteria adopted for fixing recommended dietary allowance for essential fatty acids.  The present study indicates that ALA could be an alternative source for long chain n-3 PUFA if taken at higher levels in the diet. ALA can be elongated and desaturated to long chain n-3 PUFA to a limited extent and it also has beneficial effects in lowering serum lipid levels. These results, which were observed in rats, however need to be validated in humans. (Editor`s comments)

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