Key Findings:
Studies in humans show that dietary supplementation in ALA leads to increased EPA and docosapentaenoic acid (22:5n-3, DPA) and smaller amounts of DHA. The liver is the main organ where conversion of LA and ALA to longer chain PUFAs occurs. This study showed that LA intake can reduce tissue n-3 levels. In rats, hepatic Δ6-desaturase the enzyme responsible for conversion of the EFA to the longer chain fatty acids, were elevated when either a diet high in LA or ALA was fed. Hepatic Δ5-desaturase activity was elevated only following the ALA diet. The ALA diet led to higher n-3 LC-PUFAs including DHA in brain and heart. The LA diet reduced n-3 content in blood, liver and heart. The study suggests that increasing dietary ALA and reducing LA intake can increase n-3 LC-PUFA levels in tissues.
ABSTRACT:
The intake of the essential fatty acid precursor α-linolenic acid (ALA) contributes to ensure adequate n-3 long-chain polyunsaturated fatty acid (LC-PUFA) bioavailability. Conversely, linoleic acid (LA) intake may compromise tissue n-3 PUFA status as its conversion to n-6 LC-PUFA shares a common enzymatic pathway with the n-3 family. This study aimed to measure dietary ALA and LA contribution to LC-PUFA biosynthesis and tissue composition. Rats were fed with control or experimental diets moderately enriched in ALA or LA for 8 weeks. Liver Δ6- and Δ5-desaturases were analyzed and FA composition was determined in tissues (red blood cells, liver, brain and heart). Hepatic Δ6-desaturase activity was activated with both diets, and Δ5-desaturase activity only with the ALA diet. The ALA diet led to higher n-3 LC-PUFA composition, including DHA in brain and heart. The LA diet reduced n-3 content in blood, liver and heart, without impacting n-6 LC-PUFA composition. At levels relevant with human nutrition, increasing dietary ALA and reducing LA intake were both beneficial in increasing n-3 LC-PUFA bioavailability in tissues. (Authors Abstract)
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