Abstract

Polymorphisms (SNPs) within the FADS gene cluster and the ELOVL gene family are believed to influence enzyme activities after an omega-3 (n-3) fatty acid (FA) supplementation. The objectives of the study are to test whether an n-3 supplementation is associated with indexes of desaturase and elongase activities in addition to verify whether SNPs in the FADS gene cluster and the ELOVL gene family modulate enzyme activities of desaturases and elongases. A total 208 subjects completed a 6-week supplementation period with 5 g/day of fish oil (1.9–2.2 g/day of EPA + 1.1 g/day of DHA). FA profiles of plasma phospholipids were obtained by gas chromatography (n = 210). Desaturase and elongase indexes were estimated using product-to-precursor ratios. Twenty-eight SNPs from FADS1, FADS2, FADS3, ELOVL2 and ELOVL5 were genotyped using TaqMan technology. Desaturase indexes were significantly different after the 6-week n-3 supplementation. The index of δ-5 desaturase activity increased by 25.7 ± 28.8 % (p < 0.0001), whereas the index of δ-6 desaturase activity decreased by 17.7 ± 18.2 % (p < 0.0001) post-supplementation. Index of elongase activity decreased by 39.5 ± 27.9 % (p < 0.0001). Some gene–diet interactions potentially modulating the enzyme activities of desaturases and elongases involved in the FA metabolism post-supplementation were found. SNPs within the FADS gene cluster and the ELOVL gene family may play an important role in the enzyme activity of desaturases and elongases, suggesting that an n-3 FAs supplementation may affect PUFA metabolism.

Highlights

  • Elongation and desaturation of long-chain (LC) polyunsaturated fatty acids (PUFA) of the omega-3 (n-3) family are made possible by enzymes called desaturases and elongases

  • SNPs within the FADS gene cluster and the ELOVL gene family may play an important role in the enzyme activity of desaturases and elongases, suggesting that an n-3 FAs supplementation may affect PUFA metabolism

  • Estimates of d-5 desaturase (D5D) activity increased by 25.7 ± 28.8 % (Mean ± SD, p \ 0.0001), whereas surrogate estimates of d-6 desaturases (D6D) activity decreased by 17.7 ± 18.2 % (p \ 0.0001) after the supplementation

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Summary

Introduction

Elongation and desaturation of long-chain (LC) polyunsaturated fatty acids (PUFA) of the omega-3 (n-3) family are made possible by enzymes called desaturases and elongases. Fatty acid desaturase 1 and 2 (FADS1 and FADS2, respectively) genes encode for key enzymes in the PUFA metabolism, the d-5 desaturase (D5D) and D6D, respectively (Malerba et al 2008). These desaturases are responsible for the double bond formation between two carbons leading to more unsaturated FAs. Elongases are encoded by genes within the ELOVL family and catalyzes the elongation of the aliphatic chain of carbons leading to the formation of LC-PUFAs (Jakobsson et al 2006). A high desaturase activity may lead to an increased bioavailability of arachidonic acid (AA) with dominant synthesis of AAderived proinflammatory eicosanoids, possibly leading to vascular damage, especially in populations eating a Western diet (Martinelli et al 2009). A shift from n-6 to n-3 induces changes in the eicosanoid profile, which may lead to a decrease inflammatory state (Calder 2009)

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