Highlights
- •EPA and DHA induce expression of key inflammatory genes in immune cells.
- •Changes in anti-inflammatory gene expression with EPA and DHA are coordinated.
- •CRP reduction with DHA correlates with up-regulation of anti-inflammatory genes.
Abstract
Background and aims
Whether EPA and DHA exert similar anti-inflammatory effects through modulation of
gene expression in immune cells remains unclear. The aim of the study was to compare
the impact of EPA and DHA supplementation on inflammatory gene expression in subjects
at risk for cardiometabolic diseases.
Methods
In this randomized double-blind crossover trial, 154 men and women with abdominal
obesity and low-grade inflammation were subjected to three 10-wk supplementation phases:
1) EPA (2.7 g/d); 2) DHA (2.7 g/d); 3) corn oil (3 g/d), separated by a 9-wk washout.
Pro- and anti-inflammatory gene expression was assessed in whole blood cells by RT-qPCR
after each treatment in a representative sample of 44 participants.
Results
No significant difference was observed between EPA and DHA in the expression of any
of the genes investigated. Compared with control, EPA enhanced TRAF3 and PPARA expression and lowered CD14 expression (p < 0.01) whereas DHA increased expression of PPARA and TNFA and decreased CD14 expression (p < 0.05). Variations in gene expression after EPA and after DHA were strongly correlated
for PPARA (r = 0.73, p < 0.0001) and TRAF3 (r = 0.66, p < 0.0001) and less for TNFA (r = 0.46, p < 0.005) and CD14 (r = 0.16, p = 0.30).
Conclusions
High-dose supplementation with either EPA or DHA has similar effects on the expression
of many inflammation-related genes in immune cells of men and women at risk for cardiometabolic
diseases. The effects of EPA and of DHA on anti-inflammatory gene expression may be
more consistent than their effects on expression of pro-inflammatory genes in whole
blood cells.
Keywords
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Article info
Publication history
Published online: January 20, 2017
Accepted:
January 19,
2017
Received in revised form:
January 13,
2017
Received:
November 24,
2016
Identification
Copyright
© 2017 Elsevier B.V. All rights reserved.
