n-3 PUFAs improve erythrocyte fatty acid profile in patients with small AAA: a randomized controlled trial

Abdominal aortic aneurysm (AAA) is an important cause of death in older adults, which has no current drug therapy. Inflammation and abnormal redox status are believed to be key pathogenic mechanisms for AAA. In light of evidence correlating inflammation with aberrant fatty acid profiles, this study compared erythrocyte fatty acid content in 43 AAA patients (diameter 3.0–4.5 cm) and 52 healthy controls. In addition, the effect of omega-3 PUFA (n-3 PUFA) supplementation on erythrocyte fatty acid content was examined in a cohort of 30 AAA patients as part of a 12 week randomized placebo-controlled clinical trial. Blood analyses identified associations between AAA and decreased linoleic acid (LA), and AAA and increased Δ6-desaturase activity and biosynthesis of arachidonic acid (AA) from LA. Omega-3 PUFA supplementation (1.5 g DHA + 0.3 g EPA/day) decreased red blood cell distribution width (14.8 ± 0.4% to 13.8 ± 0.2%; P = 0.003) and levels of pro-inflammatory n-6 PUFAs (AA, 12.46 ± 0.23% to 10.14 ± 0.3%, P < 0.001; adrenic acid, 2.12 ± 0.13% to 1.23 ± 0.09%; P < 0.001). In addition, Δ-4 desaturase activity increased (DHA/docosapentaenoic acid ratio, 1.85 ± 0.14 to 3.93 ± 0.17; P < 0.001) and elongase 2/5 activity decreased (adrenic acid/AA ratio, 0.17 ± 0.01 to 0.12 ± 0.01; P < 0.01) following supplementation. The findings suggest that n-3 PUFAs improve fatty acid profiles and ameliorate factors associated with inflammation in AAA patients.

Fatty acid profile in erythrocytes associated with serum cytokines in pediatric cystic fibrosis patients

ABSTRACT Objective To analyze erythrocyte fatty acid composition and its association with serum cytokine levels in pediatric cystic fibrosis patients. Methods A cross-sectional study was performed at a reference center in Rio de Janeiro, Brazil. We have included all pediatric patients aged 5-19 years with confirmed cystic fibrosis diagnosis. Erythrocyte fatty acid composition and serum cytokine (TNF-α, IL-1β, IL-6 and IL-8) and C-reactive protein levels were measured. The cut-off point to determine essential fatty acids deficiency was the linoleic acid concentration of <21%. Results Twenty-six children (<10 years old) and thirty-one adolescents were studied. Most patients were female and heterozygous for DF508 mutation and suffered from exocrine pancreatic insufficiency. Both children and adolescents had lower linoleic acid concentration (<21%). TNF-α was the only pro-inflammatory marker whose levels were increased; the increase was greater in children. An association between fatty acid composition in erythrocytes and cytokines IL-1β and IL-6 was observed (p<0.05). Conclusion The pediatric cystic fibrosis patients studied presented a deficiency of essential fatty acids, and an association between fatty acid profile in erythrocytes and serum pro-inflammatory cytokines was observed. These findings highlight the importance of this type of assessment that may open new possibilities for studying pathophysiology and treating cystic fibrosis patients, such as the dietary supplementation with n-3 fatty acids (eicosapentaenoic and docosahexaenoic acids). However, further longitudinal studies are needed for better clarification of the imbalance in lipid metabolism and inflammation in cystic fibrosis