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Racial Differences in Plasma Omega‐3 Long Chain Fatty Acid Levels in a Cohort of African Americans and European Americans with Diabetes and Metabolic Syndrome
Author(s) -
Wilson Bryan Anthony,
Sergeant Susan,
Ainsworth Hannah,
Mathias Rasika,
Chilton Floyd H.
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.266.4
Subject(s) - polyunsaturated fatty acid , docosapentaenoic acid , medicine , endocrinology , diabetes mellitus , eicosapentaenoic acid , chemistry , fatty acid , omega 3 fatty acid , fatty acid metabolism , metabolism , docosahexaenoic acid , biochemistry
Background We have shown that polymorphisms in the fatty acid desaturase 1 gene (FADS1) are associated with racial differences in omega‐6 long‐chain polyunsaturated fatty acid (LC‐PUFA) metabolism. We thus examined whether racial differences also exist in omega‐3 (ω3) LC‐PUFA metabolism. Methods We used GLC to measure levels of the LC‐PUFA precursor α‐linolenic acid (18:3, ALA) and the major ω3 LC‐PUFAs eicosapentanoic (22:5, EPA), docosapentaenoic (24:5, DPA) and docosahexanoic (24:6, DHA) acids in fasting plasma from 63 African Americans (AfAm) and 166 European Americans (EAm) with diabetes or metabolic syndrome. Results Compared to EAm, AfAm had significantly lower ALA (2.0 ± 1.2 vs 3.1 ± 2.1, p<0.001) and DPA (1.7 ± 0.5 vs 2.0 ± 0.8, p=0.006) levels, whereas DHA levels were significantly higher (6.8 ± 2.6 vs 5.6 ± 2.2, p<0.001). EPA levels were no different. Compared to EAm, fatty acid product:precursor ratios were significantly higher in AfAm for DHA:ALA, 3.8 ± 1.6 vs 2.1 ± 0.9, p<0.001; EPA:ALA, 1.2 ± 0.9 vs 0.8 ± 0.6, p<0.001, and DHA:DPA, 4.1 ± 1.4 vs 3.0 ± 1.0, P<0.001. Conclusions As product:precursor ratios of circulating ω3 PUFAs provide a surrogate measure of substrate flux through the LC‐PUFA synthesis pathway, these data suggest that AfAm display enhanced conversion of ω3 precursors to LC‐PUFA, which may be due to genetically‐determined increased activity of the FADS1 desaturase and elongase genes. Grant Funding Source : NIH Grants: 5P50AT002782‐07, 3P50AT002782‐07S1