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The impact of long chain n ‐3 polyunsaturated fatty acid supplementation on inflammation, insulin sensitivity and CVD risk in a group of overweight women with an inflammatory phenotype
Author(s) -
Browning L. M.,
Krebs J. D.,
Moore C. S.,
Mishra G. D.,
O’Connell M. A.,
Jebb S. A.
Publication year - 2007
Publication title -
diabetes, obesity and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.445
H-Index - 128
eISSN - 1463-1326
pISSN - 1462-8902
DOI - 10.1111/j.1463-1326.2006.00576.x
Subject(s) - polyunsaturated fatty acid , docosahexaenoic acid , eicosapentaenoic acid , medicine , insulin , insulin resistance , placebo , inflammation , endocrinology , body mass index , overweight , c reactive protein , crossover study , gastroenterology , fatty acid , chemistry , biochemistry , pathology , alternative medicine
Background: Inflammation is strongly related to obesity and the risk of cardiovascular disease (CVD). The metabolic benefits of long chain (LC) n ‐3 polyunsaturated fatty acid (PUFA) may be attributable to its anti‐inflammatory properties. Objective: To investigate whether an individual’s habitual inflammatory status influences the impact of a LC n ‐3 PUFA intervention on CVD risk. Design: The study was a randomized crossover design. Subjects received LC n ‐3 PUFA capsules or a placebo for 12 weeks, with 4‐week washout between phases. Thirty women, in the top and bottom tertiles of baseline sialic acid concentration, formed raised inflammatory status (top, n = 12) and reference (bottom, n = 18) groups. Baseline data were analysed using one‐way anova , differences between treatment phases were calculated at each timepoint and analysed using a random effects model. Results: At baseline, the raised inflammatory status group had significantly higher body mass index and area under the curve (AUC) insulin than the reference group. With LC n ‐3 PUFA supplementation, both groups showed significantly higher plasma eicosapentaenoic acid and docosahexaenoic acid at 4 and 12 weeks (p < 0.001), and lower triacylglycerols (4 weeks p < 0.01 and 12 weeks p < 0.05). The difference in AUC insulin between the two treatment phases at 12 weeks was significantly greater in the raised inflammatory status group compared to the reference group (p < 0.05). Inflammatory markers were significantly lower after 12 weeks LC n ‐3 PUFA supplementation compared to baseline (C‐reactive protein p < 0.05 and interleukin‐6 p < 0.01), but there was no significant group effect. Conclusions: Habitual inflammatory status influences the impact of LC n ‐3 PUFA supplementation, but it is not clear whether the effect of LC n ‐3 PUFA on AUC insulin is mediated through inflammatory mechanisms.