Journal
DIABETES OBESITY & METABOLISM
Volume 9, Issue 1, Pages 70-80Publisher
BLACKWELL PUBLISHING
DOI: 10.1111/j.1463-1326.2006.00576.x
Keywords
CRP; inflammation; insulin sensitivity; n-3 polyunsaturated fatty acids (PUFA); sialic acid
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Funding
- Medical Research Council [MC_U105960389, MC_U120063239, MC_U105960399] Funding Source: Medline
- MRC [MC_U105960399, MC_U120063239, MC_U105960389] Funding Source: UKRI
- Medical Research Council [MC_U105960399, MC_U105960389, MC_U120063239] Funding Source: researchfish
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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.
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