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.
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.


METHODS
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.
Browning
L M
LM
MRC Human Nutrition Research, Elsie Widdowson Laboratory, Fulbourn Road, Cambridge, UK. lucy.browning@mrc-hnr.cam.ac.uk
Krebs
J D
JD
Moore
C S
CS
Mishra
G D
GD
O'Connell
M A
MA
Jebb
S A
SA
D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000209:etiology / Q000517:prevention & control*; D018592:Cross-Over Studies; D019587:Dietary Supplements; D015525:Fatty Acids, Omega-3 / Q000097:blood / Q000627:therapeutic use*; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000188:drug therapy* / Q000209:etiology; D018836:Inflammation Mediators / Q000097:blood; D007333:Insulin Resistance; D019158:N-Acetylneuraminic Acid / Q000097:blood; D009765:Obesity / Q000097:blood / Q000150:complications; D050177:Overweight; D010641:Phenotype; D016896:Treatment Outcome
D001786:Blood Glucose; D015525:Fatty Acids, Omega-3; D018836:Inflammation Mediators; D002097:C-Reactive Protein; D019158:N-Acetylneuraminic Acid