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Volume 58, Issue 12, Pages 1709-1716 (December 2009)


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Modifying the n-6/n-3 polyunsaturated fatty acid ratio of a high–saturated fat challenge does not acutely attenuate postprandial changes in inflammatory markers in men with metabolic syndrome

Hilary M.F. Tulk, Lindsay E. RobinsonCorresponding Author Informationemail address

Received 18 March 2008; accepted 20 May 2009. published online 22 July 2009.

Abstract 

Metabolic syndrome (MetS) features chronic inflammation and exaggerated postprandial triacylglyceride (TAG) responses. Fasting concentrations of interleukin-6 (IL-6) and C-reactive protein (CRP), key inflammatory mediators, decrease after sustained n-3 polyunsaturated fatty acid (PUFA) intake; however, the ability of n-3 PUFA to attenuate postprandial inflammatory responses is not well studied. Thus, we examined the acute effect of modifying the n-6/n-3 PUFA ratio of a high–saturated fatty acid (SFA) oral fat tolerance test (OFTT) on postprandial TAG and inflammatory responses in men with MetS. Men (n = 8, ≥45 years old) with MetS ingested 2 high-SFA OFTTs (1 g fat per kilogram body weight), with either a 20:1 (low n-3) or 2:1 (high n-3) n-6/n-3 PUFA ratio, and a water control in a randomized crossover design. Blood samples were collected for 8 hours after treatment to measure postprandial TAG, free fatty acids, IL-6, soluble IL-6 receptor, and CRP. Postprandial TAG increased at the same rate after ingestion of the low–n-3 and high–n-3 OFTTs; however, both OFTTs were significantly different from the water control. There were no differences in the rate at which IL-6 concentrations increased after ingestion of either of the OFTTs compared with water. Furthermore, neither time nor treatment affected circulating soluble IL-6 receptor or CRP concentrations. Thus, increasing the n-3 PUFA content of a high-SFA OFTT does not acutely change postprandial TAG or inflammatory responses in men with MetS.

Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada N1G 2W1

Corresponding Author InformationCorresponding author. Tel.: +1 519 824 4120x52297; fax: +1 519 763 5902.

PII: S0026-0495(09)00240-6

doi:10.1016/j.metabol.2009.05.031


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