title: n-3 and n-6 Fatty acids are independently associated with lipoprotein-associated phospholipase A2 in the Multi-Ethnic Study of Atherosclerosis.
abstract: Lipoprotein-associated phospholipase A2 (Lp-PLA2) is an independent risk factor for CVD and has been proposed as a marker of vascular inflammation. Polyunsaturated n-3 fatty acids (FA) and several n-6 FA are known to suppress inflammation and may influence Lp-PLA2 mass and activity. The associations of n-3 and n-6 plasma FA with Lp-PLA2 mass and activity were analysed using linear regression analysis in 2246 participants of the Multi-Ethnic Study of Atherosclerosis; statistical adjustments were made to control for body mass, inflammation, lipids, diabetes, and additional clinical and demographic factors. Lp-PLA2 mass and activity were significantly lower in participants with the higher n-3 FA EPA (β = - 4·72, P< 0·001; β = - 1·53; P= 0·023) and DHA levels (β = - 4·47, β = - 1·87; both P< 0·001). Those in the highest quintiles of plasma EPA and DHA showed 12·71 and 19·15 ng/ml lower Lp-PLA2 mass and 5·7 and 8·90 nmol/min per ml lower Lp-PLA2 activity than those in the first quintiles, respectively. In addition, lower Lp-PLA2 mass and activity were associated with higher levels of n-6 arachidonic acid (β = - 1·63, β = - 1·30; both P< 0·001), while γ-linolenic acid was negatively associated with activity (β = - 27·7, P= 0·027). Lp-PLA2 mass was significantly higher in participants with greater plasma levels of n-6 linoleic (β = 0·828, P= 0·011) and dihomo-γ-linolenic acids (β = 4·17, P= 0·002). Based on their independent associations with Lp-PLA2 mass and activity, certain n-3 and n-6 FA may have additional influences on CVD risk. Intervention studies are warranted to assess whether these macronutrients may directly influence Lp-PLA2 expression or activity.
authors.affiliation: Department of Laboratory Medicine and Pathology, University of Minnesota, 420 Delaware Street, SE, Mayo Mail Code 609, Minneapolis, MN 55455-0392, USA.
authors.forename: Brian T
authors.initials: BT
authors.lastname: Steffen
authors.forename: Lyn M
authors.initials: LM
authors.lastname: Steffen
authors.forename: Shuang
authors.initials: S
authors.lastname: Liang
authors.forename: Russell
authors.initials: R
authors.lastname: Tracy
authors.forename: Nancy Swords
authors.initials: NS
authors.lastname: Jenny
authors.forename: Michael Y
authors.initials: MY
authors.lastname: Tsai
mesh_terms: D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase / Q000097:blood*; D000368:Aged; D050197:Atherosclerosis / Q000097:blood*; D004281:Docosahexaenoic Acids / Q000097:blood*; D015118:Eicosapentaenoic Acid / Q000097:blood*; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood*; D019787:Linoleic Acid / Q000097:blood*; D008297:Male; D008875:Middle Aged; D012044:Regression Analysis; D012307:Risk Factors; D017965:gamma-Linolenic Acid / Q000097:blood*
chemical_list: D004281:Docosahexaenoic Acids; D017965:gamma-Linolenic Acid; D019787:Linoleic Acid; D015118:Eicosapentaenoic Acid; D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase
references.citation: J Clin Lipidol. 2009 Oct;3(5):332-40
references.pmid: 21291831
references.citation: Biochem J. 1999 Mar 1;338 ( Pt 2):479-87
references.pmid: 10024526
references.citation: Vasc Health Risk Manag. 2006;2(2):153-6
references.pmid: 17319459
references.citation: Am J Clin Nutr. 2009 Jan;89(1):331-46
references.pmid: 19056549
references.citation: Am J Clin Nutr. 2010 Nov;92(5):1214-22
references.pmid: 20861175
references.citation: J Clin Lipidol. 2011 Nov-Dec;5(6):483-92
references.pmid: 22108152
references.citation: J Biol Chem. 2004 Aug 20;279(34):36158-65
references.pmid: 15215249
references.citation: Am J Epidemiol. 2002 Nov 1;156(9):871-81
references.pmid: 12397006
references.citation: Circulation. 2002 Nov 19;106(21):2747-57
references.pmid: 12438303
references.citation: Int J Obes (Lond). 2012 Jun;36(6):797-804
references.pmid: 21829163
references.citation: Am J Cardiol. 2005 May 1;95(9):1025-32
references.pmid: 15842965
references.citation: Circulation. 2008 Sep 9;118(11):1172-82
references.pmid: 18765397
references.citation: Cardiovasc Res. 2010 Mar 1;85(4):845-52
references.pmid: 19910444
references.citation: Clin Chem. 2005 Dec;51(12):2264-73
references.pmid: 16223884
references.citation: Atherosclerosis. 2008 Jan;196(1):420-424
references.pmid: 17157859
references.citation: Eur J Nutr. 2011 Apr;50(3):185-93
references.pmid: 20706728
references.citation: Cardiovasc Hematol Agents Med Chem. 2011 Apr 1;9(2):78-83
references.pmid: 21476960
references.citation: Am J Clin Nutr. 2010 Mar;91(3):786-93
references.pmid: 20107195
references.citation: Lancet. 1978 Jul 15;2(8081):117-9
references.pmid: 78322
references.citation: Inflamm Res. 2008 Sep;57(9):430-7
references.pmid: 18777114
references.citation: Clin Chem. 2006 Dec;52(12):2265-72
references.pmid: 17053155
references.citation: Eur J Nutr. 2009 Feb;48(1):1-5
references.pmid: 19030909
references.citation: Circ Res. 2010 Nov 12;107(10):1170-84
references.pmid: 21071715
references.citation: J Am Coll Cardiol. 2008 Apr 29;51(17):1632-41
references.pmid: 18436114
references.citation: Thromb Haemost. 2011 Sep;106(3):500-10
references.pmid: 21727988
references.citation: J Nutr Biochem. 2006 Nov;17(11):766-72
references.pmid: 16563718
references.citation: Prostaglandins Other Lipid Mediat. 2002 Aug;68-69:433-55
references.pmid: 12432935
references.citation: Clin Chem. 1995 Feb;41(2):264-70
references.pmid: 7874780
references.citation: Atherosclerosis. 2010 Apr;209(2):528-32
references.pmid: 19804884
references.citation: J Mol Cell Cardiol. 2003 Jul;35(7):769-75
references.pmid: 12818567
references.citation: J Immunol. 2007 Mar 15;178(6):3912-7
references.pmid: 17339491
references.citation: Atherosclerosis. 2008 Jul;199(1):110-5
references.pmid: 18061193
references.citation: Lancet. 2010 May 1;375(9725):1536-44
references.pmid: 20435228