Effect of fatty acids on expression of endothelial leukocyte adhesion molecules

Reißig, Dieter; Rassoul, F; Salvetter, Jürgen; Wagner, Oswald; Richter, V.

doi:10.1007/s00394-003-0408-4

Cited by 22 publications

(17 citation statements)

References 13 publications

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“…In contrast, several studies have reported anti-infl ammatory effects of LA. In one such study, LA in combination with IL-1α was found to decrease the expression of adhesion molecules ICAM-1, VCAM-1, and E-selectin from endothelial cells when compared with IL-1α treatment alone, with decreased monocyte adherence as a fi nal end point [38]. In support of the anti-infl ammatory effects reported for LA, other investigators have found that endothelial cell activation decreases as the level of unsaturation increases [39,40].…”

Section: Effects Of Fatty Acids On Vascular Infl Ammationmentioning

confidence: 86%

Inflammation associated with the postprandial lipolysis of triglyceriderich lipoproteins by lipoprotein lipase

Higgins

Rutledge²

2009

Curr Atheroscler Rep

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Although hypertriglyceridemia has repeatedly been implicated as an atherogenic condition, there are conflicting reports concerning the atherogenicity of products released from triglyceride-rich lipoproteins by lipoprotein lipase. The hydrolysis of triglyceride is a normal process by which chylomicrons and very low-density lipoproteins are metabolized and cleared from the circulation, which would suggest a beneficial role for lipoprotein lipase in reducing circulating levels of triglyceride and, therefore, reducing atherosclerotic burden. However, many in vitro studies have shown that lipolysis products such as fatty acids induce vascular cell inflammation, which can initiate or exacerbate atherosclerosis. This review summarizes the results and implications of recent studies on the effects of lipoprotein lipase on vascular inflammation, expanding upon existing controversy among human postprandial studies, animal models, and in vitro experimental models.

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Section: Effects Of Fatty Acids On Vascular Infl Ammationmentioning

confidence: 86%

Inflammation associated with the postprandial lipolysis of triglyceriderich lipoproteins by lipoprotein lipase

Higgins

Rutledge²

2009

Curr Atheroscler Rep

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“…By contrast, linoleate (C18:2 6), a polyunsaturated FFA with controversial effects on endothelial activation (25,26), did not promote IL-6 expression in CAECs and had only a minor, possibly endotoxin-mediated, IL-6Ϫinducing effect in CASMCs. As to the FFA specificity of this cellular response, palmitate was by far the most potent IL-6Ϫinduc-ing FFA in CAECs.…”

Section: Discussionmentioning

confidence: 99%

“…The molecular mechanisms underlying these associations are, however, far from clear. Whereas monoand polyunsaturated FFAs, such as oleate (C18:1 9), linoleate (C18:2 6), arachidonate (C20:4 6), eicosapentaenoate (C20:5 3), and docosahexaenoate (C22:6 3), have been convincingly demonstrated to modulate endothelial functions (23)(24)(25)(26)(27)(28), very little is known about the role of saturated FFAs in vascular complications.…”

Section: Discussionmentioning

confidence: 99%

Palmitate-Induced Interleukin-6 Expression in Human Coronary Artery Endothelial Cells

Staiger

Staiger²,

Stefan³

et al. 2004

Diabetes

142

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Obesity-linked insulin resistance is associated with chronic inflammation and cardiovascular complications. Free fatty acids (FFAs) are prominent candidates for the molecular link between these disorders. In this study, we determined whether FFAs contribute to vascular inflammation via induction of interleukin (IL)-6 in coronary artery endothelial cells (CAECs) and coronary artery smooth muscle cells (CASMCs) and whether this is reflected in vivo. In contrast to our findings regarding IL-6 and gp130 (the glycoprotein of 130 kDa) expression, IL-6 receptor mRNA expression was very low in these cells. Palmitate, but not linoleate, induced a significant increase in IL-6 mRNA expression in CAECs (P < 0.001) and, to a less relevant extent, in CASMCs (P < 0.01). gp130 remained unaffected. As to potency, palmitate was comparable with the IL-6؊inducer IL-1␤. To substantiate our in vitro data, we examined the plasma FFA pattern in 54 healthy human subjects and studied the relation of individual FFAs with plasma IL-6. IL-6 levels correlated with palmitate, but not with other abundant FFAs, even after adjusting for body fat (r ‫؍‬ 0.33, P < 0.05) and total FFAs (r ‫؍‬ 0.29, P < 0.05). We show here that the common plasma FFA palmitate induces high levels of IL-6 in CAECs. Furthermore, palmitate correlates with IL-6 in vivo. This points to a potential contribution of palmitate to vascular inflammation. Diabetes 53: 3209 -3216, 2004

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“…On the other hand, pro-atherogenic effects of SFA have been demonstrated [13,14] whereas the properties of the n-6 PUFA precursor are still discussed [15][16][17][18]. Indeed, some authors demonstrated a positive correlation between LA intake and a proinflammatory response and/or an increased risk to coronary diseases [19] whereas others showed that n-6 PUFA family intake protect against atherosclerosis through anti-inflammatory properties [8,15,[20][21][22].…”

Section: Introductionmentioning

confidence: 93%

“…Dietary fatty acids are known to modulate endothelial functions [7,8]. On one hand, some studies pointed out neutral and/or anti-atherogenic properties of monounsaturated fatty acids (MUFA) and n-3 PUFA families, respectively [9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%