Randomized placebo-controlled intervention with n-3 LC-PUFA-supplemented yoghurt: Effects on circulating eicosanoids and cardiovascular risk factors

Dawczynski, Christine; Massey, Karen A.; Ness, Christina; Kiehntopf, Michael; Stepanow, Stefanie; Platzer, Matthias; Grün, M.; Nicolaou, Anna; Jahreis, Gerhard

doi:10.1016/j.clnu.2012.12.010

Cited by 65 publications

(73 citation statements)

References 27 publications

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“…Our study contrasts with that of Dawczynski et al ( 18 ) who used a metabolomic approach to measure a large number of plasma eicosanoids by LC/ESI-/MS/MS. The authors were unable to detect 17S-HDHA, RvE1, or RvD1 before or after 10 weeks of 3g/day of n-3 fatty acids provided by yogurt in hypertriglyceridemic patients ( 18 ). The different study fi ndings may relate to the study population; our study recruited healthy volunteers.…”

Section: Discussionmentioning

confidence: 44%

Short-term n-3 fatty acid supplementation but not aspirin increases plasma proresolving mediators of inflammation

Barden

Mas

Croft

et al. 2014

Journal of Lipid Research

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the infl ammatory process ( 1, 2 ), acting on a number of G-coupled protein receptors, including the leukotriene B4 (LTB 4 ) receptor to affect resolution of infl ammation.Metabolism of EPA by acetylated cyclooxygenase (COX)-2 or cytochrome P450 monooxygenase results in the formation of 18-hydroxyeicosapentaenoic acid (18-HEPE) that can be converted by 5-lipoxygenase (LOX) to 5-hydroperoxy-18-hydroxyeicosapentaenoic acid (5-Hp-18-HEPE). The latter can undergo epoxidation and enzyme hydrolysis to yield resolvin E1 (RvE1), or reduction to yield resolvin E2 (RvE2). A third E-series resolvin, resolvin E3 (RvE3), is generated from EPA by the 12/15 LOX pathway ( 3 ). Studies using chiral chromatography indicate that acetylation of COX-2 by aspirin generates both 18S-HEPE and 18R-HEPE and their respective downstream E-series resolvins 18S-RvE1 and 18R-RvE1 ( 4 ).Metabolism of DHA by either acetylated COX-2 or 15-LOX gives rise to 17-hydroperoxydocosahexaenoic acid (17-HpDHA) that is converted to 17-hydroxydocosahexaenoic acid (17-HDHA). 15-LOX gives rise to mainly 17S-HpDHA whereas acetylated COX-2 yields 17R-HpDHA ( 5 ). The action of 5-LOX on 17-HDHA generates the Dseries resolvins RvD1-RvD6 ( 1 ). In the absence of 5-LOX, protectin D1 (PD1) is formed from 17-HpDHA. In macrophages, 12/15-LOX can act on DHA to form 14-hydroperoxydocosahexaenoic acid (14-HpDHA) that can be further metabolized to 14-hydroxydocosahexaenoic acid (14-HDHA) and the maresins ( 6 ).Most of the research on the effects of SPMs has been in animal models. The resolvins and protectins have been Abstract Resolution of infl ammation is an active process involving specialized proresolving mediators (SPM) formed from the n-3 fatty acids. This study examined the effect of n-3 fatty acid supplementation and aspirin on plasma SPMs in healthy humans. Healthy volunteers (n = 21) were supplemented with n-3 fatty acids (2.4g/day) for 7 days with random assignment to take aspirin (300 mg/day) or placebo from day 5 to day 7. Blood was collected at baseline (day 0 There is increasing interest in the role of the specialized proresolving mediators (SPMs) that actively stimulate resolution of infl ammation ( 1 ). In particular, recent attention has focused on those SPM derived from the long-chain n-3 fatty acids EPA and DHA. The SPMs formed from EPA are known as E-series resolvins, while those formed from DHA include protectins, D-series resolvins, and maresins ( 1 ). Studies have shown that SPMs increase with time during A.B., T.A.M.,)

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Section: Discussionmentioning

confidence: 44%

Short-term n-3 fatty acid supplementation but not aspirin increases plasma proresolving mediators of inflammation

Barden

Mas

Croft

et al. 2014

Journal of Lipid Research

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“…Average plasma levels of RvE1 of 0.521 nM (182.6 pg/ml) and of RvD1 of 0.0454 nM (17.1 pg/ml) were reported in a study of healthy volunteers on an ad libitum diet ( 58 ). By contrast, a randomized and placebo-controlled supplementation of 16 volunteers with 3 g/day fi sh oil over 10 weeks failed to detect RvD1 and RvE1 in plasma ( 59 ). However, labeled authentic standards were not applied in either study.…”

Section: Discussionmentioning

confidence: 99%

Bioactive products formed in humans from fish oils

Skarke

Alamuddin

Lawson

et al. 2015

Journal of Lipid Research

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The clinical cardiovascular utility of a diet rich in fi sh oils, particularly EPA and DHA, has been debated over the past 50 years ( 1-3 ). Large clinical outcome trials, such as the open-labeled GISSI-Prevenzione ( 4 ) or JELIS ( 5 ) studies, supported the notion that fi sh oil supplements confer therapeutic benefi t on patients with cardiovascular disease. However, an overview analysis of results of more than 50 randomized controlled trials and cohort studies addressing this question yielded equivocal results ( 6, 7 ). Consequently, the adoption of the dietary interventions with fi sh oil into clinical guidelines has been limited ( 8 ). Fish oil supplementation does infl uence a series of cardiovascular biomarkers: it decreases blood levels of triglycerides in patients with hypertriglyceridemia, an effect primarily driven by lowering the production of triglycerides from nonesterifi ed fatty acids ( 9 ); high doses reduce blood pressure in patients with essential hypertension ( 10, 11 ) and modestly inhibit indices of platelet activation ( 12 ). The mechanisms involved are unclear, but may involve a shift in formation of enzymatic and free radical-catalyzed prostanoids, refl ecting utilization of EPA and DHA rather than arachidonic acid (AA) as a substrate. It has been speculated also that cardiovascular benefi t might derive, in part, from anti-infl ammatory actions of fi sh oils: families of bioactive lipids which favor resolution of infl ammation have been suggested to be of particular importance ( 13 ). Synthetic versions of such specialized pro-resolving mediators (SPMs), products of transcellular metabolism of fi sh oils, exert anti-infl ammatory effects in vitro and when administered in vivo in several animal models ( 14-17 ). Quantities Abstract Resolvins, maresins, and protectins can be formed from fi sh oils. These specialized pro-resolving mediators (SPMs) have been implicated in the resolution of infl ammation. Synthetic versions of such SPMs exert anti-infl ammatory effects in vitro and when administered to animal models. However, their importance as endogenous products formed in suffi cient amounts to exert anti-infl ammatory actions in vivo remains speculative. We biased our ability to detect SPMs formed in healthy volunteers by supplementing fi sh oil in doses shown previously to infl uence blood pressure and platelet aggregation under placebo-controlled conditions. Additionally, we sought to determine the relative formation of SPMs during an acute infl ammatory response and its resolution, evoked in healthy volunteers by bacterial lipopolysaccharide (LPS). Bioactive lipids, enzymatic epoxyeicosatrienoic acids (EETs), and free radical-catalyzed prostanoids [isoprostanes (iPs)] formed from arachidonic acid and the fi sh oils, served as comparators. Despite the clear shift from -6 to -3 EETs and iPs, we failed to detect a consistent signal, in most cases, of SPM formation in urine or plasma in response to fi sh oil, and in all cases in response to LPS on a background of fi sh oil. Our results que...

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“…Subsequent studies have examined the effect of n-3 fatty acids supplementation in relation to plasma SPM formation in healthy volunteers [21,23 & ,26]; patients suffering from chronic headaches [22]; mild hypertriglyceridemia [27]; chronic renal disease [24 && ]; and peripheral artery disease [28].…”

Section: Specialized Proresolving Mediators In Humans and The Effect mentioning

confidence: 99%

“…In a controlled trial of 10 weeks, 53 patients with mild hypertriglyceridemia were randomized to one of three groups that were given a fruit yoghurt enriched with either n-3 fatty acids (0.8 g/day or 3 g/day) or placebo. The primary outcomes of the study were blood lipids (total cholesterol, triglycerides, and HDL and LDL-cholesterol) [27]. Plasma 18-HEPE was measured at baseline and after 10 weeks using a lipidomic approach in the 16 patients who received 3 g/day n-3 fatty acids.…”

Section: Specialized Proresolving Mediators In Humans and The Effect mentioning

confidence: 99%

n-3 Fatty acid supplementation and proresolving mediators of inflammation

Barden

Mas

Mori

2016

Current Opinion in Lipidology

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Resolution of inflammation is an active process with SPM playing a vital role in maintaining homeostasis. Studies in humans are providing evidence to suggest that this may be a relevant mechanism that can be stimulated by n-3 fatty acid supplementation. Further research is now required to determine SPM profiles in patients with different chronic conditions and to examine whether supplementation with n-3 fatty acids affects SPMs in relation to their clinical outcome.

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Randomized placebo-controlled intervention with n-3 LC-PUFA-supplemented yoghurt: Effects on circulating eicosanoids and cardiovascular risk factors

Cited by 65 publications

References 27 publications

Short-term n-3 fatty acid supplementation but not aspirin increases plasma proresolving mediators of inflammation

Short-term n-3 fatty acid supplementation but not aspirin increases plasma proresolving mediators of inflammation

Bioactive products formed in humans from fish oils

n-3 Fatty acid supplementation and proresolving mediators of inflammation

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