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Dose-response effects of marine omega-3 fatty acids on apolipoproteins, apolipoprotein-defined lipoprotein subclasses, and Lp-PLA2 in individuals with moderate hypertriglyceridemia.

ABSTRACT: Apolipoprotein (apo) distribution and lipoprotein (Lp)-associated markers of inflammation, such as lipoprotein-associated phospholipase A2 (Lp-PLA2), influence the atherogenicity of circulating lipids and lipoproteins. Little evidence exists regarding the dose-response effects of the marine omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on apos, apo-defined Lps, and Lp-PLA2.The purpose of this study was to compare the effects of 0, 0.85, and 3.4 g/d of EPA + DHA on Lp-PLA2 mass and activity in individuals with moderate hypertriglyceridemia. We also measured effects on concentrations of apoAI, apoAII, apoB, apoC, apoD, and apoE-defined Lp subclasses.The study was a randomized, doubleblind, crossover design with 8-week treatment periods and 6-week washout periods. During the 3 treatment periods, subjects (n = 25) received 0 g/d EPA + DHA, 0.85 g/d EPA + DHA (low dose), and 3.4 g/d EPA + DHA (high dose) in random order.apoB and apoC-III were significantly decreased by the high dose relative to placebo and low dose (P < .01), as was very low-density lipoprotein cholesterol (P < .005). The low dose had no effect on Lp outcomes compared with placebo. The high- and low-dose effects differed significantly for heparin-precipitated apoC-III, LpB, LpA-I, and apoB/apoA-I ratio (P < .05). There was a trend for a decreased Lp-PLA2 mass with the high dose (P = .1).The effects of 3.4 g/d EPA + DHA on apoB and apoC-III may reduce atherosclerotic plaque progression in individuals with elevated triglycerides.

SUBMITTER: Skulas-Ray AC

PROVIDER: S-EPMC4677829 | biostudies-literature | 2015 May-Jun

REPOSITORIES: biostudies-literature

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Dose-response effects of marine omega-3 fatty acids on apolipoproteins, apolipoprotein-defined lipoprotein subclasses, and Lp-PLA2 in individuals with moderate hypertriglyceridemia.

Skulas-Ray Ann C AC Alaupovic Petar P Kris-Etherton Penny M PM West Sheila G SG

Journal of clinical lipidology 20141211 3

<h4>Background</h4>Apolipoprotein (apo) distribution and lipoprotein (Lp)-associated markers of inflammation, such as lipoprotein-associated phospholipase A2 (Lp-PLA2), influence the atherogenicity of circulating lipids and lipoproteins. Little evidence exists regarding the dose-response effects of the marine omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on apos, apo-defined Lps, and Lp-PLA2.<h4>Objective</h4>The purpose of this study was to compare the effects o ...[more]

PMID: 26073395

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Project description:Based on the complex pathophysiology of atherosclerosis, a large number of biomarkers that relate to lipids, inflammation, immunity, thrombosis and hemostasis, have been investigated experimentally, in epidemiologic studies and in clinical trials. Interest focuses on their potential role to aid in risk stratification, as possible surrogate markers of atherosclerosis, and potential targets for therapy. More recently, one lipid associated biomarker, lipoprotein-associated phospholipase A2 (Lp-PLA₂), has gained considerable interest. In addition to a plausible pathophysiological role by generating pro-inflammatory and pro-atherogenic compounds from oxidized LDL in the vessel wall, there is a large, fairly consistent epidemiological database indicating that increased levels of Lp-PLA2 mass or activity are associated with increased risk for cardiovascular outcomes; such data further suggest that it might improve risk stratification. In addition, clinical studies indicate that increased Lp-PLA₂ levels are associated with endothelial dysfunction. Moreover, it may also serve as an interesting therapeutic target, since a specific inhibitor of the enzyme is available with promising animal data and initial positive data in humans. Recent experimental data from a hyperlipidemic diabetic pig model strongly suggest that increased Lp-PLA2 in the vessel wall is associated with a more vulnerable plaque phenotype which can be modulated by inhibiting Lp-PLA₂ activity. A biomarker study in more than 1,000 patients with CHD over three months has demonstrated a positive effect on various inflammatory molecules. In addition, an imaging study using IVUS based modalities (greyscale, virtual histology, and palpography) together with a panel of biomarkers (IBIS-2) has been done in more than 300 patients with CHD treated over 12 months and results indicate that the progression of the necrotic core of the plaque can be retarded. Inhibition of the pro-atherogenic and pro-inflammatory effects of Lp-PLA₂ may therefore contribute to decrease the residual risk in high risk patients already on polypharmacotherapy. This hypothesis is now being tested in two large phase 3 clinical trials. Thus, Lp-PLA₂ indeed may represent a biomarker and a promising target for intervention.

Project description:Introduction:Lipoprotein associated phospholipase A2 (Lp-PLA2) has been explored as a potential biomarker for Cardiovascular Disease (CVD). The human Lp-PLA2 is a serine-dependent, Ca2+- independent enzyme. It gives way to oxidised free fatty acids and lysophosphatidyl choline by hydrolysing oxidised phospholipids, that leads to smooth muscle cell apoptosis, inflammatory cell chemotaxis and endothelial cell dysfunction in CVD. Owing to its role in inflammation, it may influence the development and progression of periodontitis as well. Aim:To compare the demographic variables, Gingival Index(GI), Bleeding On Probing (BOP), Probing Pocket Depth (PPD), and Clinical Attachment Level (CAL) with serum lipid profile and Lp-PLA2 level in Chronic Periodontitis (CP) subjects. Materials and Methods:A total of 75 subjects were selected and divided into three groups; based on the inclusion and exclusion criteria: Group I - 25 subjects with severe generalized CP with CAL ? 5 mm in more than 30% of sites. Group II -25 subjects with moderate generalized CD with clinical CAL 3 mm-4 mm in more than 30% of sites. Group III- 25 systemically and periodontally healthy volunteers who served as control. Clinical parameters such as Plaque Index (PI), BOP, Probing Depth (PD) and CAL, lipid profile such as Total Cholesterol (TC), Triglyceride (TG), High density Lipoprotein (HDL), Low Density Lipoprotein (LDL), Very Low Density Lipoprotein (VLDL) as well as Lp-PLA2 were assessed. One-way ANOVA and Tukey's Post-hoc test were used for data analysis. Results:Age was higher in Group I and II when compared to Group III. Group II showed a significant correlation between PI and LDL. In Group III, lower PI was significantly correlated with high HDL and low LDL and BOP was positively correlated with TG and HDL. A significant association of Lp-PLA2 was found to be higher with increase in the TG and VLDL level in Group I and Group II when compared to Group III. Conclusion:The study concluded that Lp-PLA2, TG and VLDL already being a predictor biomarker for atherosclerotic disease can be an inflammatory marker for periodontitis.

Dataset Information

Dose-response effects of marine omega-3 fatty acids on apolipoproteins, apolipoprotein-defined lipoprotein subclasses, and Lp-PLA2 in individuals with moderate hypertriglyceridemia.

Publications

Dose-response effects of marine omega-3 fatty acids on apolipoproteins, apolipoprotein-defined lipoprotein subclasses, and Lp-PLA2 in individuals with moderate hypertriglyceridemia.

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