Omega-3 Polyunsaturated Fatty Acids Increase Plasma Adiponectin to Leptin Ratio in Stable Coronary Artery Disease

Abstract

BackgroundGrowing evidence suggests a cardioprotective role of omega-3 polyunsaturated fatty acids (PUFA). However, the exact mechanisms underlying the effects of omega-3 PUFA in humans have not yet been fully clarified.PurposeWe sought to evaluate omega-3 PUFA-mediated effects on adipokines in patients with stable coronary artery disease (CAD) undergoing elective percutaneous coronary intervention (PCI).MethodsWe conducted a prospective, double-blind, placebo-controlled, randomized study, in which adiponectin, leptin and resistin were determined at baseline, 3–5 days and 30 days during administration of omega-3 PUFA 1 g/day (n = 20) or placebo (n = 28).ResultsAs compared to controls administration of omega-3 PUFA resulted in increase of adiponectin by 13.4 % (P < 0.0001), reduction of leptin by 22 % (P < 0.0001) and increase of adiponectin to leptin (A/L) ratio by 45.5 % (P < 0.0001) at 30 days, but not at 3–5 days. Compared with placebo adiponectin was 12.7 % higher (P = 0.0042), leptin was 16.7 % lower (P < 0.0001) and A/L ratio was 33.3 % higher (P < 0.0001) in the omega-3 PUFA group at 30 days. Resistin decreased similarly in both groups after 1 month, without intergroup differences (P = 0.32). The multivariate model showed that the independent predictors of changes in adiponectin at 1 month (P < 0.001) were: omega-3 PUFA treatment, baseline platelet count, total cholesterol and those in leptin (P < 0.0001) were: omega-3 PUFA treatment and waist circumference. Independent predictors of A/L ratio changes (P < 0.0001) were: assigned treatment, current smoking and hyperlipidemia.ConclusionsIn high risk stable coronary patients after PCI omega-3 PUFA supplementation improves adipokine profile in circulating blood. This might be a novel, favourable mechanism of omega-3 PUFA action.Electronic supplementary materialThe online version of this article (doi:10.1007/s10557-013-6457-x) contains supplementary material, which is available to authorized users.

Omega-3 fatty acids’ effect on leptin and adiponectin concentrations in patients with spinal cord injury: A double-blinded randomized clinical trial

“…We did not detect any influence of 14-month administration of ω-3 PUFA on circulatory leptin concentration in patients with SCI, which is in line with the findings of Sneddon et al 33 who investigated this association in lean and obese men. By considering previous reports 30,31,34,35 that demonstrated increased adiponectin after ω-3 PUFA therapy and decreased leptin 30 concentration in patients with CVDs, this point is clarified that the effect of ω-3 PUFA is dependent on patients' background disorders. Weight was positively related with leptin concentration at the beginning of the trial (stage 0) but this association was attenuated only in the treatment group after receiving ω-3 PUFA while it remained significant in the placebo group till the end of the trial.…”

“…29 Some alterations in leptin and adiponectin concentrations have been reported after intervention with omega-3 fatty acids. Mostowik et al 30 showed increased adiponectin to leptin ratio with a 30-day administration of omega-3 fatty acids in patients with stable coronary artery disease. However, its effect on circulatory concentrations of leptin and adiponectin was not yet evaluated in spinal cord injured patients.…”

Exploration of micro- and macronutrient consumption and leverage of interaction with adipokines among Jordanian adults

“…Also, an increased dietary consumption of fish was found to be associated with a reduced level of leptin [28]. Mostowik et al (2013) found that daily supplementation of 1 g/d of omega-3 fatty acid for 30 days significantly increased adiponectin level and adiponectin/leptin ratio as well as resulted in a significant reduction in leptin level [68]. The effect of omega-3 fatty acid on adiponectin and leptin levels is suggested to be a concomitant to its modulatory effects on cytokine and proinflammatory mediators [21].…”

Beneficial Effects of n-3 Fatty Acids on Cardiometabolic and Inflammatory Markers in Type 2 Diabetes Mellitus: A Clinical Trial

“…Long-chain n-3 polyunsaturated fatty acids (PUFAs), namely, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), decrease plasma triglyceride (TG) levels, arrhythmias, and inflammation, thereby ameliorating endothelial dysfunction [2,4]. The beneficial effect of n-3 PUFA intake on the metabolic profile of patients with T2DM and obesity has been reported [5].…”

“…n-3 PUFAs accumulate in adipose tissue [4], so it could be hypothesized that some of their effects might partly be associated with improvements in adipose tissue function. Moreover, n-3 PUFAs have been found to ameliorate the low-grade inflammation in adipose tissue and regulate adipokine gene expression [4,6].…”