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Medical Principles and Practice. 2017; 26 (6): 535-541
in English | IMEMR | ID: emr-197080


Objective: Jo determine the effect of supplementation with n-3 polyunsaturated fatty acids (PUFAs) on circulatory resis-tin and monocyte chemoattractant protein 1 [MCP-1] levels in type 2 diabetes mellitus [T2DM] patients

Subjects and Methods: This was a 10-week, placebo-controlled, double-blind, randomized trial of n-3 PUFAs [2,700 mg/day] versus placebo [soft gels containing 900 mg of edible paraffin]. Forty-four T2DM patients were supplemented with n-3 PUFAs and another 44 patients received placebo (3 patients discontinued the trial]. Serum resistin, MCP-1, and the lipid profile were measured before and after supplementation. The adi-ponectin-resistin index [1 + Iog[10] [resistin] - Iog10 [adiponec-tin]] and atherogenic index [Iog[10] triglyceride/high-density lipoprotein cholesterol] of plasma [an indicator of cardiovascular complications] were assessed. The independent Student t test was used to assess the differences between the supplement and placebo groups and the paired f test to analyze the before/after changes

Results: In this study, n-3 PUFAs reduced serum MCP-1 levels [from 260.5 to 230.5 pg/ ml_;p = 0.002], but they remained unchanged in the placebo group, n-3 PUFAs could not decrease serum resistin levels. The adiponectin-resistin index was significantly reduced after supplementation with n-3 PUFAs when compared to theplacebo. The atherogenic index was also significantly improved after supplementation with n-3 PUFAs [from 1.459 to 1.412; p = 0.006]

Conclusions: The MCP-1 levels and lipid profile were improved after supplementation with n-3 PUFAs, but resistin serum levels were not changed. Hence, the anti-inflammatory effects of n-3 PUFAs might be mediated by targeting MCP-1

Archives of Iranian Medicine. 2012; 15 (11): 688-692
in English | IMEMR | ID: emr-160610


Visfatin, a novel adiopocytokine, has been proven to be a proinflammatory mediator involved in the process of atherosclerosis. Visfatin has been shown to play a role in plaque destabilization as it is found abundantly in foam cell macrophages within unstable atherosclerotic plaques. The present study is designed to investigate the potential association between serum vistafin levels and the risk of acute myocardial infarction [AMI]. There were 72 patients [mean age: 61.57 +/- 11.40 years] as cases who presented with first-time AMI that were assessed 8 hours after the incident. The control group consisted of 83 healthy volunteers [mean age: 60.30 +/- 8.32 years]. Plasma visfatin levels were measured using enzyme immunoassay in both groups. Biochemical parameters were analyzed. Blood pressure, body mass index [BMI], waist circumference, diabetes, and hypertension were recorded. Serum visfatin levels were significantly higher in patients with AMI [12.77 +/- 8.06 ng/ml] compared to controls [6.57 +/- 2.96 ng/ml, P 7.244 ng/ml [log visfatin > 0.86] had a sensitivity of 70% and a specificity of 75% for predicting AMI. We have detected high levels of visfatin in patients with AMI. It can be concluded that proinflammatory cytokines such as visfatin may play a role in the development of atherosclerosis as well as destabilization of the atherosclerotic plaque