Fenofibrate improves endothelial function and plasma myeloperoxidase in patients with type 2 diabetes mellitus: an open-label interventional study

Diabetology & Metabolic Syndrome

Nicolae Hancu¹  Mihai Porojan²  Cornelia Bala¹  Cristina Nita¹ 

[1]Department of Diabetes, Nutrition and Metabolic Diseases, “Iuliu Hatieganu” University of Medicine and Pharmacy Cluj-Napoca, 2-4 Clinicilor Street, 400006 Cluj-Napoca, Romania

[2]Department of Internal Medicine, “Iuliu Hatieganu” University of Medicine and Pharmacy Cluj-Napoca, 4-6 Clinicilor Street, 400006 Cluj-Napoca, Romania

关键词: Type 2 diabetes;    sE-selectin;    Endothelial dysfunction;    Myeloperoxidase;    Fenofibrate;   

Others  :  805134
DOI  :  10.1186/1758-5996-6-30

 received in 2013-10-08, accepted in 2014-02-13,  发布年份 2014

【 摘 要 】

Background

Fenofibrate offers a number of benefits on the cardiovascular system and it is plausible that its anti-inflammatory, anti-oxidant and anti-fibrotic effects and enhancement of cardiac metabolic performances may account for its direct cardioprotective effects.

In this study we aimed to investigate the effect of fenofibrate on endothelial function assesed by vascular studies and levels of soluble E-selectin (sE-selectin) as well as the effect on plasma myeloperoxidase (MPO) in patients with type 2 diabetes mellitus (T2DM) without previous use of lipid-lowering medication.

Methods

27 patients (14 men and 13 women) with T2DM and good glycemic control (HbA1c: min 5.9%, max: 7.1%) treated with metformin monotherapy, without previous use of lipid-lowering medication were enrolled in this study. Vascular studies included measures of brachial artery diameter before and after release of a suprasystolic ischemia. FMD was calculated as the percent (%) change in arterial diameter following reactive hyperemia. Student’s paired t test and Wilcoxon Signed Ranks Test were used to compare values before and after fenofibrate therapy.

Results

Fenofibrate therapy significantly increased post ischemia mean brachial artery diameter at 60 s (from 4.7 [4.4; 5.0] mm to 4.9 [4.6; 5.2] mm, p = 0.01) and at 90 s (from 4.7 [4.4; 5.0] mm to 4.9 [4.6; 5.1], p = 0.02). FMD response to hyperaemia at 60 s increased with 4.5 ± 13.7% (median value pre- treatment: 22.2%, median value post- treatment 25.0%, z = −2.9, p = 0.004). After 8 weeks of fenofibrate therapy, plasma MPO levels decreased to 49.5 [30.3; 71.5] ng/ml (% change from baseline = 4.6%, z = −2.2, p = 0.03) and mean plasma sE-selectin levels decreased to 67.1 [54.4; 79.8] ng/ml, (% change from baseline = 2.6%, p = 0.03).

Conclusion

In patients with T2DM without previous treatment for dyslipidemia, short-term treatment with fenofibrate improved vascular endothelial function as demonstrated by increased post ischemia mean brachial artery diameter, increased FMD and decreased plasma sE-selectin and favorably affected plasma MPO levels. Therefore, fenofibrate may be considered a protective cardiovascular drug in this group of patients.

Trial registration

(Australian New Zealand Clinical Trials Registry ANZCTR12612000734864)

【 授权许可】

   
2014 Nita et al.; licensee BioMed Central Ltd.

【 图 表 】

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