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01.12.2014 | Research | Ausgabe 1/2014 Open Access

Diabetology & Metabolic Syndrome 1/2014

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

Diabetology & Metabolic Syndrome > Ausgabe 1/2014
Cristina Nita, Cornelia Bala, Mihai Porojan, Nicolae Hancu
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​1758-5996-6-30) contains supplementary material, which is available to authorized users.
Cristina Nita, Cornelia Bala contributed equally to this work.

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

CN and CB were study coordinators, participated in the design of the study, were responsible for individual selection and characterization, carried out the statistical analysis and drafted the manuscript. MP carried out vascular studies and participated to manuscript preparation. NH participated in the design of the study and to manuscript preparation. All authors read and approved the final manuscript.



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.


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.


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).


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 ANZCTR1261200073​4864)
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