Letters to the Editor |
From the Division of Metabolic Diseases, Center of Excellence for Cardiovascular Research, University of Naples SUN, Italy.
Correspondence to Dario Giugliano, MD, PhD, Division of Metabolic Diseases, University of Naples SUN, Piazza Miraglia 2, Naples, 80021 Italy. E-mail dario.giugliano@unina2.it
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Emerging evidence indicates that in patients without diabetes but with features of the metabolic syndrome, the peroxisome proliferator-activated receptor-
(PPAR-
) ligand pioglitazone exerts direct effects on inflammation and endothelial dysfunction which may be independent of amelioration of insulin resistance.1,2 In particular, in nondiabetic patients with low high density lipoprotein cholesterol (HDL-C) and the metabolic syndrome, a 12-week treatment with pioglitazone significantly raised HDL-C and favorably affected lipoprotein particle size, markers of inflammation, and adipokines without changes in triglycerides, low density lipoprotein cholesterol, or weight.1 Improvements in endothelial function and circulating markers of inflammation were also observed in nondiabetic subjects with hypercholesterolemia or hypertension receiving a 8-week treatment with pioglitazone.2 In this perspective, PPAR-
ligands may find room among possible pharmacological treatments for the metabolic syndrome, as rosiglitazone can decrease the prevalence of the syndrome by
30%.3,4
In recent years, the interest for endothelial cellderived submicroscopic membranous vesicles, termed microparticles, has substantially increased, not only because of their procoagulant properties, but also because of their putative role in inflammatory processes and their ability to directly affect endothelial functions.5,6 To our knowledge, there are no reported studies that investigated the effect of PPAR-
ligands on circulating microparticles.
We evaluated the short-term effects of pioglitazone on circulating endothelial microparticles in subjects with the metabolic syndrome as defined by NCEP (ATPIII)7; subjects were excluded if they had diabetes mellitus, cardiovascular disease, or if they took any medication, including vitamin or mineral supplements. The 10 subjects volunteered after informed consent to participate in
This article has been cited by other articles:
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A. Tesse, G. Al-Massarani, R. Wangensteen, S. Reitenbach, M. C. Martinez, and R. Andriantsitohaina Rosiglitazone, a Peroxisome Proliferator-Activated Receptor-{gamma} Agonist, Prevents Microparticle-Induced Vascular Hyporeactivity through the Regulation of Proinflammatory Proteins J. Pharmacol. Exp. Ther., February 1, 2008; 324(2): 539 - 547. [Abstract] [Full Text] [PDF] |
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