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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:1413.)
© 2006 American Heart Association, Inc.

Letters to the Editor

Rosiglitazone Cools Down Inflammation in the Metabolic Syndrome

Katherine Esposito; Miryam Ciotola; Domenico Merante; Dario Giugliano

From the Division of Metabolic Diseases (K.E., M.C., D.G.), Center of Excellence for Cardiovascular Research, University of Naples SUN, Italy; and GlaxoSmithKline, Medical Department (D.M.), Verona, Italy.

Correspondence to Dario Giugliano, Division of Metabolic Diseases, Center of Excellence for Cardiovascular Research, University of Naples SUN, Piazza L. Miraglia 2, 80138 Naples, 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.

To the Editor:

We read with interest the article by Samaha et al¹ demonstrating a favorable effect of short-term rosiglitazone treatment on the inflammatory milieu in nondiabetic subjects with low high-density lipoprotein cholesterol and the metabolic syndrome. Almost simultaneously, the same group reported similar effects of pioglitazone in subjects with the metabolic syndrome.² The proinflammatory state that accompanies the metabolic syndrome is associated with both insulin resistance and endothelial dysfunction, providing a connection between inflammation and metabolic processes which is highly deleterious for vascular functions.³ PPAR- agonists have displayed unique characteristics, in both animal and clinical studies, indicating that they have antiatherogenic properties.⁴ These compounds may have direct beneficial effects on cardiovascular risk independent of their hypoglycemic action.⁵ Two pilot studies with troglitazone⁶ and pioglitazone⁷ have shown reduced carotid intima-media thickness in patients with type 2 diabetes mellitus. Moreover, a placebo-controlled study showed reduced progression of the intima-media thickness of the common carotid artery in nondiabetic patients who were treated with rosiglitazone.⁸ More recently, pioglitazone reduced the composite of all-cause mortality, non-fatal myocardial infarction, and stroke in patients with type 2 diabetes who have a high risk of macrovascular events.⁹

Nuclear factor B (NF-B) plays a central role in inflammation and atherogenesis. NF-B is normally bound to IB in the cytosol which prevents its movement into the nucleus. Phosphorylation of IB ( and ß) promotes its ubiquitination and subsequent degradation by the proteasome, releasing NF-B to translocate into the nucleus where it induces the transcription . . . [Full Text of this Article]