Mechanisms of Perivascular Adipose Tissue Dysfunction in Obesity
Author(s) -
María S. FernándezAlfonso,
Marta GilOrtega,
Concha F. GarcíaPrieto,
Isabel Aránguez,
Mariano RuizGayo,
Beatriz Somoza
Publication year - 2013
Publication title -
international journal of endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.875
H-Index - 60
eISSN - 1687-8345
pISSN - 1687-8337
DOI - 10.1155/2013/402053
Subject(s) - adipose tissue , medicine , paracrine signalling , adventitia , adipocyte , endocrinology , endothelial dysfunction , vasodilation , aorta , obesity , endothelium , vasoactive , leptin , receptor
Most blood vessels are surrounded by adipose tissue. Similarly to the adventitia, perivascular adipose tissue (PVAT) was considered only as a passive structural support for the vasculature, and it was routinely removed for isolated blood vessel studies. In 1991, Soltis and Cassis demonstrated for the first time that PVAT reduced contractions to noradrenaline in rat aorta. Since then, an important number of adipocyte-derived factors with physiological and pathophysiological paracrine vasoactive effects have been identified. PVAT undergoes structural and functional changes in obesity. During early diet-induced obesity, an adaptative overproduction of vasodilator factors occurs in PVAT, probably aimed at protecting vascular function. However, in established obesity, PVAT loses its anticontractile properties by an increase of contractile, oxidative, and inflammatory factors, leading to endothelial dysfunction and vascular disease. The aim of this review is to focus on PVAT dysfunction mechanisms in obesity.
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