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PMID: 23805408 Published · ppublish English Journal Article

New insights into adipose tissue VEGF-A actions in the control of obesity and insulin resistance.

Adipocyte ·Vol. 2 ·No. 2 ·2013-04-01 ·Pages 109-12

Elias I, Franckhauser S, Bosch F

Abstract

Vascular endothelial growth factor A (VEGF-A) is classically viewed as a key factor in angiogenesis and tissue remodeling. However, recent evidence suggests a potential role of this growth factor in the control of energy metabolism and adipose tissue function. In this regard, we and others have described the effects of the up and downregulation of VEGF-A in adipose tissue on the control of energy homeostasis. VEGF-A overexpression protects against diet-induced obesity and insulin resistance. The observation that VEGF-A overexpression leads to an increase in brown adipose tissue (BAT) thermogenesis and also promotes a "BAT-like" phenotype in white adipose tissue depots is of particular relevance for the understanding of the mechanisms underlying obesity development. In addition, VEGF-A may not only have pro-inflammatory but also anti-inflammatory properties, with a chemotactic activity specific for M2 anti-inflammatory macrophages. This new scientific evidence highlights the importance that VEGF-A actions on metabolism could have on the design of new treatments for obesity, insulin resistance and obesity-related disorders.

Keywords
VEGF-A adipose tissue inflammation insulin resistance obesity
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Elias Ivet
Center of Animal Biotechnology and Gene Therapy; School of Veterinary Medicine; Universitat Autònoma de Barcelona; Barcelona, Spain ; Department of Biochemistry and Molecular Biology, School of Veterinary Medicine, Universitat Autònoma de Barcelona; Barcelona, Spain ; CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM); Barcelona, Spain.
Franckhauser Sylvie
Bosch Fatima
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Article Info
Journal
Adipocyte
Abbr.
Adipocyte
ISSN
2162-3945
DOI
10.4161/adip.22880
Published
2013-04-01
Pages
109-12
Language
English
Region
United States
NLM ID
101567863
PMCID
PMC3661112
External Links
PubMed source DOI: 10.4161/adip.22880 PMC Full Text View journal details
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