The adipose tissue plays a major role in energy homeostasis as the main tissue of energy reserve but also as source of adipokines involved in the control of metabolic fluxes. Among them, many adipokines exhibit pro-angiogenic activities including leptin (1), the family of vascular endothelial growth factors, the angiopoietins, hepatocyte growth factor, angiopoietin like factor 4, apelin, visfatin, the families of fibroblast growth factors and of matrix metalloproteinases (2). Anti-angiogenic factors such as thrombospondins, Secreted Protein Acidic and Rich in Cysteine, osteopontin, resistin, the metalloproteases inhibitors and plasminogen activator inhibitor 1 are also produced by TA (2). The global angiogenic status of the human AT is modulated mainly by the adiposity degree and the AT location. Indeed, a global increase in AT angiogenic status is found with obesity. This effect might be related to the accumulation of immune-inflammatory cells within AT including macrophages shown to stimulate angiogenesis in AT (3) . Hypoxia, that may be consecutive to the increased size of adipocytes (or hypertrophy), is a condition that will increase the production of pro-angiogenic adipokines in AT (4). Distinct angiogenic statuses are described according to the fat mass location, visceral AT being considered more proangiogenic than subcutaneous fat mass (5). Angiogenesis within AT is a key event in the cellular homeostasis during fat mass development and most of the approaches to lower angiogenesis have been shown to interfere with AT growth and whole energy expenditure (6). This key mechanism may become pathological under too strong local angiogenic pressure leading to accelerated aging of endothelial cells (5) and ultimatively to endothelial cell dysfunction. Therefore the link involving adipokines in the communication between adipocytes and endothelial cells is of great interest to better understand the link between obesity and associated pathologies.