The plasticity of adipose tissue (AT) is related to its angiogenic ability. Angiogenesis is a multistep process which involves endothelial cell (EC) proliferation, migration, invasion and finally tube formation. AT as a secretory organ produces adipokines, which contributes to the development of subclinical inflammation. The inflammation-related adipokines deteriorate EC function and in consequence change the production of endothelial mediators responsible for vascular homeostasis and angiogenesis, leading to cardiovascular diseases (CVD) in obese patients. Additionally, the recent observation suggests that AT is poorly oxygenated in obesity. Hypoxia limits the healthy expansion of AT and stimulates a molecular response, enhancing nuclear factor kappa-B (NF-kB) and hypoxia-inducible factor (HIF-1) expression. HIF-1α induction does not start a normal angiogenic process but rather induces inflammatory response and fibrosis that is strongly associated with insulin resistance (IR). It is believed that EC dysfunction in obesity can be reduced by caloric restriction (CR). Moderate CR reflects a real-life situation and could be optimal to achieve an EC improvement. It reduces adiposity leading to pro-angiogenic, anti-inflammatory and—to a lesser extent—anti-oxidative cellular effects, which not only preserves the healthy EC phenotype but also leads to an improvement of AT remodeling and prevent systemic IR.
Part of the book: Endothelial Dysfunction