[Adipose tissue as a therapeutic target in obesity].
Obesity is characterized by an increase of adipose tissue as a result of a positive imbalance between food intake and energy expenditure. Recent studies have indicated that adipocyte function is more complex than expected, since these cells have multiple functions and are integrated in a homeostatic network to optimize energy resources. As metabolic sensors in the body, adipocytes and the surrounding stromal vascular cells produce and secrete autocrine, paracrine and endocrine factors, able to regulate aspects involved in the development of adipocytes, as well as effects in peripheral organs important for metabolism. Regulation of these endocrine factors could lead to new therapeutic approaches targeted at aspects related to adipogenesis, preadipocyte proliferation and differentiation, inflammatory cytokine release and secretion, adipose tissue vascularization, and regulation of lipid metabolism or, alternatively, regulation of energy dissipation in mitochondria. In the study of the mechanisms of adipogenesis and remodulation of adipose tissue with respect to adipocyte size and function, an alternative and unorthodox strategy to improve obesity-associated metabolic complications could consist of increasing the storage capacity of adipose tissue to prevent a toxic response known as lipotoxicity.
Medina-Gómez
Gema
G
Departamento de Bioquímica y Fisiología, Universidad Rey Juan Carlos, Facultad de Ciencias de la Salud, Alarcón, Madrid, España. gema.medina@urjc.es
Vidal-Puig
Antonio
A
D017667:Adipocytes / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D050156:Adipogenesis; D054392:Adipokines / Q000378:metabolism; D000273:Adipose Tissue / Q000098:blood supply / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D000818:Animals; D019440:Anti-Obesity Agents / Q000494:pharmacology*; D017209:Apoptosis; D019898:Autocrine Communication; D048429:Cell Size; D016207:Cytokines / Q000378:metabolism; D016503:Drug Delivery Systems; D004734:Energy Metabolism; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000503:physiopathology; D007333:Insulin Resistance; D050356:Lipid Metabolism; D008264:Macrophages / Q000502:physiology; D051379:Mice; D018345:Mice, Knockout; D009765:Obesity / Q000188:drug therapy* / Q000503:physiopathology; D047495:PPAR gamma / Q000502:physiology; D019899:Paracrine Communication
D054392:Adipokines; D019440:Anti-Obesity Agents; D016207:Cytokines; D047495:PPAR gamma