title: [Obesity and inflammation].
abstract: The adipose tissue produces a vast number of molecules called adipokines such as leptin, tumoral necrosis factor (TNFalpha), interleukins and adiponectin. Many of the metabolic disturbances associated with obesity and the metabolic syndrome may be due to citokine production by adipocytes. The adipose tissue increases the soluble fractions of TNFalpha leading to a rise in its biological activity. The activation of TNFalpha system causes insulin resistance through different mechanisms such as defects in receptor fosforilation and reduction in insulin-sensitive glucose transporters. TNFalpha is also involved in the pathophysiology of hypertension and dyslipidaemia associated with obesity and insulin resistance. More than one third of interleukin-6 (IL-6) concentrations come from the adipocytes. It has been demonstrated a role for IL-6 in the development of hyperlipidemia, diabetes and hypertension. In contrast to the rest of adipokines, adiponectin is reduced in obesity, diabetes or cardiovascular disease. Adiponectin improves insulin resistance, dyslipidaemia and adhesion to endothelial cells protecting from atherosclerosis development. Thus, adipokines have an important role in the pathophysiology of metabolic syndrome by different mechanisms involving metabolic and vascular effects.
authors.affiliation: Unidad de Diabetes, Endocrinología y Nutrición, Hospital Universitari de Girona, Doctor Josep Trueta.
authors.forename: M
authors.initials: M
authors.lastname: Recasens
authors.forename: W
authors.initials: W
authors.lastname: Ricart
authors.forename: J M
authors.initials: JM
authors.lastname: Fernández-Real
mesh_terms: D017667:Adipocytes / Q000378:metabolism*; D052242:Adiponectin; D000818:Animals; D001161:Arteriosclerosis / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control; D002318:Cardiovascular Diseases / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control; D016207:Cytokines / Q000502:physiology*; D003924:Diabetes Mellitus, Type 2 / Q000209:etiology / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000503:physiopathology; D007249:Inflammation / Q000209:etiology* / Q000503:physiopathology; D007333:Insulin Resistance / Q000502:physiology; D036341:Intercellular Signaling Peptides and Proteins; D015850:Interleukin-6 / Q000502:physiology; D024821:Metabolic Syndrome / Q000209:etiology* / Q000503:physiopathology; D008954:Models, Biological; D009765:Obesity / Q000150:complications* / Q000503:physiopathology; D011506:Proteins / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
chemical_list: D052242:Adiponectin; D016207:Cytokines; D036341:Intercellular Signaling Peptides and Proteins; D015850:Interleukin-6; D011506:Proteins; D014409:Tumor Necrosis Factor-alpha
vernacular_title: Obesidad e inflamación.