title: Insulin resistance and chronic cardiovascular inflammatory syndrome.
abstract: Insulin resistance is increasingly recognized as a chronic, low-level, inflammatory state. Hyperinsulinemia and insulin action were initially proposed as the common preceding factors of hypertension, low high-density lipoprotein cholesterol, hypertriglyceridemia, abdominal obesity, and altered glucose tolerance, linking all these abnormalities to the development of coronary heart disease. The similarities of insulin resistance with another inflammatory state, atherosclerosis, have been described only in the last few decades. Atherosclerosis and insulin resistance share similar pathophysiological mechanisms, mainly due to the actions of the two major proinflammatory cytokines, TNF-alpha and IL-6. Genetic predisposition to increased transcription rates of these cytokines is associated with metabolic derangement and simultaneously with coronary heart disease. Dysregulation of the inflammatory axis predicts the development of insulin resistance and type 2 diabetes mellitus. The knowledge of how interactions between metabolic and inflammatory pathways occur will be useful in future therapeutic strategies. The effective administration of antiinflammatory agents in the treatment of insulin resistance and atherosclerosis is only the beginning of a promising approach in the management of these syndromes.
authors.affiliation: Section of Diabetes, Endocrinology and Nutrition, University Hospital of Girona Dr. Josep Trueta, 17007 Girona, Spain. uden.jmfernandezreal@htrueta.scs.es
authors.forename: José Manuel
authors.initials: JM
authors.lastname: Fernández-Real
authors.forename: Wifredo
authors.initials: W
authors.lastname: Ricart
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D002318:Cardiovascular Diseases / Q000503:physiopathology*; D002908:Chronic Disease; D016207:Cytokines / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000209:etiology / Q000517:prevention & control; D006801:Humans; D006949:Hyperlipidemias / Q000503:physiopathology; D006973:Hypertension / Q000503:physiopathology; D007249:Inflammation / Q000150:complications / Q000503:physiopathology; D018836:Inflammation Mediators / Q000378:metabolism; D007333:Insulin Resistance; D013577:Syndrome
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; D018836:Inflammation Mediators