title: Pathophysiological implications between chronic inflammation and the development of diabetes and obesity.
abstract: The different theories about the mechanisms involved in the development of metabolic disease and its complications converge in the presence of an etiologic chronic proinflammatory state. Chronic inflammation is, at present, the central pathophysiological mechanism involved in the genesis of metabolic diseases. The multiple interactions between the immune system, adipose tissue, the vascular wall and the pancreas are the issues addressed in this review, focusing on specific intracellular and molecular aspects that may become new therapeutic targets. These lead to a proinflammatory, prothrombotic state as well as to proapoptotic endothelial damage that allows the development of atherosclerosis and, consequently, cardiovascular disease. The multiple immunopathological processes associated with the etiology and pathophysiology of different chronic diseases is still in the process of being fully elucidated, allowing the development of new therapeutic targets.
authors.affiliation: Unidad 308, Servicio de Medicina Interna, Hospital General de México, Secretaría de Salud, México, D. F., Mexico. antglez51@yahoo.com.mx
authors.forename: Antonio
authors.initials: A
authors.lastname: González-Chávez
authors.forename: Sandra
authors.initials: S
authors.lastname: Elizondo-Argueta
authors.forename: Gabriela
authors.initials: G
authors.lastname: Gutiérrez-Reyes
authors.forename: José Israel
authors.initials: JI
authors.lastname: León-Pedroza
mesh_terms: D000273:Adipose Tissue / Q000503:physiopathology; D050197:Atherosclerosis / Q000209:etiology / Q000503:physiopathology; D002908:Chronic Disease; D016207:Cytokines / Q000502:physiology; D003924:Diabetes Mellitus, Type 2 / Q000209:etiology* / Q000503:physiopathology; D004721:Endoplasmic Reticulum / Q000502:physiology; D005609:Free Radicals; D006801:Humans; D058847:Inflammasomes / Q000502:physiology; D007249:Inflammation / Q000150:complications / Q000503:physiopathology*; D018836:Inflammation Mediators; D007515:Islets of Langerhans / Q000473:pathology; D020738:Leptin / Q000502:physiology; D008928:Mitochondria / Q000502:physiology; D009765:Obesity / Q000209:etiology* / Q000503:physiopathology; D018384:Oxidative Stress; D011494:Protein Kinases / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology; D013879:Thioredoxins / Q000502:physiology
chemical_list: D016207:Cytokines; D005609:Free Radicals; D058847:Inflammasomes; D018836:Inflammation Mediators; D020738:Leptin; D013879:Thioredoxins; D011494:Protein Kinases