title: [Low-grade systemic inflammation and the development of metabolic diseases: from the molecular evidence to the clinical practice].
abstract: BACKGROUND
  Systemic inflammation is characterised by high circulating levels of inflammatory cytokines and increased macrophage infiltration in peripheral tissues. Most importantly, this inflammatory state does not involve damage or loss of function of the infiltrated tissue, which is a distinctive feature of the low-grade systemic inflammation. The term "meta-inflammation" has also been used to refer to the low-grade systemic inflammation due to its strong relationship with the development of cardio-metabolic diseases in obesity.
  
  
  OBJECTIVE
  A review is presented on the recent clinical and experimental evidence concerning the role of adipose tissue inflammation as a key mediator of low-grade systemic inflammation. Furthermore, the main molecular mechanisms involved in the inflammatory polarization of macrophages with the ability to infiltrate both the adipose tissue and the vascular endothelium via activation of toll-like receptors by metabolic damage-associated molecular patterns, such as advanced glycation-end products and oxidized lipoproteins, is discussed. Finally, a review is made of the pathogenic mechanisms through which the low-grade systemic inflammation contributes to develop insulin resistance, dyslipidaemia, atherogenesis, type 2 diabetes, and hypertension in obese individuals.
  
  
  CONCLUSIONS
  A better understanding of the molecular mechanisms of low-grade systemic inflammation in promoting cardio-metabolic diseases is necessary, in order to further design novel anti-inflammatory therapies that take into consideration clinical data, as well as the circulating levels of cytokines, immune cells, and metabolic damage-associated molecular patterns in each patient.
authors.affiliation: Servicio de Medicina Interna, Clínica de Obesidad y Síndrome Metabólico, Hospital General de México «Dr. Eduardo Liceaga», México, D. F., México.
authors.forename: José Israel
authors.initials: JI
authors.lastname: León-Pedroza
authors.affiliation: Servicio de Medicina Interna, Clínica de Obesidad y Síndrome Metabólico, Hospital General de México «Dr. Eduardo Liceaga», México, D. F., México.
authors.forename: Luis Alonso
authors.initials: LA
authors.lastname: González-Tapia
authors.affiliation: Servicio de Medicina Interna, Clínica de Obesidad y Síndrome Metabólico, Hospital General de México «Dr. Eduardo Liceaga», México, D. F., México.
authors.forename: Esteban
authors.initials: E
authors.lastname: del Olmo-Gil
authors.affiliation: Servicio de Medicina Interna, Clínica de Obesidad y Síndrome Metabólico, Hospital General de México «Dr. Eduardo Liceaga», México, D. F., México.
authors.forename: Diana
authors.initials: D
authors.lastname: Castellanos-Rodríguez
authors.affiliation: Laboratorio de Hígado, Páncreas y Motilidad, Unidad de Medicina Experimental, Facultad de Medicina, Universidad Nacional Autónoma de México, México, D. F., México.
authors.forename: Galileo
authors.initials: G
authors.lastname: Escobedo
authors.affiliation: Servicio de Medicina Interna, Clínica de Obesidad y Síndrome Metabólico, Hospital General de México «Dr. Eduardo Liceaga», México, D. F., México. Electronic address: antglez51@yahoo.com.mx.
authors.forename: Antonio
authors.initials: A
authors.lastname: González-Chávez
mesh_terms: D054392:Adipokines / Q000378:metabolism; D001161:Arteriosclerosis / Q000209:etiology / Q000503:physiopathology; D016207:Cytokines / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000209:etiology / Q000503:physiopathology; D050171:Dyslipidemias / Q000209:etiology / Q000503:physiopathology; D017127:Glycation End Products, Advanced / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000150:complications* / Q000503:physiopathology / Q000628:therapy; D007333:Insulin Resistance; D050417:Insulin-Secreting Cells / Q000473:pathology; D050152:Intra-Abdominal Fat / Q000503:physiopathology; D020738:Leptin / Q000502:physiology; D008264:Macrophages / Q000502:physiology; D024821:Metabolic Syndrome / Q000209:etiology* / Q000503:physiopathology; D008954:Models, Biological; D016328:NF-kappa B / Q000378:metabolism; D009765:Obesity / Q000150:complications* / Q000503:physiopathology; D051192:Receptors, Pattern Recognition / Q000502:physiology; D051193:Toll-Like Receptors / Q000502:physiology
chemical_list: D054392:Adipokines; D016207:Cytokines; D017127:Glycation End Products, Advanced; D020738:Leptin; D016328:NF-kappa B; D051192:Receptors, Pattern Recognition; D051193:Toll-Like Receptors
keywords: Adipose tissue; Arterioesclerosis; Arteriosclerosis; Diabetes mellitus tipo 2; Enfermedades metabólicas; Inflamación sistémica de grado bajo; Insulin resistance; Low-grade systemic inflammation; Macrophages; Macrófagos; Metabolic diseases; Resistencia a la insulina; Tejido adiposo; Type 2 diabetes