title: Increased levels of chemerin and its receptor, chemokine-like receptor-1, in obesity are related to inflammation: tumor necrosis factor-α stimulates mRNA levels of chemerin in visceral adipocytes from obese patients.
abstract: BACKGROUND
  Chemerin is a novel adipokine that regulates adipocyte development and metabolic function and glucose metabolism. Our aim was to determine the effect of chemerin and its receptor, chemokine-like receptor-1, in obesity-associated low-grade chronic inflammation, exploring its circulating and gene expression levels in obesity and the effect of weight loss and to analyze the effect of the stimulation with tumor necrosis factor-α in human visceral adipocytes at a University hospital.
  
  
  METHODS
  We included 52 women (16 lean and 36 obese) in the present study. The plasma concentrations of chemerin and the expression levels of chemerin and its receptor in visceral adipose tissue were analyzed. The chemerin concentrations were also measured before and after weight loss achieved by Roux-en-Y gastric bypass (n = 26).
  
  
  RESULTS
  The circulating concentrations and visceral adipose tissue expression of chemerin were increased in obese patients (P < .01) and were associated with well-established markers of inflammation (P < .001). Gene expression levels of chemokine-like receptor-1 followed the same trend and were upregulated (P < .05) in human obesity. Elevated chemerin levels in obese patients did not change after Roux-en-Y gastric bypass weight loss. Tumor necrosis factor-α treatment significantly enhanced (P < .05) the mRNA levels of chemerin in human visceral adipocytes, but the gene expression levels of chemokine-like receptor-1 were not affected.
  
  
  CONCLUSIONS
  The increased levels of chemerin in obesity and its positive association with inflammation suggest a role for this chemoattractant protein in the changes that take place in visceral adipose tissue in the presence of energy surplus, establishing a link between inflammation and the greater risk of the development of metabolic disease.
authors.affiliation: Metabolic Research Laboratory, Clínica Universidad de Navarra, Pamplona, Spain.
authors.forename: Victoria
authors.initials: V
authors.lastname: Catalán
authors.forename: Javier
authors.initials: J
authors.lastname: Gómez-Ambrosi
authors.forename: Amaia
authors.initials: A
authors.lastname: Rodríguez
authors.forename: Beatriz
authors.initials: B
authors.lastname: Ramírez
authors.forename: Fernando
authors.initials: F
authors.lastname: Rotellar
authors.forename: Víctor
authors.initials: V
authors.lastname: Valentí
authors.forename: Camilo
authors.initials: C
authors.lastname: Silva
authors.forename: María J
authors.initials: MJ
authors.lastname: Gil
authors.forename: Javier
authors.initials: J
authors.lastname: Salvador
authors.forename: Gema
authors.initials: G
authors.lastname: Frühbeck
mesh_terms: D017667:Adipocytes / Q000378:metabolism*; D000328:Adult; D018925:Chemokines / Q000378:metabolism*; D005260:Female; D015390:Gastric Bypass; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D036341:Intercellular Signaling Peptides and Proteins; D050152:Intra-Abdominal Fat / Q000378:metabolism*; D009765:Obesity / Q000378:metabolism* / Q000601:surgery; D012333:RNA, Messenger / Q000378:metabolism; D019707:Receptors, Chemokine / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*; D015431:Weight Loss / Q000502:physiology
chemical_list: C102741:CMKLR1 protein, human; D018925:Chemokines; D036341:Intercellular Signaling Peptides and Proteins; C478630:RARRES2 protein, human; D012333:RNA, Messenger; D019707:Receptors, Chemokine; D014409:Tumor Necrosis Factor-alpha