title: [Chemerin induces insulin resistance in C2C12 cells through nuclear factor-κB pathway-mediated inflammatory reaction].
abstract: OBJECTIVE
  To explore the insulin resistance-inducing effect of chemerin on murine C2C12 myoblasts and the underlying molecular mechanism.
  
  
  METHODS
  Following 24-hour treatment with various concentrations of chemerin (0, 10, 100) ng/mL and 30-minute insulin stimulation in C2C12 cells, the glucose uptake was evaluated using a fluorescence microplate reader. ELISA was used to detect the levels of interleukin-6 (IL-6), IL-8 and tumor necrosis factor α (TNF-α) in culture fluid. In addition, the expression of nuclear factor κB (NF-κB) was determined by Western blotting. The underlying mechanism involved in chemerin-induced insulin resistance was evaluated with the precondition of NF-κB blocker pyrrolidine dithiocarbamate (PDTC).
  
  
  RESULTS
  Chemerin inhibited the glucose uptake of C2C12 cells in a dose-dependent manner, concomitant with the increases of IL-6, IL-8, TNF-α levels. Furthermore, chemerin stimulation improved the expression of NF-κB. However, pretreatment with NF-κB blocker PDTC significantly abated the inhibitory effect of chemerin on glucose uptake, and also obviously decreased the levels of IL-6, IL-8 and TNF-α induced by chemerin.
  
  
  CONCLUSIONS
  Chemerin might induce insulin resistance in C2C12 cells through NF-κB pathway-mediated inflammatory reaction.
authors.affiliation: Out-patient Department, General Political Department of Chinese PLA, Beijing 100120, China.
authors.forename: Zefeng
authors.initials: Z
authors.lastname: Huang
authors.affiliation: Ministry of Education Key Laboratory of Resource Biology and Biotechnology in Western China, College of Life Science, Northwest University, Xi'an 710032; Department of Translational Medicine, Institute of Integrated Medical Information, Xi'an 710032, China.
authors.forename: Xin
authors.initials: X
authors.lastname: Xie
mesh_terms: D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D018925:Chemokines / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D005947:Glucose / Q000378:metabolism; D018836:Inflammation Mediators / Q000378:metabolism; D007333:Insulin Resistance; D036341:Intercellular Signaling Peptides and Proteins / Q000494:pharmacology*; D051379:Mice; D032446:Myoblasts / Q000166:cytology* / Q000187:drug effects* / Q000378:metabolism; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000378:metabolism*; D011759:Pyrrolidines / Q000494:pharmacology; D015398:Signal Transduction / Q000187:drug effects*; D013859:Thiocarbamates / Q000494:pharmacology
chemical_list: D018925:Chemokines; D018836:Inflammation Mediators; D036341:Intercellular Signaling Peptides and Proteins; D016328:NF-kappa B; D011759:Pyrrolidines; D013859:Thiocarbamates; C523686:chemerin protein, mouse; C020972:pyrrolidine dithiocarbamic acid; D005947:Glucose