title: [Role of c-Jun NH (2)-terminal kinase in insulin resistance after burn].
abstract: OBJECTIVE
  To investigate the role of c-Jun NH (2)-terminal kinase (JNk) in insulin resistance after burn and its mechanism.
  
  
  METHODS
  Twenty-four Sprague-Dawley rats were randomized to control, burn and burn + anisomycin groups. The rats in control group received sham burn trauma, and burn and burn + anisomycin groups received 30% total body surface area (TBSA) full thickness burn injury. Anisomycin (5 mg/kg) together with 250 microl dimethyl sulfoxide (DMSO) was injected to the rats in anisomycin group intravenously, and only 250 microl DMSO in the other two groups. Euglycemic-hyperinsulinemic glucose clamps was performed 2 hours after the injection. The changes of phospho-serine 307, phospho-tyrosine of insulin receptor substrate (IRS)-1 and phospho-JNK in muscle tissues were determined and compared using immunoprecipitation and Western blot analysis or immunohistochemistry in the three groups.
  
  
  RESULTS
  The infusing rates of total 10% glucose (mg x kg(-1) x min(-1)) in control, burn and burn + anisomycin group were 12.3 +/- 0.4, 6.6 +/- 0.3, 6.5 +/- 0.4, respectively. The level of IRS-1 Serine 307 phosphorylation and phospho-JNK in muscle increased significantly, while insulin-induced tyrosine phosphorylation of IRS-1 decreased markedly after burn.
  
  
  CONCLUSIONS
  The activation of JNK elevates the level of IRS-1 phospho-serine 307 and might play a role in insulin resistance after burn in rats.
authors.affiliation: Department of Burn, The Affiliated Hospital of Medical College of Chinese People's Armed Police, Tianjin 300162, China.
authors.forename: Xin-long
authors.initials: XL
authors.lastname: Chen
authors.forename: Zhao-fan
authors.initials: ZF
authors.lastname: Xia
authors.forename: Duo
authors.initials: D
authors.lastname: Wei
authors.forename: Dao-feng
authors.initials: DF
authors.lastname: Ben
authors.forename: Hong-tai
authors.initials: HT
authors.lastname: Tang
authors.forename: Sheng-de
authors.initials: SD
authors.lastname: Ge
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000378:metabolism; D000818:Animals; D000841:Anisomycin / Q000008:administration & dosage; D000900:Anti-Bacterial Agents / Q000008:administration & dosage; D015153:Blotting, Western; D002056:Burns / Q000201:enzymology / Q000378:metabolism / Q000503:physiopathology*; D004121:Dimethyl Sulfoxide / Q000008:administration & dosage; D004195:Disease Models, Animal; D005260:Female; D015309:Glucose Clamp Technique; D007150:Immunohistochemistry; D007275:Injections, Intravenous; D007328:Insulin / Q000008:administration & dosage; D055504:Insulin Receptor Substrate Proteins; D007333:Insulin Resistance / Q000502:physiology*; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism*; D008297:Male; D009132:Muscles / Q000378:metabolism; D010766:Phosphorylation / Q000187:drug effects; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012694:Serine / Q000378:metabolism; D014443:Tyrosine / Q000378:metabolism
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D000900:Anti-Bacterial Agents; D007328:Insulin; D055504:Insulin Receptor Substrate Proteins; C526296:Irs1 protein, rat; D014443:Tyrosine; D012694:Serine; D000841:Anisomycin; D048031:JNK Mitogen-Activated Protein Kinases; D004121:Dimethyl Sulfoxide