title: Prolonged exposure to resistin inhibits glucose uptake in rat skeletal muscles.
abstract: OBJECTIVE
  To assess the effects and mechanisms of the action of resistin on basal and insulin-stimulated glucose uptake in rat skeletal muscle cells.
  
  
  METHODS
  Rat myoblasts (L6) were cultured and differentiated into myotubes followed by stimulation with single commercial resistin (130 ng/mL, 0-24 h) or cultured supernatant from 293-T cells transfected with resistin-expressing vectors (130 ng/mL, 0-24 h). Liquid scintillation counting was used to quantitate [3H] 2-deoxyglucose uptake. The translocation of insulin-sensitive glucose transporters GLUT4 and GLUT1, synaptosomal-associated protein 23 (SNAP23) and GLUT protein content, as well as the tyrosine phosphorylation status and protein content of insulin receptor substrate (IRS)-1, were assessed by Western blotting.
  
  
  RESULTS
  Treatment of L6 myotubes with single resistin or cultured supernatant containing recombinant resistin reduced basal and insulin-stimulated 2-deoxyglucose uptake and impaired insulin-stimulated GLUT4 translocation. While SNAP23 protein content was decreased, no effects were noted in GLUT4 or GLUT1 protein content. Resistin also diminished insulin-stimulated IRS-1 tyrosine phosphorylation levels without affecting its protein content. The effects of recombinant resistin from 293-T cells transfected with resistin-expressing vectors were greater than that of single resistin treatment.
  
  
  CONCLUSIONS
  Resistin regulated IRS-1 function and decreased GLUT4 translocation and glucose uptake in response to insulin. The downregulated expression of SNAP23 may have been partly attributed to the decrease of glucose uptake by resistin treatment. These observations highlight the potential role of resistin in the pathophysiology of type 2 diabetes related to obesity.
authors.affiliation: Department of Pediatrics, Nanjing Maternal and Child Health Hospital of Nanjing Medical University, Nanjing 210004, China.
authors.forename: Hong-Qi
authors.initials: HQ
authors.lastname: Fan
authors.forename: Nan
authors.initials: N
authors.lastname: Gu
authors.forename: Feng
authors.initials: F
authors.lastname: Liu
authors.forename: Li
authors.initials: L
authors.lastname: Fei
authors.forename: Xiao-Qin
authors.initials: XQ
authors.lastname: Pan
authors.forename: Mei
authors.initials: M
authors.lastname: Guo
authors.forename: Rong-Hua
authors.initials: RH
authors.lastname: Chen
authors.forename: Xi-Rong
authors.initials: XR
authors.lastname: Guo
mesh_terms: D000818:Animals; D000963:Antimetabolites; D002454:Cell Differentiation / Q000187:drug effects; D002478:Cells, Cultured; D003847:Deoxyglucose; D005947:Glucose / Q000378:metabolism*; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007328:Insulin / Q000494:pharmacology; D018485:Muscle Fibers, Skeletal / Q000187:drug effects / Q000378:metabolism; D018482:Muscle, Skeletal / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D032446:Myoblasts / Q000187:drug effects / Q000378:metabolism; D010957:Plasmids / Q000235:genetics; D051381:Rats; D052243:Resistin / Q000494:pharmacology*; D014162:Transfection
chemical_list: D000963:Antimetabolites; D007004:Hypoglycemic Agents; D007328:Insulin; D052243:Resistin; D003847:Deoxyglucose; D005947:Glucose