title: Exercise training increases insulin-stimulated glucose disposal and GLUT4 (SLC2A4) protein content in patients with type 2 diabetes.
abstract: OBJECTIVE
  Exercise enhances insulin-stimulated glucose transport in skeletal muscle through changes in signal transduction and gene expression. The aim of this study was to assess the impact of acute and short-term exercise training on whole-body insulin-mediated glucose disposal and signal transduction along the canonical insulin signalling cascade.
  
  
  METHODS
  A euglycaemic-hyperinsulinaemic clamp, with vastus lateralis skeletal muscle biopsies, was performed at baseline and 16 h after an acute bout of exercise and short-term exercise training (7 days) in obese non-diabetic (n=7) and obese type 2 diabetic (n=8) subjects.
  
  
  RESULTS
  Insulin-mediated glucose disposal was unchanged following acute exercise in both groups. Short-term exercise training increased insulin-mediated glucose disposal in obese type 2 diabetic (p<0.05), but not in obese non-diabetic subjects. Insulin activation of (1) IRS1, (2) IRS2, (3) phosphotyrosine-associated phosphatidylinositol-3 kinase activity and (4) the substrate of phosphorylated Akt, AS160, a functional Rab GTPase activating protein important for GLUT4 (now known as solute carrier family 2 [facilitated glucose transporter], member 4 [SLC2A4]) translocation, was unchanged after acute or chronic exercise in either group. GLUT4 protein content was increased in obese type 2 diabetic subjects (p<0.05), but not in obese non-diabetic subjects following chronic exercise.
  
  
  CONCLUSIONS
  Exercise training increased whole-body insulin-mediated glucose disposal in obese type 2 diabetic patients. These changes were independent of functional alterations in the insulin-signalling cascade and related to increased GLUT4 protein content.
authors.affiliation: Metabolic Research Unit, St James's Hospital, Trinity College, Dublin, Ireland.
authors.forename: D J
authors.initials: DJ
authors.lastname: O'Gorman
authors.forename: H K R
authors.initials: HK
authors.lastname: Karlsson
authors.forename: S
authors.initials: S
authors.lastname: McQuaid
authors.forename: O
authors.initials: O
authors.lastname: Yousif
authors.forename: Y
authors.initials: Y
authors.lastname: Rahman
authors.forename: D
authors.initials: D
authors.lastname: Gasparro
authors.forename: S
authors.initials: S
authors.lastname: Glund
authors.forename: A V
authors.initials: AV
authors.lastname: Chibalin
authors.forename: J R
authors.initials: JR
authors.lastname: Zierath
authors.forename: J J
authors.initials: JJ
authors.lastname: Nolan
mesh_terms: D001706:Biopsy; D001786:Blood Glucose / Q000378:metabolism*; D001794:Blood Pressure; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications / Q000378:metabolism*; D003927:Diet, Diabetic; D015444:Exercise / Q000502:physiology*; D005080:Exercise Test; D005260:Female; D015309:Glucose Clamp Technique; D051275:Glucose Transporter Type 4 / Q000378:metabolism*; D006801:Humans; D007328:Insulin / Q000097:blood / Q000502:physiology; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000378:metabolism / Q000473:pathology; D009765:Obesity / Q000097:blood / Q000150:complications / Q000378:metabolism / Q000503:physiopathology; D019869:Phosphatidylinositol 3-Kinases / Q000097:blood
chemical_list: D001786:Blood Glucose; D051275:Glucose Transporter Type 4; D007328:Insulin; D019869:Phosphatidylinositol 3-Kinases