title: Physical exercise increases the expression of TNFalpha and GLUT 1 in muscle tissue of diabetes prone Psammomys obesus.
abstract: BACKGROUND
  Tumor necrosis factor-alpha (TNFalpha) is a major mediator of insulin resistance. On the other hand, it has been suggested that TNFalpha may facilitate glucose uptake through GLUT 1 expression. We recently found that physical exercise prevented the progression to type 2 diabetes mellitus in diabetes prone Psammomys obesus (sand rat).
  
  
  OBJECTIVE
  The aim of the present study was to characterize the influence of physical exercise on the expression of TNFalpha, its receptor R1 and GLUT 1 in muscle tissue of this animal model.
  
  
  METHODS
  Animals were assigned for 4 weeks to four groups: high-energy diet (HC), high-energy diet and exercise (HE), low-energy diet (LC), low-energy diet and exercise (LE). TNFalpha, R1 and GLUT 1 expression were analyzed using Western blot technique.
  
  
  RESULTS
  None of the animals in the HE group became diabetic while all the animals in the HC group became diabetic. TNFalpha, its receptor (R1) and GLUT 1 expressions were significantly higher in the two exercising groups (LE and HE) and significantly lower in the HC group compared to the control LC group.
  
  
  CONCLUSIONS
  Physical exercise augments the expression of TNFalpha, its receptor R1 and the glucose transporter GLUT 1 in muscle tissue. We suggest that this mechanism may improve glucose uptake through pathways parallel and unrelated to insulin signaling that may include MAPK and/or NO. These biochemical processes contribute to the beneficial effects of physical exercise on the prevention of type 2 diabetes mellitus.
authors.affiliation: Heller Institute of Medical Research, Sheba Medical Center and Sackler School of Medicine, Tel Aviv University, Ramat Gan 52621, Israel.
authors.forename: Y
authors.initials: Y
authors.lastname: Heled
authors.forename: Y
authors.initials: Y
authors.lastname: Dror
authors.forename: D S
authors.initials: DS
authors.lastname: Moran
authors.forename: T
authors.initials: T
authors.lastname: Rosenzweig
authors.forename: S R
authors.initials: SR
authors.lastname: Sampson
authors.forename: Y
authors.initials: Y
authors.lastname: Epstein
authors.forename: J
authors.initials: J
authors.lastname: Meyerovitch
mesh_terms: D000818:Animals; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism* / Q000517:prevention & control; D004038:Diet, Reducing; D004195:Disease Models, Animal; D002149:Energy Intake; D005849:Gerbillinae; D051272:Glucose Transporter Type 1; D008297:Male; D009004:Monosaccharide Transport Proteins / Q000378:metabolism*; D009124:Muscle Proteins / Q000378:metabolism; D018482:Muscle, Skeletal / Q000378:metabolism*; D010805:Physical Conditioning, Animal; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
chemical_list: D051272:Glucose Transporter Type 1; D009004:Monosaccharide Transport Proteins; D009124:Muscle Proteins; D047888:Receptors, Tumor Necrosis Factor, Type I; D014409:Tumor Necrosis Factor-alpha