title: Exercise training-induced improvement in skeletal muscle PGC-1α-mediated fat metabolism is independent of dietary glycemic index.
abstract: This study hypothesized that a low-glycemic diet combined with exercise would increase expression of nuclear regulators of fat transport and oxidation in insulin-resistant skeletal muscle.
  
  
  
  Nineteen subjects (64 ± 1 y; 34 ± 1 kg/m2) were randomized to receive isocaloric high-glycemic-index (HiGIX; 80 ± 0.6 units, n = 10) or low-glycemic-index (LoGIX; 40 ± 0.3 units, n = 9) diets combined with supervised exercise (1 h/d, 5 d/wk at ∼85% HRmax) for 12 weeks. Insulin sensitivity was determined by hyperinsulinemic-euglycemic clamp. Skeletal muscle biopsies were obtained before and after the intervention to assess fasting gene and protein expression.
  
  
  
  Weight loss was similar for both groups (9.5 ± 1.3 kg). Likewise, improvements in insulin sensitivity (P < 0.002) and PPARγ (P < 0.002), PGC-1α (P = 0.003), CD36 (P = 0.003), FABP3 (mRNA, P = 0.01 and protein, P = 0.02), and CPT1B (mRNA, P = 0.03 and protein, P = 0.008) expression were similar for both interventions. Increased insulin sensitivity correlated with increased PGC-1α expression (P = 0.04), and increased fasting fat oxidation correlated with increased FABP3 (P = 0.04) and CPT1B (P = 0.05) expression.
  
  
  
  An exercise/diet program resulting in 8% to 10% weight loss improved insulin sensitivity and key molecular mechanisms in skeletal muscle that are controlled by PGC-1α. These effects were independent of the glycemic index of the diets.
authors.affiliation: Department of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio.
authors.forename: Anny
authors.initials: A
authors.lastname: Mulya
authors.affiliation: Department of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio.
authors.forename: Jacob M
authors.initials: JM
authors.lastname: Haus
authors.affiliation: Department of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio.
authors.forename: Thomas P J
authors.initials: TP
authors.lastname: Solomon
authors.affiliation: Department of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio.
authors.forename: Karen R
authors.initials: KR
authors.lastname: Kelly
authors.affiliation: Department of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio.
authors.forename: Steven K
authors.initials: SK
authors.lastname: Malin
authors.affiliation: Department of Preventive Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio.
authors.forename: Michael
authors.initials: M
authors.lastname: Rocco
authors.affiliation: Department of Nutrition, School of Medicine, Case Western Reserve University, Cleveland, Ohio.
authors.forename: Hope
authors.initials: H
authors.lastname: Barkoukis
authors.affiliation: Department of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio.|Department of Nutrition, School of Medicine, Case Western Reserve University, Cleveland, Ohio.|Metabolic Translational Research Center, Endocrine and Metabolism Institute, Cleveland Clinic, Cleveland, Ohio.
authors.forename: John P
authors.initials: JP
authors.lastname: Kirwan
mesh_terms: D000368:Aged; D004032:Diet / Q000379:methods*; D015444:Exercise / Q000502:physiology; D005081:Exercise Therapy / Q000379:methods; D005260:Female; D015309:Glucose Clamp Technique; D038321:Glycemic Index; D006801:Humans; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance / Q000502:physiology; D050356:Lipid Metabolism; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000378:metabolism*; D009765:Obesity / Q000378:metabolism* / Q000628:therapy; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha / Q000502:physiology*; D016896:Treatment Outcome; D015431:Weight Loss / Q000502:physiology
chemical_list: D007328:Insulin; C486497:PPARGC1A protein, human; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha