Exercise training-induced improvement in skeletal muscle PGC-1α-mediated fat metabolism is independent of dietary glycemic index

Obesity (Silver Spring). 2017 Apr;25(4):721-729. doi: 10.1002/oby.21799.

Abstract

Objective: 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.

Method: 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.

Results: 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.

Conclusions: 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.

MeSH terms

  • Aged
  • Diet / methods*
  • Exercise / physiology
  • Exercise Therapy / methods
  • Female
  • Glucose Clamp Technique
  • Glycemic Index*
  • Humans
  • Insulin / metabolism
  • Insulin Resistance / physiology
  • Lipid Metabolism
  • Male
  • Middle Aged
  • Muscle, Skeletal / metabolism*
  • Obesity / metabolism*
  • Obesity / therapy
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha / physiology*
  • Treatment Outcome
  • Weight Loss / physiology

Substances

  • Insulin
  • PPARGC1A protein, human
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha