title: Impaired resting muscle energetics studied by (31)P-NMR in diet-induced obese rats.
abstract: OBJECTIVE
  Mitochondrial activity is altered in skeletal muscle of obese, insulin-resistant or type 2 diabetic patients. We hypothesized that this situation was associated with profound adaptations in resting muscle energetics. For that purpose, we used in vivo (31)P-nuclear magnetic resonance ((31)P-NMR) in male sedentary Wistar rats fed with obesogenic diets known to induce alterations in muscle mitochondrial activity.
  
  
  METHODS
  Two experimental diets (high sucrose and high fat) were provided for 6 weeks at two levels of energy (standard, N and high, H) and compared to control diet. The rates of the adenosine triphosphate (ATP) exchange between phosphocreatine (PCr) and gamma-ATP (k(a)) and beta-adenosine diphosphate (beta-ADP) to beta-ATP (k(b)) were evaluated using (31)P-NMR in resting gastrocnemius muscle. Muscle contents in phosphorylated compounds as well as creatine, were assessed using (31)P-NMR and biochemical assays, respectively.
  
  
  RESULTS
  ATP content increased by 6.7-8.5% in standard-energy high-sucrose (NSU), high-energy high-fat (HF) and high-energy high-sucrose (HSU) groups compared to control (P < 0.05), whereas PCr content decreased by 4.2-6.4% (P < 0.01). Consequently, PCr to ATP ratio decreased in NSU, HF, and HSU groups, compared to control (P < 0.01). Furthermore in high-energy groups (HF and HSU) compared to control, creatine contents were decreased by 14-19% (P < 0.001), whereas k(a) and k(b) fluxes were increased by 89-133% (P < 0.001) and 243-277% (P < 0.01), respectively.
  
  
  CONCLUSIONS
  Our in vivo data showed adaptations of resting skeletal muscle energetics in response to high-energy diets. Increased activity of enzymes catalyzing ATP production may reflect a compensatory mechanism to face impaired mitochondrial ATP synthesis in order to preserve intracellular energy homeostasis.
authors.affiliation: INRA, UMR1019, Clermont-Ferrand, France.
authors.forename: Emilie
authors.initials: E
authors.lastname: Chanseaume
authors.forename: Guy
authors.initials: G
authors.lastname: Bielicki
authors.forename: Anne-Laure
authors.initials: AL
authors.lastname: Tardy
authors.forename: Jean-Pierre
authors.initials: JP
authors.lastname: Renou
authors.forename: Damien
authors.initials: D
authors.lastname: Freyssenet
authors.forename: Yves
authors.initials: Y
authors.lastname: Boirie
authors.forename: Béatrice
authors.initials: B
authors.lastname: Morio
mesh_terms: D000222:Adaptation, Physiological; D000244:Adenosine Diphosphate / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D004041:Dietary Fats / Q000009:adverse effects; D019422:Dietary Sucrose / Q000009:adverse effects; D004195:Disease Models, Animal; D004734:Energy Metabolism; D006863:Hydrogen-Ion Concentration; D007700:Kinetics; D009682:Magnetic Resonance Spectroscopy / Q000379:methods; D008297:Male; D008931:Mitochondria, Muscle / Q000378:metabolism* / Q000473:pathology; D018482:Muscle, Skeletal / Q000378:metabolism* / Q000473:pathology; D009765:Obesity / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D010725:Phosphocreatine / Q000378:metabolism; D010759:Phosphorus Isotopes; D051381:Rats; D017208:Rats, Wistar
chemical_list: D004041:Dietary Fats; D019422:Dietary Sucrose; D010759:Phosphorus Isotopes; D010725:Phosphocreatine; D000244:Adenosine Diphosphate; D000255:Adenosine Triphosphate