1. Carnitine Acetyltransferase Mitigates Metabolic Inertia and Muscle Fatigue during Exercise.

    Cell Metabolism 22(1):65 (2015) PMID 26154055

    Acylcarnitine metabolites have gained attention as biomarkers of nutrient stress, but their physiological relevance and metabolic purpose remain poorly understood. Short-chain carnitine conjugates, including acetylcarnitine, derive from their corresponding acyl-CoA precursors via the action of c...
  2. HIF-1 Alpha Regulates the Response of Primary Sarcomas to Radiation Therapy through a Cell Autonomous Mechanism.

    Radiation Research 183(6):594 (2015) PMID 25973951

    Hypoxia is a major cause of radiation resistance, which may predispose to local recurrence after radiation therapy. While hypoxia increases tumor cell survival after radiation exposure because there is less oxygen to oxidize damaged DNA, it remains unclear whether signaling pathways triggered by...
  3. Muscle-Specific Overexpression of PGC-1α Does Not Augment Metabolic Improvements in Response to Exercise and Caloric Restriction.

    Diabetes 64(5):1532 (2015) PMID 25422105 PMCID PMC4407850

    This study used mice with muscle-specific overexpression of PGC-1α, a transcriptional coactivator that promotes mitochondrial biogenesis, to determine whether increased oxidative potential facilitates metabolic improvements in response to lifestyle modification. MCK-PGC1α mice and nontransgenic ...
  4. Metabolomic analysis reveals altered skeletal muscle amino acid and fatty acid handling in obese humans.

    Obesity 23(5):981 (2015) PMID 25864501 PMCID PMC4414721

    Investigate the effects of obesity and high-fat diet (HFD) exposure on fatty acid oxidation and TCA cycle intermediates and amino acids in skeletal muscle to better characterize energy metabolism. Plasma and skeletal muscle metabolomic profiles were measured from lean and obese males before and ...
  5. Neuronal CRTC-1 Governs Systemic Mitochondrial Metabolism and Lifespan via a Catecholamine Signal

    Cell 160(5):842 (2015)

    Low energy states delay aging in multiple species, yet mechanisms coordinating energetics and longevity across tissues remain poorly defined. The conserved energy sensor AMP-activated protein kinase (AMPK) and its corresponding phosphatase calcineurin modulate longevity via the CREB re...
  6. Neuronal CRTC-1 Governs Systemic Mitochondrial Metabolism and Lifespan via a Catecholamine Signal.

    Cell 160(5):842 (2015) PMID 25723162 PMCID PMC4392909

    Low energy states delay aging in multiple species, yet mechanisms coordinating energetics and longevity across tissues remain poorly defined. The conserved energy sensor AMP-activated protein kinase (AMPK) and its corresponding phosphatase calcineurin modulate longevity via the CREB regulated tr...
  7. Neuronal CRTC-1 Governs Systemic Mitochondrial Metabolism and Lifespan via a Catecholamine Signal.

    Cell 160(5):842 (2015) PMID 25723162

    Low energy states delay aging in multiple species, yet mechanisms coordinating energetics and longevity across tissues remain poorly defined. The conserved energy sensor AMP-activated protein kinase (AMPK) and its corresponding phosphatase calcineurin modulate longevity via the CREB regulated tr...
  8. Acyl-CoA thioesterase-2 facilitates mitochondrial fatty acid oxidation in the liver.

    Journal of Lipid Research 55(12):2458 (2014) PMID 25114170 PMCID PMC4242439

    Acyl-CoA thioesterase (Acot)2 localizes to the mitochondrial matrix and hydrolyses long-chain fatty acyl-CoA into free FA and CoASH. Acot2 is expressed in highly oxi-dative tissues and is poised to modulate mitochondrial FA oxidation (FAO), yet its biological role is unknown. Using a model of ad...
  9. Acyl-CoA thioesterase-2 facilitates mitochondrial fatty acid oxidation in the liver.

    Journal of Lipid Research 55(12):2458 (2014) PMID 25114170 PMCID PMC4242439

    Acyl-CoA thioesterase (Acot)2 localizes to the mitochondrial matrix and hydrolyses long-chain fatty acyl-CoA into free FA and CoASH. Acot2 is expressed in highly oxi-dative tissues and is poised to modulate mitochondrial FA oxidation (FAO), yet its biological role is unknown. Using a model of ad...
  10. Acyl-CoA thioesterase-2 facilitates mitochondrial fatty acid oxidation in the liver.

    Journal of Lipid Research 55(12):2458 (2014) PMID 25114170 PMCID PMC4242439

    Acyl-CoA thioesterase (Acot)2 localizes to the mitochondrial matrix and hydrolyses long-chain fatty acyl-CoA into free FA and CoASH. Acot2 is expressed in highly oxi-dative tissues and is poised to modulate mitochondrial FA oxidation (FAO), yet its biological role is unknown. Using a model of ad...
  11. Acyl-CoA thioesterase-2 facilitates mitochondrial fatty acid oxidation in the liver.

    Journal of Lipid Research 55(12):2458 (2014) PMID 25114170 PMCID PMC4242439

    Acyl-CoA thioesterase (Acot)2 localizes to the mitochondrial matrix and hydrolyses long-chain fatty acyl-CoA into free FA and CoASH. Acot2 is expressed in highly oxi-dative tissues and is poised to modulate mitochondrial FA oxidation (FAO), yet its biological role is unknown. Using a model of ad...
  12. Energy metabolic reprogramming in the hypertrophied and early stage failing heart: a multisystems approach.

    Circulation: Heart Failure 7(6):1022 (2014) PMID 25236884 PMCID PMC4241130

    An unbiased systems approach was used to define energy metabolic events that occur during the pathological cardiac remodeling en route to heart failure (HF). Combined myocardial transcriptomic and metabolomic profiling were conducted in a well-defined mouse model of HF that allows comparative as...
  13. Energy metabolic reprogramming in the hypertrophied and early stage failing heart: a multisystems approach.

    Circulation: Heart Failure 7(6):1022 (2014) PMID 25236884 PMCID PMC4241130

    An unbiased systems approach was used to define energy metabolic events that occur during the pathological cardiac remodeling en route to heart failure (HF). Combined myocardial transcriptomic and metabolomic profiling were conducted in a well-defined mouse model of HF that allows comparative as...
  14. Energy metabolic reprogramming in the hypertrophied and early stage failing heart: a multisystems approach.

    Circulation: Heart Failure 7(6):1022 (2014) PMID 25236884 PMCID PMC4241130

    An unbiased systems approach was used to define energy metabolic events that occur during the pathological cardiac remodeling en route to heart failure (HF). Combined myocardial transcriptomic and metabolomic profiling were conducted in a well-defined mouse model of HF that allows comparative as...
  15. Metabolite signatures of exercise training in human skeletal muscle relate to mitochondrial remodelling and cardiometabolic fitness.

    Diabetologia 57(11):2282 (2014) PMID 25091629 PMCID PMC4182127

    Targeted metabolomic and transcriptomic approaches were used to evaluate the relationship between skeletal muscle metabolite signatures, gene expression profiles and clinical outcomes in response to various exercise training interventions. We hypothesised that changes in mitochondrial metabolic ...
  16. Energy metabolic reprogramming in the hypertrophied and early stage failing heart: a multisystems approach.

    Circulation: Heart Failure 7(6):1022 (2014) PMID 25236884 PMCID PMC4241130

    An unbiased systems approach was used to define energy metabolic events that occur during the pathological cardiac remodeling en route to heart failure (HF). Combined myocardial transcriptomic and metabolomic profiling were conducted in a well-defined mouse model of HF that allows comparative as...
  17. Metabolite signatures of exercise training in human skeletal muscle relate to mitochondrial remodelling and cardiometabolic fitness.

    Diabetologia 57(11):2282 (2014) PMID 25091629 PMCID PMC4182127

    Targeted metabolomic and transcriptomic approaches were used to evaluate the relationship between skeletal muscle metabolite signatures, gene expression profiles and clinical outcomes in response to various exercise training interventions. We hypothesised that changes in mitochondrial metabolic ...
  18. Neuronal CRTC-1 governs systemic mitochondrial metabolism and lifespan via a catecholamine signal

    Cell (2014)

    Low energy states delay aging in multiple species, yet mechanisms coordinating energetics and longevity across tissues remain poorly defined. The conserved energy sensor AMP-activated protein kinase (AMPK) and its corresponding phosphatase calcineurin modulate longevity via the CREB re...
  19. Treatment with the 3-ketoacyl-CoA thiolase inhibitor trimetazidine does not exacerbate whole-body insulin resistance in obese mice.

    Journal of Pharmacology and Experimental Therap... 349(3):487 (2014) PMID 24700885 PMCID PMC4019316

    There is a growing need to understand the underlying mechanisms involved in the progression of cardiovascular disease during obesity and diabetes. Although inhibition of fatty acid oxidation has been proposed as a novel approach to treat ischemic heart disease and heart failure, reduced muscle f...
  20. Treatment with the 3-ketoacyl-CoA thiolase inhibitor trimetazidine does not exacerbate whole-body insulin resistance in obese mice.

    Journal of Pharmacology and Experimental Therap... 349(3):487 (2014) PMID 24700885 PMCID PMC4019316

    There is a growing need to understand the underlying mechanisms involved in the progression of cardiovascular disease during obesity and diabetes. Although inhibition of fatty acid oxidation has been proposed as a novel approach to treat ischemic heart disease and heart failure, reduced muscle f...