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Exercise training decreases the concentration of malonyl-CoA and increases the expression and activity of malonyl-CoA decarboxylase in human muscle

2006/01/25 by Jeanette Kuhl, Neil B. Ruderman, Nicolas Musi +14 · 1 citation
Biochemistry, Genetics and Molecular Biology · Chemistry · Medicine · #AMP-activated protein kinase #AMPK #Adipose Tissue and Metabolism #Beta oxidation #Biochemistry #Chemistry #Coactivator #Endocrinology #Enzyme #Gene #Internal medicine #Malonyl-CoA #Medicine #Metabolism #Metabolism, Diabetes, and Cancer #Peroxisome Proliferator-Activated Receptors #Phosphorylation #Protein kinase A #Pyruvate carboxylase #Transcription factor

paper · doi:10.1152/ajpendo.00341.2005

openalex publication_date 2006/01/25 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/01

Abstract

The study was designed to evaluate whether changes in malonyl-CoA and the enzymes that govern its concentration occur in human muscle as a result of physical training. Healthy, middle-aged subjects were studied before and after a 12-wk training program that significantly increased VO2 max by 13% and decreased intra-abdominal fat by 17%. Significant decreases (25-30%) in the concentration of malonyl-CoA were observed after training, 24-36 h after the last bout of exercise. They were accompanied by increases in both the activity (88%) and mRNA (51%) of malonyl-CoA decarboxylase (MCD) in muscle but no changes in the phosphorylation of AMP kinase (AMPK, Thr172) or of acetyl-CoA carboxylase. The abundance of peroxisome proliferator-activated receptor (PPAR)gamma coactivator-1alpha (PGC-1alpha), a regulator of transcription that has been linked to the mediation of MCD expression by PPARalpha, was also increased (3-fold). In studies also conducted 24-36 h after the last bout of exercise, no evidence of increased whole body insulin sensitivity or fatty acid oxidation was observed during an euglycemic hyperinsulinemic clamp. In conclusion, the concentration of malonyl-CoA is diminished in muscle after physical training, most likely because of PGC-1alpha-mediated increases in MCD expression and activity. These changes persist after the increases in AMPK activity and whole body insulin sensitivity and fatty acid oxidation, typically caused by an acute bout of exercise in healthy individuals, have dissipated.

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