GW28-e0914 A Novel Mechanism Underlying Energy Metabolic Disorders in Failing Heart: Defective Branched Chain Amino Acid Catabolism-Induced Mitochondrial Metabolic Enzyme Hyper-Succinylation

GW28-e0914 A Novel Mechanism Underlying Energy Metabolic Disorders in Failing Heart: Defective Branched Chain Amino Acid Catabolism-Induced Mitochondrial Metabolic Enzyme Hyper-Succinylation

Methods MI was induced by coronary artery ligation in a mouse model of defective BCAA catabolism (protein phosphatase-2Cm [PP2Cm] knockout [KO]) or in wild type (WT) mice. In KO heart, chronic BCAA accumulation obviously suppressed cardiac glucose and lipid metabolism through inhibition of mitochond...

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Veröffentlicht in:Journal of the American College of Cardiology 2017-10, Vol.70 (16), p.C34-C34
Hauptverfasser: Zhang, Fuyang, Chen, Xiyao, Ma, Xinliang, Pei, Jianming, Tao, Ling
Format: Artikel
Sprache:eng
Schlagworte:
Amino acids
Cardiology
Catabolism
Chain branching
Coronary artery
Enzymes
Heart failure
Metabolic disorders
Mitochondria
Rodents
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Zusammenfassung:Methods MI was induced by coronary artery ligation in a mouse model of defective BCAA catabolism (protein phosphatase-2Cm [PP2Cm] knockout [KO]) or in wild type (WT) mice. In KO heart, chronic BCAA accumulation obviously suppressed cardiac glucose and lipid metabolism through inhibition of mitochondrial pyruvate dehydrogenase (PDH) and carnitine palmitoyltransferase-1 (CPT-1) activity.
ISSN:0735-1097
1558-3597
DOI:10.1016/j.jacc.2017.07.116