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Ablation of PGC-1beta results in defective mitochondrial activity, thermogenesis, hepatic function, and cardiac performance.
Disruption of the circadian clock within the cardiomyocyte influences myocardial contractile function, metabolism, and gene expression.
Type 1 diabetic akita mouse hearts are insulin sensitive but manifest structurally abnormal mitochondria that remain coupled despite increased uncoupling protein 3.
Impaired insulin signaling accelerates cardiac mitochondrial dysfunction after myocardial infarction.
Loss of bradykinin signaling does not accelerate the development of cardiac dysfunction in type 1 diabetic akita mice.
PGC-1? deficiency accelerates the transition to heart failure in pressure overload hypertrophy.
Genetic loss of insulin receptors worsens cardiac efficiency in diabetes.
Antioxidant treatment normalizes mitochondrial energetics and myocardial insulin sensitivity independently of changes in systemic metabolic homeostasis in a mouse model of the metabolic syndrome.