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The cardiac phenotype induced by PPARalpha overexpression mimics that caused by diabetes mellitus.
TLDR
PPARalpha is a critical regulator of myocardial fatty acid uptake and utilization, activation of cardiac PPARalpha regulatory pathways results in a reciprocal repression of glucose uptake and usage pathways, and derangements in myocardian energy metabolism typical of the diabetic heart can become maladaptive, leading to cardiomyopathy. Expand
Peroxisome proliferator-activated receptor gamma coactivator-1 promotes cardiac mitochondrial biogenesis.
TLDR
It is found that PGC-1 gene expression is induced in the mouse heart after birth and in response to short-term fasting, conditions known to increase cardiac mitochondrial energy production. Expand
Restoration of insulin-sensitive glucose transporter (GLUT4) gene expression in muscle cells by the transcriptional coactivator PGC-1
TLDR
It is shown that adenovirus-mediated expression of the transcriptional coactivator PGC-1, which is expressed in muscle in vivo but is also deficient in cultured muscle cells, causes the total restoration of GLUT4 mRNA levels to those observed in vivo. Expand
PGC-1α Deficiency Causes Multi-System Energy Metabolic Derangements: Muscle Dysfunction, Abnormal Weight Control and Hepatic Steatosis
TLDR
It is demonstrated that PGC-1α is necessary for appropriate adaptation to the metabolic and physiologic stressors of postnatal life. Expand
Cardiac-Specific Induction of the Transcriptional Coactivator Peroxisome Proliferator-Activated Receptor &ggr; Coactivator-1&agr; Promotes Mitochondrial Biogenesis and Reversible Cardiomyopathy in a
TLDR
Results indicate that PGC-1&agr; drives mitochondrial biogenesis in a developmental stage-dependent manner permissive during the neonatal period, and this unique murine model should prove useful for the study of the molecular regulatory programs governing mitochondrialBiogenesis. Expand
A Role for the Transcriptional Coactivator PGC-1α in Muscle Refueling*
TLDR
Findings identify PGC-1α as a critical regulator of skeletal muscle fuel stores via several mechanisms including stimulation of glucose import, suppression of glycolytic flux, and by down-regulation of the expression of glycogen phosphorylase and its activating kinase, phosphoryLase kinase α. Expand
Gene Regulatory Mechanisms Governing Energy Metabolism during Cardiac Hypertrophic Growth
TLDR
This review describes results of recent molecular studies aimed at delineating the gene regulatory events which facilitate myocardial energy substrate switches during hypertrophic growth of the heart, and defines whether energy metabolic derangements play a primary role in the development of pathologic cardiac hypertrophy and eventual progression to heart failure. Expand
Transcriptional Activation Of Energy Metabolic Switches In The Developing And Hypertrophied Heart
1. The present review focuses on the gene regulatory mechanisms involved in the control of cardiac mitochondrial energy production in the developing heart and following the onset of pathologicalExpand
A role for the transcriptional coactivator PGC-1alpha in muscle refueling.
TLDR
Findings identify PGC-1alpha as a critical regulator of skeletal muscle fuel stores after it was shown to increase muscle glycogen stores via several mechanisms including stimulation of glucose import, suppression of glycolytic flux, and by down-regulation of the expression of glycogen phosphorylase and its activating kinase, phosphorus kinase alpha. Expand
The transcriptional coactivator PGC-1alpha is essential for maximal and efficient cardiac mitochondrial fatty acid oxidation and lipid homeostasis.
High-capacity mitochondrial ATP production is essential for normal function of the adult heart, and evidence is emerging that mitochondrial derangements occur in common myocardial diseases. PreviousExpand
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