John J. Lehman

TL;DR: 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.

TL;DR: It is demonstrated that PGC-1α is necessary for appropriate adaptation to the metabolic and physiologic stressors of postnatal life.

TL;DR: 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.

TL;DR: 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.

TL;DR: 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.