Cardiac energy dependence on glucose activates metabolic genes controlled by mTOR. Mus musculus

Mice lacking the expression of Acsl1 in the heart (Acsl1H-/-) have impaired cardiac fatty acid oxidation and develop spontaneous cardiac hypertrophy due to increased mTOR activation. To explore how the loss of ACSL1 alters gene expression, we performed a global gene expression analysis on ventricular RNA isolated from Acsl1H-/- and Acsl1flox/flox mice ten weeks after tamoxifen treatment when ACSL1 protein is completely lost and the specific activity of ACSL1 in Acsl1H-/- hearts is reduced 90% Overall design: Two-condition experiment, cadiac gene expression of Acsl1H-/- vs Acsl1flox/flox mice 10 weeks after tamoxifen treatment. Biological replicates: 3-4 per condition.