Key result
Temporal ACSL1 inactivation in mouse hearts altered 60 metabolites and 568 genes, revealing that the switch from fatty acid to glucose use causes mTOR-dependent metabolic changes.
In a mouse model of inactivated fatty acid oxidation, the switch to glucose utilization causes mTOR-dependent alterations in cardiac metabolism and gene expression, suggesting that substrate switching to glucose is not entirely benign.
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May challenge assumption of benign glucose preference in myocardium; hypothesis-generating for mTOR modulation in human HF.
Schisler et al. (2015) studied Cardiac hypertrophy and altered metabolism. Temporal ACSL1 inactivation (Acsl1(H-/-)) was evaluated on Metabolomic and gene expression alterations. Temporal ACSL1 inactivation in mouse hearts altered 60 metabolites and 568 genes, revealing that the switch from fatty acid to glucose use causes mTOR-dependent metabolic changes.
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