Shiraj Sen, Bijoy K Kundu, Henry Cheng-Ju Wu, S Shahrukh Hashmi, Patrick Guthrie, Landon W Locke, R Jack Roy, G Paul Matherne, Stuart S Berr, Matthew Terwelp, Brian Scott, Sylvia Carranza, O Howard Frazier, David K Glover, Wolfgang H Dillmann, Michael J Gambello, Mark L Entman, Heinrich Taegtmeyer
BACKGROUND: Changes in energy substrate metabolism are first responders to hemodynamic stress in the heart. We have previously shown that hexose-6-phosphate levels regulate mammalian target of rapamycin (mTOR) activation in response to insulin. We now tested the hypothesis that inotropic stimulation and increased afterload also regulate mTOR activation via glucose 6-phosphate (G6P) accumulation. METHODS AND RESULTS: We subjected the working rat heart ex vivo to a high workload in the presence of different energy-providing substrates including glucose, glucose analogues, and noncarbohydrate substrates...
May 17, 2013: Journal of the American Heart Association