GLUT1 deficiency in cardiomyocytes does not accelerate the transition from compensated hypertrophy to heart failure

Abstract The aim of this study was to determine whether endogenous GLUT1 induction and the increased glucose utilization that accompanies pressure overload hypertrophy (POH) are required to maintain cardiac function during hemodynamic stress, and to test the hypothesis that lack of GLUT1 will accele...

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Veröffentlicht in:	Journal of molecular and cellular cardiology 2014-07, Vol.72, p.95-103
Hauptverfasser:	Pereira, Renata O, Wende, Adam R, Olsen, Curtis, Soto, Jamie, Rawlings, Tenley, Zhu, Yi, Riehle, Christian, Abel, E. Dale
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Biological Transport Cardiac hypertrophy Cardiac metabolism Cardiac Output Cardiovascular Gene Expression Glucose - metabolism Glucose transport Glucose Transporter Type 1 - deficiency Glucose Transporter Type 1 - genetics Heart Failure - metabolism Heart Failure - pathology Heart Failure - physiopathology Hypertrophy, Left Ventricular - metabolism Hypertrophy, Left Ventricular - pathology Hypertrophy, Left Ventricular - physiopathology Male Mice Mice, Inbred C57BL Mice, Knockout Mitochondria, Heart - metabolism Myocardial Contraction Myocardium - metabolism Myocardium - pathology Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology Organ Culture Techniques Oxygen Consumption Primary Cell Culture
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