Cardiac Metabolic Deregulation Induced by the Tyrosine Kinase Receptor Inhibitor Sunitinib is rescued by Endothelin Receptor Antagonism.

Accordingly, hearts from sunitinib-treated mice showed a trend for higher expression of the glucose transporter protein GLUT1 and of Hexokinase II, the glucose phosphorylating enzyme, together with reduced expression of PGC1α, a key regulator of energy metabolism ( Figure 3 E ).

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Kinetics analysis of dynamic FDG-PET scans of the heart showed a trend towards a higher metabolic flux and a higher metabolic rate of glucose (MRGlu) after 1 and 2 weeks of sunitinib treatment that did not reach statistical significance ( Figure 5 A ).

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