All Phenotypes Tg(Ckm-Prkaa2*K45R)1Mbb MGI Mouse

abnormal myocardial fiber morphology ( J:91969 )

• trend toward reduced myocyte diameter

• hypoxia-stimulated and 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR)-stimulated hexose uptake is completely blocked in skeletal and cardiac muscle

• partial reduction (40%) in contraction-stimulated hexose uptake in muscle

decreased heart left ventricle muscle contractility ( J:91969 )

• in vivo left ventricular dP/dt is lower than in wild-type, however mutants have normal fractional shortening, and no heart failure, cardiac hypertrophy or fibrosis

impaired exercise endurance ( J:110092 )

• display a 20-30% reduction in voluntary wheel running activities during the active phase but no differences during the light/resting phase

abnormal response to cardiac infarction ( J:91969 )

• during low-flow ischemia and postischemic reperfusion in vitro, hearts fail to augment glucose uptake and glycolysis, although glucose transporter content and insulin-stimulated glucose uptake are normal

• hearts fail to increase fatty acid oxidation during reperfusion and show impaired recovery of left ventricular contractile function during postischemic reperfusion that is associated with lower ATP content and increased injury

abnormal circulating glucose level ( J:110092 )

• 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) does not lower blood glucose levels to the same extent as in wild-type