Short-term Calorie Restriction Improves Post-ischemic Recovery in the Spontaneously Hypertensive Rat

• Author / Creator

  Lozyk, Mira D

• Ischemic heart disease is the leading cause of death in Western countries. We demonstrated how alterations in energy metabolism and the activation of Reperfusion Injury Salvage Kinase (RISK) pathway induced by short-term calorie restriction (CR) contribute to protecting the diseased heart from ischemia/reperfusion (I/R) injury. Our findings using the Spontaneously Hypertensive Rat (SHR) validate that short-term CR exhibits cardioprotection in the rat model of hypertension and cardiac hypertrophy. Our data also suggest that improving glucose oxidation at the time of reperfusion and activating two members of the pro-survival anti-apoptotic RISK pathway, Akt and Erk1/2 MAPK, are possible mechanism by which short-term CR contributes to improving mechanical recovery of the heart during reperfusion following ischemia. Additionally, our data suggest that the effects of short-term CR in I/R injury may be mediated by an AMPK-independent mechanism as the hearts from SHRs exhibited improved metabolic status in presence of significantly reduced AMPK activity.

• Subjects / Keywords

  • Ischemia-Reperfusion Injury
  • Cardiac Energy Metabolism
  • Ischemic Preconditioning
  • Cardiac Preconditioning
  • Spontaneously Hypertensive Rat
  • Post-ischemic Recovery
  • Calorie Restriction
  • Cardiac Metabolism

• Graduation date

  Fall 2012

• Type of Item

  Thesis

• Degree

  Master of Science

• DOI

  https://doi.org/10.7939/R3MS8D

• License

  This thesis is made available by the University of Alberta Libraries with permission of the copyright owner solely for non-commercial purposes. This thesis, or any portion thereof, may not otherwise be copied or reproduced without the written consent of the copyright owner, except to the extent permitted by Canadian copyright law.