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Publication : Acute consumption of a high-fat diet prior to ischemia-reperfusion results in cardioprotection through NF-κB-dependent regulation of autophagic pathways.

First Author  Haar L Year  2014
Journal  Am J Physiol Heart Circ Physiol Volume  307
Issue  12 Pages  H1705-13
PubMed ID  25239807 Mgi Jnum  J:220723
Mgi Id  MGI:5635978 Doi  10.1152/ajpheart.00271.2014
Citation  Haar L, et al. (2014) Acute consumption of a high-fat diet prior to ischemia-reperfusion results in cardioprotection through NF-kappaB-dependent regulation of autophagic pathways. Am J Physiol Heart Circ Physiol 307(12):H1705-13
abstractText  Previous studies have demonstrated improvement of cardiac function occurs with acute consumption of a high-fat diet (HFD) after myocardial infarction (MI). However, no data exist addressing the effects of acute HFD upon the extent of injury after MI. This study investigates the hypothesis that short-term HFD, prior to infarction, protects the heart against ischemia-reperfusion (I/R) injury through NF-kappaB-dependent regulation of cell death pathways in the heart. Data show that an acute HFD initiates cardioprotection against MI (>50% reduction in infarct size normalized to risk region) after 24 h to 2 wk of HFD, but protection is completely absent after 6 wk of HFD, when mice are reported to develop pathophysiology related to the diet. Furthermore, cardioprotection after 24 h of HFD persists after an additional 24 h of normal chow feeding and was found to be dependent upon NF-kappaB activation in cardiomyocytes. This study also indicates that short-term HFD activates autophagic processes (beclin-1, LC-3) preischemia, as seen in other protective stimuli. Increases in beclin-1 and LC-3 were found to be NF-kappaB-dependent, and administration of chloroquine, an inhibitor of autophagy, abrogated cardioprotection. Our results support that acute high-fat feeding mediates cardioprotection against I/R injury associated with a NF-kappaB-dependent increase in autophagy and reduced apoptosis, as has been found for ischemic preconditioning.
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