Abstract| Volume 10, ISSUE 4, SUPPLEMENT , S89, August 2004

Cardioprotective potential of intermittent fasting in rats

      Background: Intermittent Food Deprivation (IF), i.e., the feeding regimen when ad lib food is available only every other day, increases the life span and reduces the incidence of age-associated diseases including cancer, diabetes and kidney disease. We have reported the neuroprotective effects of IF against ischemic injury of the brain (Yu and Mattson, J. Neurosci. Res. 57:830–9; 1999). The mechanisms of neuroprotection of IF is not clear, but diminishing free-radical production, a mild cellular stress response, and attenuated inflammatory response are implicated. Here we investigated the cardioprotective effect of IF in rats. Method: After three months of IF or regular, daily, feeding ad libitum (AF), 5-mo old rats were subjected to coronary ligation or sham operation. A subset of rats was sacrificed 24 hours later to measure the size of myocardial infarction (MI) and the extent of apoptosis. The remaining animals were continued for 10 weeks on the same food regimen, during which time the progression of left ventricular (LV) remodeling was assessed by serial echocardiography. After ten weeks LV function was measured by pressure-volume loops analyses, and hearts were evaluated histologically. Results: 24 hrs following coronary ligation the ischemic area of myocardium, i.e., the area at risk (AAR), was similar in both groups, but in IF rats MI size, expressed as a percent of AAR, was more than 2-fold smaller, apoptosis in the AAR was reduced by more than 4-fold (Fig.1), and the inflammatory response was significantly reduced. At 10-wks late LV remodeling and MI expansion occurred in AF rats but did not occur in IF rats, and LV pump function and arterio-ventricular coupling were superior in IF vs AF rats. The myocyte hypertrophy in areas remote from the MI was also absent in IF rats. Conclusion: Intermittent Food Deprivation protects the heart from ischemic injury in part, at least, via an anti-apoptotic mechanism.
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