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CARDIOVASCULAR

Fructose-Fed Rats Are Protected against Ischemia/Reperfusion Injury

Department of Physiology and Pharmacology, Wake Forest University Health Sciences, Winston-Salem, North Carolina

This study examines the relationship between insulin resistance (IR) induced by fructose feeding (FF) and susceptibility to myocardial ischemia/reperfusion injury (MI/R). Six-week-old male Sprague-Dawley rats were randomized into control (CON; n = 59) or FF (n = 58) groups. After 4 weeks, rats were further randomized into one of the following groups: placebo, ischemic preconditioning (IPC), 5-hydroxydecanoic acid (5-HD) (10 mg/kg), or 5-HD + IPC. Moreover, to determine the role of fructose, a second model of IR (Zucker obese) and rats fed fructose diet for 3 days (FF-3) were also subjected to MI/R. In all experiments, rats were subjected to 30 min of myocardial ischemia and 4 h of reperfusion. In rats randomized to placebo, infarct size was significantly reduced by FF (24 ± 5%) compared with CON (54 ± 1%, p < 0.05). Pretreatment with 5-HD did not alter the infarct size in CON (45 ± 5%) but inhibited the protection afforded by FF (53 ± 7%). IPC reduced the infarct size to an equivalent level in both groups, whereas 5-HD administration prior to IPC blunted the IPC effect. In Zucker obese rats, infarct size was significantly larger (57 ± 4%) compared with lean controls (37 ± 4%, p < 0.05). In FF-3 rats, infarct size was also decreased (20 ± 2%, p < 0.01) compared with CON. This study suggests that fructose feeding affords protection against MI/R that is related to or mimics preconditioning. This protection is not consistent with other models of IR and is likely related to the fructose diet itself.

Address correspondence to: Dr. Allison W. Miller, Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Hanes 1050, Medical Center Boulevard, Winston-Salem, NC 27157. E-mail: amiller{at}wfubmc.edu

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