Fructose-fed rat hearts are protected against ischemia-reperfusion injury.
High fructose-fed (HFF) rat model is known to develop the insulin-resistant syndrome with a very similar metabolic profile to the human X syndrome. Such metabolic modifications have been associated with a high incidence of cardiovascular disease. The role of free radical attack in diabetes mellitus and its cardiovascular complications have been abundantly documented. The present study examined the susceptibility to myocardial ischemic injury and the involvement of free radical attack and/or protection in the metabolic disorders of high FF rats. Rats were divided into two experimental groups that received diet for 4 weeks: a control group (C, n=28) receiving a standard diet and a HFF group (FF, n=28), in which 58% of the total carbohydrate was fructose. The euglycemic clamp technique was performed to assess insulin resistance. For the ischemia-reperfusion procedure, rat hearts were isolated and perfused at constant pressure before they were subjected to a 30-min occlusion of the left coronary artery followed by 120 mins of reperfusion. Hemodynamic parameters were measured throughout the protocol. Infarct-to-risk ratio (I/R) was assessed at the end of the protocol by 2,3,4-triphenyltetrazolium chloride staining and planimetric analysis. Lipid peroxidation, antioxidant enzyme activity, level of vitamin E, and trace element status were measured in blood samples from both groups. Rats of the FF group developed an insulin resistance indicated by the glucose infusion rate, which was decreased by 47%. Infarct size was significantly reduced in rats from the FF group (19.9% +/- 6.6%) compared to rats from the control group (34.6% +/- 4.9%), and cardiac functional recovery at reperfusion was improved in the FF group. Lipid peroxidation and oxidative stress were higher in the FF group, as indicated by higher malonedialdehyde level, whereas plasma vitamin E/triacylglycerol ratio was also enhanced in this group. This study indicates that fructose feeding affords protection against in vitro ischemia-reperfusion injury, potentially implicating vitamin E.
Joyeux-Faure
Marie
M
Laboratoire HP2, Hypoxie Physio-Pathologie Respiratoire et Cardiovasculaire, Faculté de Médecine-Pharmacie, Université Grenoble I, Domaine de la Merci, 38706 La Tronche, France. Marie.Faure@ujf-grenoble.fr
Rossini
Eliane
E
Ribuot
Christophe
C
Faure
Patrice
P
D000818:Animals; D000975:Antioxidants / Q000378:metabolism / Q000494:pharmacology; D004032:Diet; D005632:Fructose / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects* / Q000502:physiology; D066298:In Vitro Techniques; D007328:Insulin / Q000494:pharmacology; D015227:Lipid Peroxidation; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar; D014810:Vitamin E / Q000097:blood
D000975:Antioxidants; D007328:Insulin; D014810:Vitamin E; D005632:Fructose