Fructose overload promotes functional and metabolic derangements in humans and in animal experimental models. Evidence suggests that dietary
flavonoids have the ability to prevent/attenuate the development of
metabolic diseases. In this work we investigated the effects of (-)-
epicatechin on the modifications induced by
fructose overload in the rat heart in terms of
nitric oxide and
superoxide metabolism. Male Sprague Dawley rats received 10% (w/v)
fructose in the
drinking water for 8 weeks, with or without (-)-
epicatechin (20 mg per kg
body weight per day) in the rat chow diet. These conditions of
fructose overload did not lead to overt manifestations of
heart hypertrophy or tissue remodeling. However, biochemical and molecular changes were observed and could represent the onset of functional alterations. (-)-
Epicatechin prevented a compromised NO bioavailability and the development of oxidative stress produced by
fructose overload essentially acting on
superoxide anion metabolism. In this line, the increase in
superoxide anion production, the overexpression of NOX2 subunit p47phox and of NOX4, the decrease in
superoxide dismutase activity, and the higher oxidized/
reduced glutathione ratio installed by
fructose overload were absent in the rats receiving (-)-
epicatechin. These results support the hypothesis that diets rich in (-)-
epicatechin could prevent the onset and progression of heart dysfunctions associated with metabolic alterations.