Sunday, November 21, 2010

A high fructose diet worsens eccentric left ventricular hypertrophy in experimental volume overload.

Am J Physiol Heart Circ Physiol. 2010 Oct 22. [Epub ahead of print]




A high fructose diet worsens eccentric left ventricular hypertrophy in experimental volume overload.

Bouchard-Thomassin AA, Lachance D, Drolet MC, Couet J, Arsenault MC.



1Centre de recherche Institut universitaire de cardiologie et pneumologie de Québec.



Abstract

Aims: The development of left ventricular hypertrophy (LVH) can be affected by diet manipulation. Concentric LVH resulting from pressure overload can be worsened by feeding rats with a high-fructose diet. Eccentric LVH is a different type of hypertrophy and is associated with volume overload (VO) diseases. The impact of an abnormal diet on the development of eccentric LVH and on ventricular function in chronic volume overload is unknown. This study therefore examined the effects of a fructose-rich diet on left ventricular eccentric hypertrophy, ventricular function and myocardial metabolic enzymes in rats with chronic VO caused by severe aortic valve regurgitation (AR). Methods: Wistar rats were divided in four groups: Sham-operated on control or fructose-rich diet (SC (n=13) and SF (n=12)) and severe aortic regurgitation fed with the same diets (ARC (n=16) and ARF (n=13)). Fructose-rich diet (F) was started one week before surgery and the animals were sacrificed 9 weeks later. Results: SF and ARF had high circulating triglycerides. ARC and ARF developed significant LV eccentric hypertrophy after 8 weeks as expected. However ARF developed more LVH than ARC. LV ejection fraction was slightly lower in the ARF compared to ARC. The increased LVH and decreased ejection fraction could not be explained by differences in hemodynamic load. SF, ARC and ARF had lower phosphorylation levels of the AMP kinase compared to SC. Conclusion: A fructose-rich diet worsened LV eccentric hypertrophy and decreased LV function in a model of chronic VO caused by AR in rats. Normal animals fed the same diet did not develop these abnormalities. Hypertriglyceridemia may play a central role in this phenomenon as well as AMP kinase activity.