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

Authors: Bouchard Thomassin, Andrée-AnneLachance, DominicDrolet, Marie-ClaudeCouët, JacquesArsenault, Marie
Other Title(s): Fructose-fed rats and eccentric LVH
Abstract: The development of left ventricular (LV) 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 VO is unknown. This study therefore examined the effects of a fructose-rich diet on LV eccentric hypertrophy, ventricular function, and myocardial metabolic enzymes in rats with chronic VO caused by severe aortic valve regurgitation (AR). Wistar rats were divided in four groups: sham-operated on control diet (SC; n = 13) or fructose-rich diet (SF; n = 13) and severe aortic regurgitation fed with the same diets [aortic regurgitation on control diet (ARC), n = 16, and aortic regurgitation on fructose-rich diet (ARF), n = 13]. Fructose-rich diet was started 1 wk before surgery, and the animals were euthanized 9 wk later. SF and ARF had high circulating triglycerides. ARC and ARF developed significant LV eccentric hypertrophy after 8 wk as expected. However, ARF developed more LVH than ARC. LV ejection fraction was slightly lower in the ARF compared with 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 with SC. 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.
Document Type: Article de recherche
Issue Date: 22 October 2010
Open Access Date: 15 November 2017
Document version: AM
Permalink: http://hdl.handle.net/20.500.11794/15840
This document was published in: American journal of physiology. Heart and circulatory physiology, Vol. 300 (1), H125 (2011)
American Physiological Society
Alternative version: 10.1152/ajpheart.00199.2010
Collection:Articles publiés dans des revues avec comité de lecture

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