Metformin reduces left ventricular eccentric remodeling in experimental volume overload in the rat

Auteur(s): Dhahri, WahibaRoussel, ÉliseDrolet, Marie-Claude; Gascon, Suzanne; Sarrhini, Otman; Rousseau, Jacques A.; Lecomte, Roger; Couët, JacquesArsenault, Marie
Résumé: Left ventricular hypertrophy (LVH) is often associated with a change in myocardial energy substrate preference from fatty acids to glucose. A possible anti hypertrophic treatment strategy could aim at stimulating or restoring normal myocardial energy metabolism. Metformin, an adenosine monophosphate-activated protein kinase (AMPK) activator used in the management of glucose metabolism in diabetes, is also a fatty acid oxidation stimulator. The effect of metformin on the development of eccentric LVH and ventricular function in chronic left ventricular (LV) volume overload (VO) is unknown. This study was designed to study this question in a VO rat model caused by severe aortic valve regurgitation (AR). Male Wistar rats were divided in four groups (13-15 animals / group): Shams (S) treated or not (C) with metformin (M; 100 mg/kg/d PO) and severe ARreceiving or not metformin. Treatment was started one week before surgery and the animals were sacrificed 9 weeks later. As expected AR rats developed severe eccentric LVH during the course of the protocol. Metformin treatment did not influence the total heart weight. However, LV remodeling associated with the severe VO was severe in ARM than in ARC. Fractional shortening, a marker of systolic function, was significantly higher in ARM compared to ARC group. Metformin also increased the activity of enzymes associated with fatty acid oxidation while inhibiting phosphofructokinase, a glycolytic enzyme. A 2 month treatment with metformin reduced LV eccentric remodeling associated with severe VO and helped maintain a better systolic function.
Type de document: Article de recherche
Date de publication: 1 novembre 2012
Date de la mise en libre accès: 14 novembre 2017
Version du document: AM
Lien permanent: http://hdl.handle.net/20.500.11794/15847
Ce document a été publié dans: Journal of Clinical & Experimental Cardiology, Vol. 3 (11) (2012)
https://doi.org/10.4172/2155-9880.1000217
OMICS Publishing Group
Autre version disponible: 10.4172/2155-9880.1000217
Collection :Articles publiés dans des revues avec comité de lecture

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