Soy Diet Worsens Heart Disease in Mice

Department of Medicine, Division of Cardiology, University of Colorado Health Sciences Center, Denver, Colorado, USA.
Journal of Clinical Investigation (Impact Factor: 13.22). 02/2006; 116(1):209-16. DOI: 10.1172/JCI24676
Source: PubMed


We report that dietary modification from a soy-based diet to a casein-based diet radically improves disease indicators and cardiac function in a transgenic mouse model of hypertrophic cardiomyopathy. On a soy diet, males with a mutation in the alpha-myosin heavy chain gene progress to dilation and heart failure. However, males fed a casein diet no longer deteriorate to severe, dilated cardiomyopathy. Remarkably, their LV size and contractile function are preserved. Further, this diet prevents a number of pathologic indicators in males, including fibrosis, induction of beta-myosin heavy chain, inactivation of glycogen synthase kinase 3beta (GSK3beta), and caspase-3 activation.

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Available from: John P Konhilas, Dec 23, 2013
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    • "These results suggest that genistein may afford greater cardioprotection in females than in males. In contrast, soy phytoestrogen supplementation augments cardiac growth in male mice but not in females (Stauffer et al., 2006), and a soy-based diet worsens hypertrophic cardiomyopathy more in male mice than in females (Haines et al., 2012a). These results strongly suggest that caution should be used before recommending estrogenic compound supplementation, at least in patients with cardiac disease (Haines et al., 2012b). "
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    • "To identify putative AMPK-target specific miRs, we performed a real-time PCR screen using the R403Q transgenic mouse model of HCM to identify disease-associated miRs [22], [23]. R403Q HCM mice express a mutant myosin heavy chain (R403Q) corresponding to a human mutation causing HCM and possess multiple phenotypic similarities with their human counterparts [22], [24]. More importantly, this R403Q model also demonstrates the energetic abnormalities that occur in cardiac disease states [25], [26]. "
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    • "We have studied sex dimorphisms in R403Q mice and characterized some of the cellular and molecular mechanisms behind the sex differences [43] [92]. These include a number of pathologic indicators such as fibrosis, induction of β-myosin heavy chain, inactivation of glycogen synthase kinase-3β, and activation of proapoptotic pathways in males but not females [43] [92] [94]. Males harboring the R403Q mutation show progressive deterioration in ventricular function associated with chamber dilation whereas females R403Q mice do not [92] [95] [96]. "
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