Currently, a high carbohydrate/low fat diet is recommended for patients with heart failure and/or hypertension; however, the potentially important role that the composition of dietary fat and carbohydrate might play in the development of LVH and heart failure has not been well characterized. Recent studies demonstrate that cardiomyocyte hypertrophy can also be triggered by activation of insulin signalling pathways, altered adipokine levels or the activity of peroxisome proliferator-activated receptors (PPARs), suggesting that metabolic alterations play a role in the pathophysiology of LVH and heart failure. Hypertensive patients with high plasma insulin or metabolic syndrome have a greater occurrence of LVH, which could be due to insulin activation of the serine-threonine kinase Akt and its downstream targets in the heart, resulting in cellular hypertrophy. PPARs also activate cardiac gene expression and growth, and are stimulated by fatty acids and consumption of a high fat diet. Dietary intake of fats and carbohydrate, the resultant effects of plasma insulin, adipokine, and lipid concentrations, may affect cardiomyocyte size and function, particularly following cardiac injury or with chronic hypertension. This review discusses potential mechanisms by which dietary carbohydrates and fats can affect cardiac growth, metabolism and function, particularly in the context of pressure overload LVH.
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Comput Methods Biomech Biomed Engin
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