Copyright © 2006, European Society of Cardiology
Potential impact of carbohydrate and fat intake on pathological left ventricular hypertrophy
aDepartment of Physiology and Biophysics, School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA
bDepartment of Nutrition, School of Medicine, Case Western Reserve University, Cleveland, Ohio, USA
* Corresponding author. Division of Cardiology, Department of Medicine, University of Maryland-Baltimore, 22 S. Greene Street, S3B08, Baltimore, MD 21201, USA. Tel.: +1 216 368 5585; fax: +1 410 328 3292. Email address: wstanley{at}medicine.umaryland.edu
Currently, a high carbohydrate/low fat diet is recommended for patients with hypertension; however, the potentially important role that the composition of dietary fat and carbohydrate plays in hypertension and the development of pathological left ventricular hypertrophy (LVH) has not been well characterized. Recent studies demonstrate that LVH can also be triggered by activation of insulin signaling 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. 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 and the resultant effects of plasma insulin, adipokine, and lipid concentrations may affect cardiomyocyte size and function, particularly in the setting of chronic hypertension. This review discusses potential mechanisms by which dietary carbohydrates and fats ca affect cardiac growth, metabolism, and function, mainly in the context of pressure overload-induced LVH.
KEYWORDS Diet; Fat; Glucose; Hypertension; Hypertrophy; Metabolism
Time for primary review 31 days
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