Docosahexaenoic Acid Supplementation Does Not Improve Western Diet-Induced Cardiomyopathy in RatsReportar como inadecuado

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Obesity increases risk for cardiomyopathy in the absence of hypertension, diabetes or ischemia. The fatty acid milieu, modulated by diet, may modify myocardial structure and function, lending partial explanation for the array of cardiomyopathic phenotypy. We sought to identify gross, cellular and ultrastructural myocardial changes associated with Western diet intake, and subsequent modification with docosahexaenoic acid DHA supplementation. Wistar and Sprague-Dawley SD rats received 1 of 3 diets: control CON; Western WES; Western + DHA WES+DHA. After 12 weeks of treatment, echocardiography was performed and myocardial adiponectin, fatty acids, collagen, area occupied by lipid and myocytes, and ultrastructure were determined. Strain effects included higher serum adiponectin in Wistar rats, and differences in myocardial fatty acid composition. Diet effects were evident in that both WES and WES+DHA feeding were associated with similarly increased left ventricular LV diastolic cranial wall thickness LVWcr-d and decreased diastolic internal diameter LVIDd, compared to CON. Unexpectedly, WES+DHA feeding was associated additionally with increased thickness of the LV cranial wall during systole LVWcr-s and the caudal wall during diastole LVWca-d compared to CON; this was observed concomitantly with increased serum and myocardial adiponectin. Diastolic dysfunction was present in WES+DHA rats compared to both WES and CON. Myocyte cross sectional area CSA was greater in WES compared to CON rats. In both fat-fed groups, transmission electron microscopy TEM revealed myofibril degeneration, disorganized mitochondrial cristae, lipid inclusions and vacuolation. In the absence of hypertension and whole body insulin resistance, WES+DHA intake was associated with more global LV thickening and with diastolic dysfunction, compared to WES feeding alone. Myocyte hypertrophy, possibly related to subcellular injury, is an early change that may contribute to gross hypertrophy. Strain differences in adipokines and myocardial fatty acid accretion may underlie heterogeneous data from rodent studies.

Autor: Kimberly M. Jeckel, D. N. Rao Veeramachaneni, Adam J. Chicco, Phillip L. Chapman, Christopher M. Mulligan, Jennifer R. Hegarty, M



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