Abstract
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.
Highlights
Obese individuals are at higher risk for the development of cardiomyopathy leading to heart failure.[1]
Averaged across intake and body weight and not accounting for feed loss in bedding, rats consumed approximately 0.26 gm docosahexaenoic acid (DHA)/day; the American Heart Association recommends that individuals consume 1–4 gm of eicosapentaenoic acid (EPA)+DHA daily.[33]
The results of this study support the idea that diet alone, in the absence of hypertension or overt insulin resistance, is associated with changes in myocardial structure and function that are relevant to human Obesity-mediated cardiomyopathy (OC)
Summary
Obese individuals are at higher risk for the development of cardiomyopathy leading to heart failure.[1]. Increased LV mass and myocardial dysfunction have been associated with obesity in otherwise healthy humans, in the absence of these comorbidities.[3,4,5,6,7] Often present in healthy obese individuals,[4,5,7,8] LV hypertrophy (LVH) is an early echocardiographic change that reflects increased LV mass. LVH is an independent risk factor for development of systolic dysfunction,[9] and is associated with an increased risk for cardiovascular and all-cause mortality.[10,11,12] Collectively, this information suggests that early obesity may not be entirely benign, and that important cardiomyopathic changes occur in the absence of conventional comorbidities
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