Abstract
BackgroundObesity increases the risk for development of cardiomyopathy in the absence of hypertension, diabetes or myocardial ischemia. Not all obese individuals, however, progress to heart failure. Indeed, obesity may provide protection from cardiovascular mortality in some populations. The fatty acid milieu, modulated by diet, may modify obesity-induced myocardial structure and function, lending partial explanation for the array of cardiomyopathic phenotypy in obese individuals.MethodsAdult male Sprague-Dawley rats were fed 1 of the following 4 diets for 32 weeks: control (CON); 50% saturated fat (SAT); 40% saturated fat + 10% linoleic acid (SAT+LA); 40% saturated fat + 10% α-linolenic acid (SAT+ALA). Serum leptin, insulin, glucose, free fatty acids and triglycerides were quantitated. In vivo cardiovascular outcomes included blood pressure, heart rate and echocardiographic measurements of structure and function. The rats were sacrificed and myocardium was processed for fatty acid analysis (TLC-GC), and evaluation of potential modifiers of myocardial structure including collagen (Masson's trichrome, hydroxyproline quantitation), lipid (Oil Red O, triglyceride quantitation) and myocyte cross sectional area.ResultsRats fed SAT+LA and SAT+ALA diets had greater cranial LV wall thickness compared to rats fed CON and SAT diets, in the absence of hypertension or apparent insulin resistance. Treatment was not associated with changes in myocardial function. Myocardial collagen and triglycerides were similar among treatment groups; however, rats fed the high-fat diets, regardless of composition, demonstrated increased myocyte cross sectional area.ConclusionsUnder conditions of high-fat feeding, replacement of 10% saturated fat with either LA or ALA is associated with thickening of the cranial LV wall, but without concomitant functional changes. Increased myocyte size appears to be a more likely contributor to early LV thickening in response to high-fat feeding. These findings suggest that myocyte hypertrophy may be an early change leading to gross LV hypertrophy in the hearts of "healthy" obese rats, in the absence of hypertension, diabetes and myocardial ischemia.
Highlights
Obesity increases the risk for development of cardiomyopathy in the absence of hypertension, diabetes or myocardial ischemia
Rats fed diets supplemented with polyunsaturated fatty acids (PUFA), whether linoleic acid (LA) or alinolenic acid (ALA), had higher body weights than CON rats; further, saturated fat (SAT) + ALA rats had higher body weights compared to SAT rats
There were no differences in % body fat by Dual Energy X-Ray Absorptiometry (DEXA) or in postmortem visceral adipose mass; visceral adipose mass was correlated with body weight (r = 0.69, p < 0.0001)
Summary
Obesity increases the risk for development of cardiomyopathy in the absence of hypertension, diabetes or myocardial ischemia. Obese individuals hypertrophy (LVH) is an early echocardiographic change that reflects increased LV mass. LVH is an independent risk factor for development of systolic dysfunction,[15] and is associated with an increased risk for cardiovascular and all-cause mortality in people[16,17,18]. It is unknown why some obese individuals progress to heart failure, while others appear to be protected from mortality[19]. There is evidence that the fatty acid milieu predicts structural and functional changes in the heart that occur with obesity. Dietary fat composition may differentially impact LV structure and contractile function, [25,26] and studies of cultured myocytes support this idea[27]
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