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Biochemical, Molecular, and Genetic Mechanisms

Dietary Soy Protein Reduces Cardiac Lipid Accumulation and the Ceramide Concentration in High-Fat Diet-Fed Rats and ob/ob Mice^1–3,

⁴ Department Fisiología de la Nutrición and ⁵ Department Endocrinología y Metabolismo, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, México, DF. 14000, México

Obesity is an epidemic condition strongly associated with cardiovascular morbidity and mortality. Heart disease secondary to obesity is associated with myocardial steatosis, leading to ceramide synthesis and cell dysfunction in a process known as lipotoxicity. Soy protein has been demonstrated to reduce lipotoxicity in the liver and pancreas in different rodent models of obesity. Thus, our purpose in the present work was to assess the effect of dietary soy protein on cardiac lipid accumulation and ceramide formation during obesity and to evaluate its effect in the following 2 rodent models of obesity: 1) a diet-induced obesity model in Sprague-Dawley rats was produced by feeding rats a control or a high-fat casein or soy protein diet for 180 d; and 2) wild-type and ob/ob mice were fed a casein or soy protein diet for 90 d. Soy protein intake led to lower cholesterol and triglyceride concentrations in the hearts of rats and ob/ob mice in association with a greater PPAR mRNA concentration and a lower level of sterol regulatory element binding protein-1 mRNA than those fed casein. The ceramide concentration was also lower in hearts of rats and ob/ob mice that were fed soy protein in association with lower serine palmitoyl transferase (SPT)-1 and tumor necrosis factor- mRNA concentrations. These results indicate that dietary soy protein can reduce the heart ceramide concentration by reducing the expression of SPT-1, a key enzyme in the formation of this sphingolipid in the heart of obese rodents, and by reducing lipid accumulation. Thus, soy protein consumption may be considered as a dietary therapeutic approach for lipotoxic cardiomyopathy prevention.

^* To whom correspondence should be addressed. E-mail: nimbester{at}gmail.com.

Manuscript received 5 May 2009. Initial review completed 2 July 2009. Revision accepted 22 September 2009.

Published online 14 October 2009.