Obesity progression causes liver steatosis and co-morbidities without apparent cardiac metabolic and functional decline

The goal of this study was to test if obesity progression can be a risk factor to alter cardiac metabolism and function along the time. Male Wistar rats were randomly divided to receive either chow diet (12.0% calories from fat) [C group] or high-fat diet (49.7% calories from fat) plus sucrose in the drinking water (100% from carbohydrate) [H group] for 6, 12 and 24 weeks. The Western diet significantly increased adiposity index of rats in all three experimental periods compared to C group. This was associated with increased plasma levels of insulin, resistin, leptin, glucose, triacylglycerol and decreased adiponectin, however, all variables were stable along the time except insulin and leptin. Plasma free fatty acid was only elevated with 24 weeks treatment. The obesity status resulted in hepatic steatosis progression in H group, while oxidative stress, hepatic inflammatory foci as well as TNF-α and IL-6 mRNA levels were not affected. There are no cardiac performance decline as well as metabolism cardiac changes in H group when compared with C. In conclusion, Western diet induced and promoted obesity, co-morbidities and hepatic steatosis progression while was not associated with apparent alterations of cardiac metabolism and function. These results suggest that obesity progression seems to affect the organs of distinct ways, and cardiac dysfunction is a question of tim