Energy expenditure and oxygen consumption as novel biomarkers of obesity-induced cardiac disease in rats.

The purpose of the present study was to determine calorimetric parameters to predict obesity adverse effects on oxidative stress and cardiac energy metabolism. Male Wistar 24 rats were divided into three groups (n = 8): given standard chow and water (C), receiving standard chow and 30% sucrose in its drinking water (S), and given sucrose-rich diet and water (SRD). After 45 days, both S and SRD rats had obesity, serum oxidative stress, and dyslipidemic profile, but the body weight gain and feed efficiency (FE) were higher in SRD than in S, whereas the obesity-related oxidative stress, myocardial triacylglycerol accumulation, and enhanced cardiac lactate dehydrogenase (LDH) activity were higher in S than in SRD rats. Myocardial beta-hydroxyacyl coenzyme-A-dehydrogenase was lower in SRD and in S than in C, whereas glycogen was only depleted in S rats. Myocardial pyruvate dehydrogenase (PDH) was lowest in S rats indicating depressed glucose oxidation. There was higher myocardial LDH/citrate synthase (CS) ratio and lower adenosine triphosphate (ATP)-synthetase indicating delayed aerobic metabolism in S rats than in the others. Cardiac ATP-synthetase was positively correlated with energy expenditure, namely resting metabolic rate (RMR), and with oxygen consumption per body weight (VO(2)/body weight). Myocardial lipid hydroperoxide (LH)/ total antioxidant substances (TAS) ratio and triacylglycerol accumulation were negatively correlated with RMR and with VO(2)/body weight. In conclusion, the present study brought new insights into obesity because the study demonstrated for the first time that reduced energy expenditure and oxygen consumption may provide novel risk factors of obesity-induced reduced energy generation for myocardial contractile function. The results serve to highlight the role of calorimetric changes as novel biomarkers of risk to obesity-induced cardiac effects.