Diet compounds, glycemic index and obesity-related cardiac effects
Introduction
The concept that obesity is the result of energy intake exceeding energy expenditure underlies most conventional weight loss strategies [1], [2]. On this simplistic view, to lose weight, energy intake should be less than energy expenditure, and diet compounds would have little effects. However, dietary factors other than energy cardiovascular disease. The conversion of carbohydrate to fat is energetically a very costly synthesis, and there is consensus that more energy is required to gain body weight on carbohydrate than on isoenergetic amount of fat [2]. Interestingly, the impact of diet compounds on obesity-related cardiac effects had drawn little attention until recently.
Obesity is an important cardiovascular risk factor [1], [3], [4] and the effectiveness of obesity to induce myocardial damage may be related to the metabolic pathway and fuel utilization for energy generation [5]. However, the basis for such observation has not been completely established.
There is increasing evidence that the mechanisms by which obesity and increased energy intake exert deleterious effects on health are the remarkable abilities to induce oxidative stress [3], [4], [6], an imbalance between oxidants and antioxidants systems in favor of the former. During energy metabolism, the mitochondrial respiratory chain represents a major intracellular source of reactive oxygen species (ROS) [6]. As the use of oxygen is vital for oxidative phosphorylation by the electron transport system, alterations in food constituents, or fuel for energy generation may result in higher ROS production, thus inducing oxidative stress [1], [3], [4]. So, oxidative stress not only may be associated with energy intake and obesity but may also depend upon which nutrient was used for energy production.
Recent research in our laboratory has shown that ROS depress myocardial energy [1], [7] and promote an inhibitory effect on myocardial function [8], [9]. The cardiovascular disease and its relation to dyslipidemia have been extensively studied [1], [10], [11], [12] but little information is available on obesity-induced oxidative stress and metabolic shifting in cardiac tissue. Moreover, serum variables other than the traditional lipid profile may be further improving the discrimination of obesity effects on cardiac health.
Thus, the major purpose of this study was to investigate the influence of diet compounds on obesity-related cardiac oxidative stress and metabolic shifting. It was hypothesized that carbohydrate-rich diet may be disadvantageous from fat-rich diet to cardiac tissue, and that glycemic index rather than lipid profile may predict the obesity-related cardiac effects.
Section snippets
Animals and diet
Male Wistar, 24 rats, weighing 200.0 ± 5 g, 60 days of age were individually housed in polypropylene cages in an environmentally controlled, clean-air room with a temperature of 22 ± 3 °C, 12 h light-and-dark cycle, and a relative humidity of 60 ± 5%. Rats received water and food ad libitum and were randomly assigned to one of three groups (n = 8/group). The control group (C) was fed with a standard Purina rodent chow (3074 SIF, Purina Ltd., Campinas, São Paulo, Brazil), containing 3.2% fat, 22.0%
General characteristics of rats
The body weight gain of the rats enhanced over the study had no significant differences between the groups at 28 days of treatments. After 35 days, FRD rats had higher body weight than CRD and C rats (Fig. 1). The specific rate of body mass gain, Lee index and BMI were higher in FRD than in CRD and C rats. Body length, heart weight (HW) and heart weight/body weight (HW/BW) ratio were comparable in all three groups. The food consumption was lower in FRD and CRD, while energy intake was higher in
Discussion
Although the adverse effects of obesity have been extensively studied, there is still a lack of information linking a specific diet compound and obesity-related cardiac effects. Data involving obesity process have been reported in a scattered fashion and, in most of these studies, only food intake and serum lipids were examined. Since the majority of the metabolic conditions that lead to cardiac dysfunction remains clinically silent, and only become manifest when cardiac alteration is
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