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Abstract

Introduction Obesity is an epidemic problem that impairs human health. It can be defined as the accumulation of excessive body fat mass, leading to abnormal changes. The world is witness an explosion in the number of obesity cases. Worldwide obesity prevalence has more than doubled since 1980s as reported by World Health Organization (WHO). Indeed, the American Medical Association announced that obesity should be classified as a chronic disease. Qatar ranks sixth globally in the prevalence of obesity according to the International Association for the Study of Obesity. There are several causes considered to contribute in the development of obesity such as: genetics, health, diet and lifestyle. However, access to high energy-dense food, and physical inactivity makes a significant contribution to the increasing rate of obesity. Increasing body weight is closely associated with cardiovascular morbidity and mortality. It has a total impact on cardiovascular disease (CVDs) in the general population approximately equal to that of smoking. The relationship and the exact role by which obesity induces the cardiovascular risk are poorly investigated. This study aims to establish a diet-induced obesity rat model and to investigate the cardiovascular diseases risk factors associated with obesity. It also aimed to examine the effect of dietary weight loss on the reversibility of these risk factors. Methodology Male Sprague Dawly (SD) rats 8-9 weeks age old, were grouped into three categories: NC group fed with Normal chow (NC) and had access to regular water ad libitum, CAF group fed with a combination of cafeteria style diet (CAF) and normal chow with 5% sugar water ad libitum for 15 weeks, and reversibility group fed with CAF diet and NC ad libitum to induced weight gain and then switched to NC only for four weeks. The nutritional contents for each diet was: NC (49% CHO, 14.37% protein, 4.65% fat) and CAF (60-70% CHO, 9-12% protein, 10% fat). Body weight, food and water intake were measured weekly throughout the study. Blood was collected to test the changes in the metabolic parameters. Large vessels responsiveness was examined by using organ bath, in response to noradrenaline (NA) and acetylcholine (Ach). Results Results showed that CAF diet has an effect on body weight. All CAF fed-rats gained weight significantly with higher consumption of CAF diet compared to NC. A significant change in their lipid profile was also observed; it showed a significant increase in triglycerides and a decrease in HDL levels. In the reversible group, rats showed a slight weight loss of approximately 6% in 4 weeks. This weight loss was associated with a more favorable lipid profile; triglycerides and HDL returned to normal levels when CAF diet stopped. The vascular studies data suggests noradrenergic contractions in the CAF-fed group were muted compared with the control (NC-fed group). Similar effect was observed in the reversibility, when CAF diet stopped for 4 weeks. The Ach relaxation pattern suggests CAF feeding was associated with endothelial dysfunction. This effect was not reversed when the diet changed to normal chow. Conclusion In conclusion, this study developed a diet-induced obesity rat model with metabolic changes associated with obesity. It specifically examined the vascular changes caused by dietary weight gain and loss. Further investigations are in progress in order to investigate the mechanisms underlying these changes.

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/content/papers/10.5339/qfarc.2018.HBPD970
2018-03-15
2020-10-25
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