Abstract
Aim: Obesity is a risk factor for the development of cardiovascular diseases. Recently it was shown that overexpression of the Mas-receptor antagonist angiotensin(1-7) could prevent from diet-induced obesity. However, it remained unclear whether diet-induced obesity and angiotensin(1-7) overexpression might also have effects on the cardiovascular system in these rats.Methods:Twenty three male Sprague Dawley rats were fed with standard chow (SD+chow, n = 5) or a cafeteria diet (SD+CD, n = 6) for 5 months. To investigate the effect of angiotensin(1-7) transgenic rats, expressing an angiotensin(1-7)-producing fusion protein in testis were used. These transgenic rats also received a 5 month's feeding period with either chow (TGR+chow, n = 6) or cafeteria diet (TGR+CD, n = 6), respectively. Hemodynamic measurements (pressure-volume loops) were carried out to assess cardiac function and blood pressure. Subsequently, hearts were explanted and investigated according to the Langendorff technique. Furthermore, cardiac remodeling in these animals was investigated histologically.Results:After 5 months cafeteria diet feeding rats showed a significantly increased body weight, which could be prevented in transgenic rats. However, there was no effect on cardiac performance after cafeteria diet in non-transgenic and transgenic rats. Moreover, overexpression of angiotensin(1-7) deteriorated cardiac contractility as indicated by impaired dp/dt. Furthermore, histological analysis revealed that cafeteria diet led to myocardial fibrosis in both, control and transgenic rats and this was not inhibited by an overproduction of angiotensin(1-7).Conclusion:These results indicate that an overexpression of circulating angiotensin(1-7) prevents a cafeteria diet-induced increase in body weight, but does not affect cardiac performance in this experimental rat model of obesity. Furthermore, overexpression of angiotensin(1-7) alone resulted in an impairment of cardiac function.
Highlights
MATERIALS AND METHODSAccording to the World Health Organization obesity is one of the leading risks for global deaths
In their experimental study Müller-Fielitz et al demonstrated that 19 weeks of high-caloric diet in rats resulted in metabolic syndrome, characterized by obesity, insulin resistance, hyperphagia, hyperlipidaemia and hypertension (Müller-Fielitz et al, 2015)
The body weight of wild type (WT) rats, which received chow and cafeteria diet (CD) was significantly elevated compared to WT rats, only fed with chow (Figure 1A)
Summary
MATERIALS AND METHODSAccording to the World Health Organization obesity is one of the leading risks for global deaths. Since the midTwentieth century, the prevalence of obesity has increased substantially and its importance as a main risk factor for the development of metabolic disorders like diabetes and metabolic syndrome, and cardiovascular diseases has been rapidly evolving. Several animal models of obesity have been described, including diet-induced obesity in rats, which closely reflects the situation of human obesity (Lutz and Woods, 2012). In their experimental study Müller-Fielitz et al demonstrated that 19 weeks of high-caloric diet in rats resulted in metabolic syndrome, characterized by obesity, insulin resistance, hyperphagia, hyperlipidaemia and hypertension (Müller-Fielitz et al, 2015). There is evidence that an association exists between the renin-angiotensin-aldosterone system (RAAS) and a number of cardiac and metabolic disorders (Santos et al, 2005, 2008, 2010, 2012; Müller-Fielitz et al, 2015)
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