Abstract
Overconsumption of fructose leads to metabolic syndrome as a result of hypertension, insulin resistance, and hyperlipidemia. In this study, the renal function of animals submitted to high fructose intake was analyzed from weaning to adulthood using in vivo and ex vivo methods, being compared with a normal control group. We investigated in ex vivo model of the role of the renin Angiotensin system (RAS) in the kidney. The use of perfused kidney from animals submitted to 8-week fructose treatment showed that high fructose intake caused metabolic and cardiovascular alterations that were consistent with other studies. Moreover, the isolated perfused kidneys obtained from rats under high fructose diet showed a 33% increase in renal perfusion pressure throughout the experimental period due to increased renal vascular resistance and a progressive fall in the glomerular filtration rate, which reached a maximum of 64% decrease. Analysis of RAS peptides in the high fructose group showed a threefold increase in the renal concentrations of angiotensin I (Ang I) and a twofold increase in angiotensin II (Ang II) levels, whereas no change in angiotensin 1-7 (Ang 1-7) was observed when compared with the control animals. We did not detect changes in angiotensin converting enzyme (ACE) activity in renal tissues, but there is a tendency to decrease. These observations suggest that there are alternative ways of producing Ang II in this model. Chymase the enzyme responsible for Ang II formation direct from Ang I was increased in renal tissues in the fructose group, confirming the alternative pathway for the formation of this peptide. Neprilysin (NEP) the Ang 1-7 forming showed a significant decrease in activity in the fructose vs. control group, and a tendency of reduction in ACE2 activity. Thus, these results suggest that the Ang 1-7 vasodilator peptide formation is impaired in this model contributing with the increase of blood pressure. In summary, rats fed high fructose affect renal RAS, which may contribute to several deleterious effects of fructose on the kidneys and consequently an increase in blood pressure.
Highlights
Metabolic syndrome (MS) is a disease of modern civilization, being strongly correlated with lifestyle, and increase has been linked to the intake of high-fructose corn syrup associate a cluster of common pathologies (Zimmet et al, 2001; Ferder et al, 2010; De Angelis et al, 2012; Chou et al, 2017)
Rats under normal (CG) or high fructose (FG) diets, received the same energy intake and there was no significant change in body weight, the adipose tissue was increased in fructose group (FG) when compared to control group (CG) (Figures 1C,D)
We evaluated renal function and the role of the kidney renin Angiotensin system (RAS) in animals submitted to high fructose intake from weaning to adulthood by using in vivo and ex vivo methods in this model
Summary
Metabolic syndrome (MS) is a disease of modern civilization, being strongly correlated with lifestyle (diet and physical activity), and increase has been linked to the intake of high-fructose corn syrup associate a cluster of common pathologies (Zimmet et al, 2001; Ferder et al, 2010; De Angelis et al, 2012; Chou et al, 2017). Fructose fed rats have been used as a model for MS exhibiting several metabolic changes, similar to those observed in the clinical presentation in humans (Rayssiguier et al, 2006; Sanchez-Lozada et al, 2007). High fructose consumption induces hypertension, dyslipidemia, central obesity, body weight increase, insulin resistance, and hepatic steatosis (Suzuki et al, 1997; Farah et al, 2006; Tran et al, 2009a; Mamikutty et al, 2015; Xu et al, 2017). NaCl exacerbated fructose-induced cardiac functional damage, as evaluated by echocardiography and documented in cardiac morphology and diastolic function (Araujo et al, 2016)
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