Effects of fructose rich diet on reactive oxygen species production in Acute Kidney Injury Zebrafish model

Abstract

Acute Kidney Injury (AKI) is defined by the impairment of renal filtration capacity, with loss of structural integrity of the kidney, altering the organ function. AKI is a complex disease with a high incidence and mortality rate. Clinically, the levels of creatinine and nitrogen in the blood can evaluate the renal capacity. However, there are still many doubts regarding the pathophysiology of the disease. With the worldwide increase consumption of industrialized food healthy problems are arising, such as obesity, hypertension, diabetes, as well as renal dysfunction. Moreover, studies indicate the association between excessive fructose consumption and poor health. Fructose abuse might precede such diseases since its distinct metabolization. Fructose is absorbed into liver cells by the GLUT2 and GLUT5 transporters. Once inside the cells, it is metabolized through frutokinase enzyme (KHK). However, when ingested in high concentrations, fructose is also metabolized in adipose tissue and kidney. Due to the absence of negative feedback, as fructose is ingested, the cell will metabolize it, even if it compromises the ATP level. However, low levels of ATP affect mitochondrial function, producing more Reactive Oxygen Species (ROS) and NADPH oxidase (NOX) activation. The exacerbated presence of ROS and activation of NOX are factors observed in the LRA. However, it is still unclear the influence of ROS, NOX and fructose in the pathophysiology of the disease. Thus, the present project aims to evaluate the pattern of kidney injury resulting from high fructose consumption, as well as the association of AKI with ROX and NOX. Since the Danio rerio kidney is analogous anatomical to human and it is a well-established model to study AKI, the project chose to use this fish to evaluate the high fructose diet and its consequences. (AU)