Fructose-rich diet leads to reduced aerobic capacity and to liver injury in rats

Abstract

The main purpose of this research was to investigate the alterations in the aerobic capacity and appearance of metabolic alterations in Wistar rats fed on fructose-rich diet. We separated twenty-eight rats into two groups according to diet: a control group (C) (balanced diet) and a fructose-rich diet group (F). The animals were fed these diets for 60 d (d 120 to 180). We performed insulin, glucose as well as a minimum lactate test, at d 120 and 180. At the end of the experiment, sixteen animals were euthanized, and the following main variables were analysed: aerobic capacity, the serum aspartate aminotransferase (AST) to alanine aminotransferase (ALT) ratio, serum and liver triglyceride concentrations, serum and liver thiobarbituric acid reactive substance (TBARS) concentrations, serum and liver catalase and superoxide dismutase (SOD) activity and haematoxylin-eosin histology (HE) in hepatocytes. The remaining twelve animals were submitted to an analysis of their hepatic lipogenic rate. The animals fed a fructose-rich diet exhibited a reduction in aerobic capacity, glucose tolerance and insulin sensitivity and increased concentrations of triglycerides and TBARS in the liver. Catalase and SOD activities were reduced in the livers of the fructose-fed animals. In addition, the serum AST/ALT ratio was higher than that of the C group, which indicates hepatic damage, and the damage was confirmed by histology. In conclusion, the fructose-rich diet caused significant liver damage and a reduction in insulin sensitivity in the animals, which could lead to deleterious metabolic effects.

The aspartate aminotransferase-to-alanine aminotransferase ratio predicts all-cause and cardiovascular mortality in patients with type 2 diabetes

“…Of interest, rats with fructose-induced liver damage showed a higher AAR coupled with a reduced aerobic capacity compared with control rats. In these animals, markers of oxidative stress were also increased [35] . Similar findings have been reported in subjects with alcoholic hepatitis, who showed a parallel increase both in the AAR and in oxidative stress markers.…”

Mitoneet mediates TNFα induced necroptosis promoted by fructose and ethanol exposure

“…Hepatocytes of the liver express the highest levels of the fructose specific transporter Glut5 and express the highest levels of fructokinase, which rapidly metabolizes fructose (Douard and Ferraris, 2008). Fructose bypasses the controls exerted on glucose metabolism, and as such exhibits a much greater ability to induce de novo lipogenesis and promote the development of nonalcoholic fatty liver disease (NAFLD) (Botezelli et al, 2012;Ouyang et al, 2008;Rutledge and Adeli, 2007). In this regard, the metabolism of fructose in the liver is similar to that of ethanol, in that the metabolism of ethanol brings about a stimulation of de novo lipogenesis, eventually resulting in the development of liver steatosis, which can progress to alcoholic fatty liver disease (AFLD).…”

Catalase deletion promotes prediabetic phenotype in mice

“…For example, the consumption of fructose, a commonly-used sweetener and food additive, is strongly linked to insulin resistance [70]. This same sugar has been shown to lower hepatic catalase mRNA and activity in experimental animals [21, 71]. These data support the intriguing possibility that modulation of catalase by fructose could contribute to the development of insulin resistance induced by this sugar.…”