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Additional file 4: Table S2. Table with additional information about the study.

Additional file 2: Figure S2. Scheme of experimental design showing the different stages for the development of the model, allocation of animals in different groups and main experimental tests carried out in this study. Weaned rats from CCA-UFOP were fed diets containing 68% carbohydrates, 33% standard commercial feed, 33% condensed milk, 7% sucrose and the remaining water or standard pellet diet for 12 weeks since weaning. In the 4th week, the rats were adapted (4 days) to the aquatic environment and the animals related to the trained groups underwent swimming training for 8 weeks. The exhaustion time protocol was performed at weeks 4 and 12 to assess the animals' physical performance. The measurements of water intake and urinary volume performed in a metabolic cage were performed on the 12nd week, in addition to the renal (for analysis of renal function and histology) and body composition (BAI, LI and RAT weight) experiments, which were performed 48 h after last T session at the end of the 12nd week, at which time the rats were euthanized and samples of blood and kidney tissue were collected for analysis. Body weight measurements were taken at weeks 1, 4, 5, 7 and 11 and food intake measurements were taken at weeks 1, 5 and 10. CCA-UFOP (Center of Animal Science of UFOP); SD (standart diet); SUD (sucrose diet); T (swimming training).

Additional file 1: Figure S1. Body adiposity index values (panel A), *different from S-SD, T-SD and T-SUD groups, +different from S-SD group. Lee index values (panel B), *different from S-SD, T-SD, T-SUD groups. Retroperitoneal adipose tissue weight values (panel C), *different from S-SD, T-SD and T-SUD groups, **different from S-SD group. It was used the parametric test, two-way ANOVA followed by Tukey’s post-test; p

Although fructose consumption has dramatically increased and is suspected to be causally linked to metabolic abnormalities, the mechanisms involved are still only partially understood. We discuss the available data and investigate the effects of dietary fructose on risk factors associated with metabolic disorders. The evidence suggests that fructose may be a predisposing cause in the development of insulin resistance in association with the induction of hypertriglyceridemia. Experiments in animals have shown this relation when they are fed diets very high in fructose or sucrose, and human studies also show this relation, although with conflicting results due to the heterogeneity of the studies. The link between increased fructose consumption and increases in uric acid also has been confirmed as a potential risk factor for metabolic syndrome, and insulin resistance/hyperinsulinemia may be causally related to the development of hypertension. Collectively, these results suggest a link between high fructose intake and insulin resistance, although future studies must be of reasonable duration, use defined populations, and improve comparisons regarding the effects of relevant doses of nutrients on specific endpoints to fully understand the effect of fructose intake in the absence of potential confounding factors.