Abstract
The increase in the use of refined food, which is rich in fructose, is of particular concern in children and adolescents, since the total caloric intake and the prevalence of metabolic syndrome are increasing continuously in these populations. Nevertheless, the effects of high fructose diet have been mostly investigated in adults, by focusing on the effect of a long-term fructose intake. Notably, some reports evidenced that even short-term fructose intake exerts detrimental effects on metabolism. Therefore, the aim of this study was to compare the metabolic changes induced by the fructose-rich diet in rats of different age, i.e., young (30 days old) and adult (90 days old) rats. The fructose-rich diet increased whole body lipid content in adult, but not in young rats. The analysis of liver markers of inflammation suggests that different mechanisms depending on the age might be activated after the fructose-rich diet. In fact, a pro-inflammatory gene-expression analysis showed just a minor activation of macrophages in young rats compared to adult rats, while other markers of low-grade metabolic inflammation (TNF-alpha, myeloperoxidase, lipocalin, haptoglobin) significantly increased. Inflammation was associated with oxidative damage to hepatic lipids in young and adult rats, while increased levels of hepatic nitrotyrosine and ceramides were detected only in young rats. Interestingly, fructose-induced hepatic insulin resistance was evident in young but not in adult rats, while whole body insulin sensitivity decreased both in fructose-fed young and adult rats. Taken together, the present data indicate that young rats do not increase their body lipids but are exposed to metabolic perturbations, such as hepatic insulin resistance and hepatic oxidative stress, in line with the finding that increased fructose intake may be an important predictor of metabolic risk in young people, independently of weight status. These results indicate the need of corrective nutritional interventions for young people and adults as well for the prevention of fructose-induced metabolic alterations.
Highlights
In the last decades, high fructose intake has been associated with increased risk of obesity development and the consequent metabolic and inflammatory diseases (Bray and Popkin, 2014; Campos and Tappy, 2016)
We focused for the first time on the effects of a short term fructose diet in young and adult rats, in order to highlight potential age-dependent responses
One of the main evidence arising from the here presented results is that a short-term high fructose intake induces a condition of low-grade metabolic inflammation in liver of young and adult rats
Summary
High fructose intake has been associated with increased risk of obesity development and the consequent metabolic and inflammatory diseases (Bray and Popkin, 2014; Campos and Tappy, 2016). Liver function is vulnerable to an increasing fructose intake, since this organ is responsible for about 90% of the total metabolism of this sugar (Tappy and Lê, 2010). Different studies in both human and animal models evidenced liver morphological and functional damage following high intake of fructose or fructosecontaining sweeteners (Crescenzo et al, 2013, 2014, 2017; Jin and Vos, 2015). It has been recently reported that even perinatal exposure to maternal consumption of sucrose or high fructose corn syrup exerts detrimental effects on the offspring, on adiposity, plasma non-esterified fatty acids (NEFA) and hepatic lipid content (Toop et al, 2017). It has been shown that 2 weeks of high fructose diet in weaning rats have a prooxidant effect on different tissues (Busserolles et al, 2002). Hepatic metabolic alterations and increased markers of oxidative stress and inflammation were detected after 3 weeks of fructose administration in drinking water in rats (Francini et al, 2010; Castro et al, 2012, 2013, 2014, 2015) or after 4 and 8 weeks of increased fructose in the diet (Alwahsh et al, 2014, 2017)
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