Abstract
Evidence indicates that many forms of fructose-induced metabolic disturbance are associated with oxidative stress and mitochondrial dysfunction. Mitochondria are prominent targets of oxidative damage; however, it is not clear whether mitochondrial DNA (mtDNA) damage and/or its lack of repair are events involved in metabolic disease resulting from a fructose-rich diet. In the present study, we evaluated the degree of oxidative damage to liver mtDNA and its repair, in addition to the state of oxidative stress and antioxidant defense in the liver of rats fed a high-fructose diet. We used male rats feeding on a high-fructose or control diet for eight weeks. Our results showed an increase in mtDNA damage in the liver of rats fed a high-fructose diet and this damage, as evaluated by the expression of DNA polymerase γ, was not repaired; in addition, the mtDNA copy number was found to be significantly reduced. A reduction in the mtDNA copy number is indicative of impaired mitochondrial biogenesis, as is the finding of a reduction in the expression of genes involved in mitochondrial biogenesis. In conclusion, a fructose-rich diet leads to mitochondrial and mtDNA damage, which consequently may have a role in liver dysfunction and metabolic diseases.
Highlights
Over the last few decades, the daily intake of fructose, either free or as high-fructose corn syrup, has markedly increased [1]
Previous studies have shown that fructose-rich diets can induce many features of metabolic syndrome, including hypertension, insulin resistance, abdominal obesity, hepatic steatosis, endothelial dysfunction, and inflammation [5,6,7,8,9,10]
The determination of MPO activity can be used as a surrogate marker of inflammation, since it has been shown that the activity of MPO solubilized from the inflamed tissue is directly proportional to the number of neutrophils seen in histologic sections [27]
Summary
Over the last few decades, the daily intake of fructose, either free or as high-fructose corn syrup, has markedly increased [1]. These forms of fructose are used in the food industry for their enhanced sweetness, palatability, solubility, lower cost, and high production efficiency compared to sugar [2]. The increase in fructose consumption has coincided with a rise in the incidence of obesity, metabolic syndrome, and type 2 diabetes [3,4]. Several researchers have even suggested that increased fructose consumption has directly contributed to the obesity and type 2 diabetes epidemic [3,4]. Fructose is a highly lipogenic substrate which can induce profound metabolic alterations in the liver [11], where 90% of ingested sugar is metabolized [12]
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