Fructose-Rich Diet Affects Mitochondrial DNA Damage and Repair in Rats

被引:72
作者
Cioffi, Federica [1 ]
Senese, Rosalba [2 ]
Lasala, Pasquale [1 ]
Ziello, Angela [2 ]
Mazzoli, Arianna [3 ]
Crescenzo, Raffaella [3 ]
Liverini, Giovanna [3 ]
Lanni, Antonia [2 ]
Goglia, Fernando [1 ]
Iossa, Susanna [3 ]
机构
[1] Univ Sannio, Dept Sci & Technol, I-82100 Benevento, Italy
[2] Univ Naples 2, Dept Environm Biol & Pharmaceut Sci & Technol, I-81100 Caserta, Italy
[3] Univ Naples Federico II, Dept Biol, I-80100 Naples, Italy
关键词
fructose-rich diet; mitochondrial biogenesis; mitochondrial DNA (mtDNA); oxidative damage; repair mechanisms; FATTY LIVER-DISEASE; OXIDATIVE STRESS; INSULIN-RESISTANCE; CORN SYRUP; INTESTINAL INFLAMMATION; HEPATIC MITOCHONDRIAL; METABOLIC SYNDROME; GLUCOSE; PATHOGENESIS; CONSUMPTION;
D O I
10.3390/nu9040323
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
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 gamma, 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.
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页数:14
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