Abstract
Fructose consumption (FC) has caused much concern due to its prominence in today's diet and its link to cardiovascular disease. We hypothesized that the effects of FC are mediated by overactivation of NADPH oxidase (Nox), which increases superoxide (O2−) production, reducing NO bioavailability. SD rats were fed either a normal or a 60% fructose diet for 21 days. FC animals showed increases in blood pressure and plasma insulin (3.1 ± 0.4 to 5.4 ± 0.4 ng/mL). In pregnancy, fetal weights of FC rats were significantly lower (5.84 ± .06 to 4.71 ± .06 g, ~20%). Furthermore, the reduction of myocardial O2 consumption (MVO2) ex vivo by bradykinin was impaired in FC (28 ± 2% to 17 ± 2%), an effect reversed by apocynin or tiron, a Nox inhibitor and O2− scavenger, respectively. Finally, microarray of mRNA revealed significant changes in 237 genes (p < .05, fold change > ± 1.5), including upregulation of cholesterol transporter caveolin 1 and endothelin receptor B, and repression of mitochondrial protein Mrpl12, and mitochondrial ATP synthase subunit Atp5S. Analysis of miRs showed repression of miRs associated with upregulated genes and vice versa, including trends seen in heart failure: upregulation of miR126, a regulator of angiogenesis, and miR21. In conclusion, FC triggers gene expression changes in the heart with involvement of miRs, which leads to the lowering of NO bioavailability through the generation of O2−. Supported by PO43023.
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