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    High-fructose diet elevates myocardial superoxide generation in mice in the absence of cardiac hypertrophy

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    Author
    Mellor, K; Ritchie, RH; Meredith, G; Woodman, OL; Morris, MJ; Delbridge, LMD
    Date
    2010-07-01
    Source Title
    NUTRITION
    Publisher
    ELSEVIER SCIENCE INC
    University of Melbourne Author/s
    MELLOR, KIMBERLEY; Delbridge, Leanne; MEREDITH, GRETA
    Affiliation
    Physiology
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Mellor, K., Ritchie, R. H., Meredith, G., Woodman, O. L., Morris, M. J. & Delbridge, L. M. D. (2010). High-fructose diet elevates myocardial superoxide generation in mice in the absence of cardiac hypertrophy. NUTRITION, 26 (7-8), pp.842-848. https://doi.org/10.1016/j.nut.2009.08.017.
    Access Status
    This item is currently not available from this repository
    URI
    http://hdl.handle.net/11343/28901
    DOI
    10.1016/j.nut.2009.08.017
    Description

    C1 - Journal Articles Refereed

    Abstract
    OBJECTIVE: Dietary fructose intake has increased considerably in recent decades and this has been paralleled by an increase in the incidence of insulin resistance, especially in children and adolescents. The impact of a high-fructose diet on the myocardium is not fully understood. The aims of this study were to characterize the murine metabolic and cardiac phenotypes associated with a high-fructose diet and to determine whether this diet imparts differential effects with age. METHODS: Juvenile (4 wk) and adult (14 wk) C57Bl/6 mice were fed a 60% fructose diet or isoenergetic control (starch) diet for 6 wk. RESULTS: At completion of the dietary intervention (at ages 10 and 20 wk), fructose-fed mice were normotensive; hyperinsulinemia and cardiac hypertrophy were not evident. Interestingly, fructose-fed mice exhibited lower blood glucose levels (10 wk: 4.81+/-0.28 versus 5.42+/-0.31 mmol/L; 20 wk: 4.88+/-0.30 versus 5.96+/-0.42 mmol/L, P<0.05) compared with controls. Nicotinamide adenosine dinucleotide phosphate-driven myocardial superoxide production was significantly increased in fructose-fed mice at both ages (by approximately 29% of control at 10 wk of age and 16% at 20 wk, P<0.01). No increase in aortic superoxide production was observed. Fructose feeding did not alter gene expression of the antioxidant thioredoxin-2, suggesting an imbalance between myocardial reactive oxygen species generation and antioxidant induction. CONCLUSION: These findings indicate that increased myocardial superoxide production may represent an early and primary cardiac pathologic response to the metabolic challenge of excess dietary fructose in juveniles and adults that can be detected in the absence of cardiac hypertrophy and hypertension.
    Keywords
    Systems Physiology; Cardiovascular System and Diseases

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