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Endogenous fructose production and metabolism in the liver contributes to the development of metabolic syndrome

Author

Listed:
  • Miguel A. Lanaspa

    (University of Colorado, 12700 East 19th Avenue, Room 7015, Denver, Colorado 80045, USA)

  • Takuji Ishimoto

    (University of Colorado, 12700 East 19th Avenue, Room 7015, Denver, Colorado 80045, USA)

  • Nanxing Li

    (University of Colorado, 12700 East 19th Avenue, Room 7015, Denver, Colorado 80045, USA)

  • Christina Cicerchi

    (University of Colorado, 12700 East 19th Avenue, Room 7015, Denver, Colorado 80045, USA)

  • David J. Orlicky

    (University of Colorado)

  • Philip Ruzycki

    (University of Colorado)

  • Christopher Rivard

    (University of Colorado, 12700 East 19th Avenue, Room 7015, Denver, Colorado 80045, USA)

  • Shinichiro Inaba

    (University of Colorado, 12700 East 19th Avenue, Room 7015, Denver, Colorado 80045, USA)

  • Carlos A. Roncal-Jimenez

    (University of Colorado, 12700 East 19th Avenue, Room 7015, Denver, Colorado 80045, USA)

  • Elise S. Bales

    (University of Colorado)

  • Christine P. Diggle

    (Leeds Institute of Molecular Medicine, University of Leeds)

  • Aruna Asipu

    (Leeds Institute of Molecular Medicine, University of Leeds)

  • J. Mark Petrash

    (University of Colorado)

  • Tomoki Kosugi

    (University of Colorado, 12700 East 19th Avenue, Room 7015, Denver, Colorado 80045, USA
    Nagoya University Graduate School of Medicine)

  • Shoichi Maruyama

    (Nagoya University Graduate School of Medicine)

  • Laura G. Sanchez-Lozada

    (University of Colorado, 12700 East 19th Avenue, Room 7015, Denver, Colorado 80045, USA
    INC Ignacio Chavez)

  • James L. McManaman

    (University of Colorado)

  • David T. Bonthron

    (Leeds Institute of Molecular Medicine, University of Leeds)

  • Yuri Y. Sautin

    (University of Florida)

  • Richard J. Johnson

    (University of Colorado, 12700 East 19th Avenue, Room 7015, Denver, Colorado 80045, USA
    Eastern Colorado Health Care System)

Abstract

Carbohydrates with high glycaemic index are proposed to promote the development of obesity, insulin resistance and fatty liver, but the mechanism by which this occurs remains unknown. High serum glucose concentrations are known to induce the polyol pathway and increase fructose generation in the liver. Here we show that this hepatic, endogenously produced fructose causes systemic metabolic changes. We demonstrate that mice unable to metabolize fructose are protected from an increase in energy intake and body weight, visceral obesity, fatty liver, elevated insulin levels and hyperleptinaemia after exposure to 10% glucose for 14 weeks. In normal mice, glucose consumption is accompanied by aldose reductase and polyol pathway activation in steatotic areas. In this regard, we show that aldose reductase-deficient mice are protected against glucose-induced fatty liver. We conclude that endogenous fructose generation and metabolism in the liver represents an important mechanism by which glucose promotes the development of metabolic syndrome.

Suggested Citation

  • Miguel A. Lanaspa & Takuji Ishimoto & Nanxing Li & Christina Cicerchi & David J. Orlicky & Philip Ruzycki & Christopher Rivard & Shinichiro Inaba & Carlos A. Roncal-Jimenez & Elise S. Bales & Christin, 2013. "Endogenous fructose production and metabolism in the liver contributes to the development of metabolic syndrome," Nature Communications, Nature, vol. 4(1), pages 1-9, December.
    • Handle: RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms3434
    DOI: 10.1038/ncomms3434
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