University Library
  • Login
A gateway to Melbourne's research publications
Minerva Access is the University's Institutional Repository. It aims to collect, preserve, and showcase the intellectual output of staff and students of the University of Melbourne for a global audience.
View Item 
  • Minerva Access
  • Medicine, Dentistry & Health Sciences
  • Melbourne Medical School
  • Physiology
  • Physiology - Research Publications
  • View Item
  • Minerva Access
  • Medicine, Dentistry & Health Sciences
  • Melbourne Medical School
  • Physiology
  • Physiology - Research Publications
  • View Item
JavaScript is disabled for your browser. Some features of this site may not work without it.

    Interleukin-18 Activates Skeletal Muscle AMPK and Reduces Weight Gain and Insulin Resistance in Mice

    Thumbnail
    Download
    Published version (1.305Mb)

    Citations
    Scopus
    Web of Science
    Altmetric
    48
    44
    Author
    Lindegaard, B; Matthews, VB; Brandt, C; Hojman, P; Allen, TL; Estevez, E; Watt, MJ; Bruce, CR; Mortensen, OH; Syberg, S; ...
    Date
    2013-09-01
    Source Title
    Diabetes
    Publisher
    AMER DIABETES ASSOC
    University of Melbourne Author/s
    Watt, Matthew
    Affiliation
    Physiology
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Lindegaard, B., Matthews, V. B., Brandt, C., Hojman, P., Allen, T. L., Estevez, E., Watt, M. J., Bruce, C. R., Mortensen, O. H., Syberg, S., Rudnicka, C., Abildgaard, J., Pilegaard, H., Hidalgo, J., Ditlevsen, S., Alsted, T. J., Madsen, A. N., Pedersen, B. K. & Febbraio, M. A. (2013). Interleukin-18 Activates Skeletal Muscle AMPK and Reduces Weight Gain and Insulin Resistance in Mice. DIABETES, 62 (9), pp.3064-3074. https://doi.org/10.2337/db12-1095.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/255743
    DOI
    10.2337/db12-1095
    Abstract
    Circulating interleukin (IL)-18 is elevated in obesity, but paradoxically causes hypophagia. We hypothesized that IL-18 may attenuate high-fat diet (HFD)-induced insulin resistance by activating AMP-activated protein kinase (AMPK). We studied mice with a global deletion of the α-isoform of the IL-18 receptor (IL-18R(-/-)) fed a standard chow or HFD. We next performed gain-of-function experiments in skeletal muscle, in vitro, ex vivo, and in vivo. We show that IL-18 is implicated in metabolic homeostasis, inflammation, and insulin resistance via mechanisms involving the activation of AMPK in skeletal muscle. IL-18R(-/-) mice display increased weight gain, ectopic lipid deposition, inflammation, and reduced AMPK signaling in skeletal muscle. Treating myotubes or skeletal muscle strips with IL-18 activated AMPK and increased fat oxidation. Moreover, in vivo electroporation of IL-18 into skeletal muscle activated AMPK and concomitantly inhibited HFD-induced weight gain. In summary, IL-18 enhances AMPK signaling and lipid oxidation in skeletal muscle implicating IL-18 in metabolic homeostasis.

    Export Reference in RIS Format     

    Endnote

    • Click on "Export Reference in RIS Format" and choose "open with... Endnote".

    Refworks

    • Click on "Export Reference in RIS Format". Login to Refworks, go to References => Import References


    Collections
    • Minerva Elements Records [45770]
    • Physiology - Research Publications [361]
    Minerva AccessDepositing Your Work (for University of Melbourne Staff and Students)NewsFAQs

    BrowseCommunities & CollectionsBy Issue DateAuthorsTitlesSubjectsThis CollectionBy Issue DateAuthorsTitlesSubjects
    My AccountLoginRegister
    StatisticsMost Popular ItemsStatistics by CountryMost Popular Authors