Cardiac contraction-induced GLUT4 translocation requires dual signaling input

Joost J. F. P. Luiken*, Jan F. C. Glatz, Dietbert Neumann

*Corresponding author for this work

    Research output: Contribution to journalArticleAcademicpeer-review

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    Contraction-induced translocation of glucose transporter type-4 (GLUT4) to the sarcolemma is essential to stimulate cardiac glucose uptake during increased energy demand. As such, this process is a target for therapeutic strategies aiming at increasing glucose uptake in insulin-resistant and/or diabetic hearts. AMP-activated protein kinase (AMPK) and its upstream kinases form part of a signaling axis essential for contraction-induced GLUT4 translocation. Recently, activation of protein kinase-D1 (PKD1) was also shown to be as obligatory for contraction-induced GLUT4 translocation in cardiac muscle. However, contraction-induced PKD1 activation in this context occurs independently from AMPK signaling, suggesting that contraction-induced GLUT4 translocation requires the input of two separate signaling pathways. Necessity for dual input would more tightly couple GLUT4 translocation to stimuli that are inherent to cardiac contraction.
    Original languageEnglish
    Pages (from-to)404-410
    JournalTrends in Endocrinology and Metabolism
    Issue number8
    Publication statusPublished - Aug 2015


    • cardiac contraction
    • glucose uptake
    • signaling pathway
    • diabetes
    • heart

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