Munc18c provides stimulus-selective regulation of GLUT4 but not fatty acid transporter trafficking in skeletal muscle

Swati S. Jain, Laelie A. Snook, Jan F. C. Glatz, Joost J. F. P. Luiken, Graham P. Holloway, Debbie C. Thurmond, Arend Bonen*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

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Abstract

Insulin-, and contraction-induced GLUT4 and fatty acid (FA) transporter translocation may share common trafficking mechanisms. Our objective was to examine the effects of partial Munc18c ablation on muscle glucose and FA transport, FA oxidation, GLUT4 and FA transporter (FAT/CD36, FAB-Ppm, FATP1, FATP4) trafficking to the sarcolemma, and FAT/CD36 to mitochondria. In Munc18c(-/+) mice, insulin-stimulated glucose transport and GLUT4 sarcolemmal appearance were impaired, but were unaffected by contraction. Insulin- and contraction-stimulated FA transport, sarcolemmal FA transporter appearance, and contraction-mediated mitochondrial FAT/CD36 were increased normally in Munc18c(-/+) mice. Hence, Munc18c provides stimulus-specific regulation of GLUT4 trafficking, but not FA transporter trafficking.
Original languageEnglish
Pages (from-to)2428-2435
JournalFebs Letters
Volume586
Issue number16
DOIs
Publication statusPublished - 30 Jul 2012

Keywords

  • FAT/CD36
  • FABPpm
  • FATP1
  • FATP4
  • Fatty acid transport
  • Glucose transport

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