GLUT4 ablation in mice results in redistribution of IRAP to the plasma membrane

Hua Jiang, Jing Li, Ellen B. Katz, Maureen J. Charron

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

Glucose transporter (GLUT) 4 is the insulin responsive glucose transporter in adipose tissue, skeletal muscle, and heart. Insulin elicits increased glucose uptake by recruiting GLUT4 from a specialized intracellular storage site to the cell surface. Expression of various proteins that colocalize with GLUT4 and/or are involved in insulin-stimulated GLUT4 translocation was examined in adipocytes as well as skeletal and cardiac muscles from GLUT4 null mice. Our data demonstrate that expression of insulin-regulated aminopeptidase (IRAP) is divergently regulated in GLUT4 null tissues, e.g., upregulated 1.6-fold in GLUT4 null adipocytes and downregulated in GLUT4 null skeletal muscle (40%) and heart (60%). IRAP exhibited abnormal subcellular distribution and impaired insulin-stimulated translocation in GLUT4-deficient tissues. We propose the compartment containing IRAP and proteins normally associated with GLUT4 vesicle traffics constitutively to the cell surface in GLUT4 null adipocytes and skeletal muscle.

Original languageEnglish (US)
Pages (from-to)519-525
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume284
Issue number2
DOIs
StatePublished - 2001

Fingerprint

Aminopeptidases
Cell membranes
Ablation
Cell Membrane
Insulin
Muscle
Skeletal Muscle
Adipocytes
Tissue
Glucose Transporter Type 4
Facilitative Glucose Transport Proteins
Adipose Tissue
Myocardium
Proteins
Down-Regulation
Glucose

Keywords

  • GLUT4 translocation
  • Insulin action
  • Insulin-regulated aminopeptidase
  • Vesicle trafficking

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

GLUT4 ablation in mice results in redistribution of IRAP to the plasma membrane. / Jiang, Hua; Li, Jing; Katz, Ellen B.; Charron, Maureen J.

In: Biochemical and Biophysical Research Communications, Vol. 284, No. 2, 2001, p. 519-525.

Research output: Contribution to journalArticle

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