Absence of insulin receptor substrate-1 expression does not alter GLUT1 or GLUT4 abundance or contraction-stimulated glucose uptake by mouse skeletal muscle

C. L. Dumke, A. C. Wetter, E. B. Arias, C. R. Kahn, G. D. Cartee

Research output: Contribution to journalArticlepeer-review

Abstract

The purpose of this study was to determine the influence of insulin receptor substrate-1 (IRS-1) expression on GLUT1 and GLUT4 glucose transporter protein abundance, contraction-stimulated glucose uptake, and contraction-induced glycogen depletion by skeletal muscle. Mice (6 months old) from three genotypes were studied: wild-type (IRS-1+/+), heterozygous (IRS-1+/-) for the null allele, and IRS-1 knockouts (IRS-1-/-) lacking a functional IRS-1 gene. In situ muscle contraction was induced (electrical stimulation of sciatic nerve) in one hindlimb using contralateral muscles as controls. Soleus and extensor digitorum longus were dissected and 2-deoxyglucose uptake was measured in vitro. 2-Deoxyglucose uptake was higher in basal muscles (no contractions) from IRS-1-/- vs. both other genotypes. Contraction-stimulated 2-deoxyglucose uptake and glycogen depletion did not differ among genotypes. Muscle IRS-1 protein was undetectable for IRS-1-/- mice, and values were approximately 40% lower in IRS-1+/- than in IRS-1+/+ mice. No difference was found in IRS-1+/+ compared to IRS-1-/- groups regarding muscle abundance of GLUT1 and GLUT4. Substantial reduction or elimination of IRS-1 did not alter the hallmark effects of contractions on muscle carbohydrate metabolism - activation of glucose uptake and glycogen depletion.

Original languageEnglish
Pages (from-to)696-700
Number of pages5
JournalHormone and Metabolic Research
Volume33
Issue number12
DOIs
StatePublished - 2001

Keywords

  • Contractile Activity
  • Exercise
  • Glucose Transport
  • Glycogen
  • Insulin Signaling

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