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Measurement of Insulin- and Contraction-Stimulated Glucose Uptake in Isolated and Incubated Mature Skeletal Muscle from Mice
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Chemical denervation using botulinum toxin increases Akt expression and reduces submaximal insulin-stimulated glucose

Zhencheng Li1, Lui Näslund-Koch2, Carlos Henriquez-Olguin1

  • 1Section of Molecular Physiology, Department of Nutrition, Exercise and Sports, University of Copenhagen, Denmark.

Cellular Signalling
|October 24, 2018
PubMed

Insights

Botulinum toxin A (botox) impacts muscle insulin signaling and glucose uptake, potentially mimicking surgical denervation effects. Further research is needed to understand these implications for human muscle health.

Area of Science:

  • Biochemistry
  • Physiology
  • Molecular Biology

Background:

  • Botulinum toxin A (botox) is used for spasticity and cosmetic treatments, inducing chemical denervation by blocking acetylcholine release.
  • Surgical denervation alters insulin signaling, glucose transporter (GLUT4), and hexokinase II (HKII) expression, leading to insulin resistance.

Purpose of the Study:

  • To investigate whether botox-induced chemical denervation affects insulin-stimulated glucose transport and related signaling pathways in mouse skeletal muscle.
  • To compare the effects of botox-induced chemical denervation with surgical denervation on muscle physiology.

Main Methods:

  • A time-course study was conducted on mouse soleus muscles ex vivo.
  • Muscles were subjected to supra-maximal and submaximal insulin stimulation at various time points after intramuscular botox injection.
  • Expression and phosphorylation of key proteins, including Akt, GLUT4, HKII, and TBC1D4, were analyzed.

Main Results:

  • Botox treatment did not affect glucose transport responsiveness to supra-maximal insulin stimulation at days 1, 7, and 21.
  • Despite no change in transport, botox decreased GLUT4, HKII, and TBC1D4 expression and phosphorylation.
  • At day 21, botox increased Akt protein expression and phosphorylation, and decreased submaximal insulin-stimulated glucose transport.

Conclusions:

  • Botox treatment induces significant alterations in insulin signaling, glucose handling proteins (GLUT4, HKII), and glucose transport in mouse muscle.
  • These findings suggest botox may induce insulin resistance, warranting further investigation in human muscle.
  • The botox-induced chemical denervation model offers a potentially less invasive alternative to surgical denervation for research.
Keywords:
AtrophyGLUT4HexokinaseInsulin signalingTBC1D4

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