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Expression of the glucose transporter GLUT4 in the muscular dystrophic mdx mouse

C Olichon-Berthe1, N Gautier, E Van Obberghen

  • 1INSERM U 145, Faculté de Médecine, Nice, France.

Insights

Glucose transporter protein levels, specifically GLUT4, are altered in mdx mice muscles. Skeletal muscle shows increased GLUT4, while diaphragm GLUT4 decreases with age, independent of mRNA levels in skeletal muscle.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Physiology

Background:

  • Glucose transporters are crucial for cellular energy metabolism.
  • Duchenne muscular dystrophy (DMD) is characterized by progressive muscle degeneration.
  • Investigating glucose transporter alterations in DMD models can reveal metabolic dysfunctions.

Purpose of the Study:

  • To quantify glucose transporter protein and mRNA levels in various tissues of mdx mice, a model for DMD.
  • To compare these levels with age-matched control mice (C57Bl/10).
  • To elucidate the regulatory mechanisms of glucose transporter expression in DMD.

Main Methods:

  • Western blot analysis was used to measure glucose transporter protein levels (GLUT4 in muscle, GLUT1 in brain).
  • Northern blot analysis was performed to assess glucose transporter mRNA levels.
  • Tissues analyzed included skeletal muscle, heart, diaphragm, and brain from young and adult mice.

Main Results:

  • Skeletal muscle (hindlegs) showed a ~55% increase in GLUT4 protein in mdx mice at both ages, without changes in GLUT4 mRNA.
  • Diaphragm GLUT4 protein was unchanged in young mdx mice but decreased by ~37% in older mdx mice, accompanied by reduced GLUT4 mRNA.
  • No significant differences in GLUT4 or GLUT1 protein were found in heart or brain, respectively.

Conclusions:

  • GLUT4 protein levels are differentially affected in mdx mouse muscles based on tissue type and age.
  • Increased skeletal muscle GLUT4 in mdx mice is not regulated at the mRNA level.
  • Diaphragm GLUT4 downregulation in older mdx mice involves both protein and mRNA level changes, suggesting age-dependent metabolic adaptations.

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