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Persistent Postirradiation Skeletal Muscle Protein and Insulin Sensitivity Changes in Nonhuman Primates.

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Whole-body irradiation causes persistent skeletal muscle insulin resistance in nonhuman primates, leading to type 2 diabetes. This dysfunction involves impaired insulin signaling and altered mitochondrial dynamics in muscle tissue.

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Area of Science:

  • Endocrinology
  • Radiation Biology
  • Muscle Physiology

Background:

  • Whole-body irradiation is linked to increased diabetes incidence in cancer survivors and animal models.
  • Type 2 diabetes post-irradiation occurs without obesity, implicating skeletal muscle dysfunction.
  • Skeletal muscle is crucial for glucose disposal and minute-to-minute glucose regulation.

Purpose of the Study:

  • To investigate the persistent effects of whole-body irradiation on skeletal muscle insulin sensitivity.
  • To identify molecular mechanisms underlying radiation-induced skeletal muscle insulin resistance.

Main Methods:

  • Analysis of skeletal muscle from control and irradiated male rhesus macaques 4 years post-irradiation (6.5 Gy).
  • Evaluation of basal and insulin-stimulated receptor activation in skeletal muscle.
  • Proteomic analysis (shotgun proteomics, immunoblotting) to identify protein changes, including post-translational modifications like sulfenylation.
  • Assessment of mitochondrial dynamics markers (fission and fusion).

Main Results:

  • Irradiated skeletal muscle exhibited deficient basal and insulin-stimulated receptor activation.
  • Akt2, a key insulin signaling protein, showed radiation-induced sulfenylation, indicating dysregulation.
  • Proteomics revealed upregulation of mitochondrial and peroxisome-associated proteins in irradiated muscle.
  • Increased markers for mitochondrial fission and fusion suggest altered mitochondrial turnover and dynamics.

Conclusions:

  • Irradiated skeletal muscle demonstrates persistent insulin resistance.
  • Radiation exposure leads to intracellular protein oxidation and altered mitochondrial function in muscle.
  • These molecular and functional changes in skeletal muscle contribute to radiation-induced glycemic dysregulation and diabetes.