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Caloric restriction and combined caloric restriction with high-intensity interval training improve peripheral neuropathy (PN) by activating AMPK in Schwann cells. These interventions offer potential therapeutic strategies for PN linked to metabolic dysfunction.

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Area of Science:

  • Metabolic Neuroscience
  • Neurobiology
  • Endocrinology

Background:

  • Peripheral neuropathy (PN) is a common complication of obesity and diabetes, with limited treatment options.
  • Diet and exercise show promise for managing PN, but underlying mechanisms require further investigation.

Purpose of the Study:

  • To investigate the effects of caloric restriction (CR) and high-intensity interval training (HIIT) on metabolic dysfunction and PN in mice fed a high-fat diet (HFD).
  • To explore the neuroprotective mechanisms, including Schwann cell insulin signaling and AMPK activation, underlying these interventions.

Main Methods:

  • Mice were fed a HFD to induce obesity, impaired glucose tolerance, and PN.
  • Interventions included CR, HIIT, and a combination (HIIT-CR).
  • Metabolic parameters, PN, nerve insulin resistance, and AMPK activation in Schwann cells were assessed.

Main Results:

  • HFD induced obesity, glucose intolerance, and PN with associated nerve insulin resistance.
  • CR and HIIT-CR improved metabolic dysfunction; all interventions (CR, HIIT, HIIT-CR) ameliorated PN.
  • CR and HIIT-CR activated AMPK in peripheral nerves.
  • In vitro, palmitate-induced Schwann cell insulin resistance was reversed by an AMPK activator (AICAR).

Conclusions:

  • Dietary and exercise interventions can improve PN associated with metabolic dysfunction.
  • AMPK activation in Schwann cells is a key mechanism for the neuroprotective effects of CR and HIIT-CR.
  • Schwann cells play a critical role in nerve insulin signaling and PN progression.