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Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells
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NAD+ Precursors Reverse Experimental Diabetic Neuropathy in Mice.

Krish Chandrasekaran1, Neda Najimi1, Avinash R Sagi1

  • 1Department of Neurology, University of Maryland School of Medicine, Baltimore, MD 21201, USA.

International Journal of Molecular Sciences
|January 23, 2024
PubMed
Summary
This summary is machine-generated.

Supplementing with NAD+ precursors like Nicotinamide Riboside (NR) or Nicotinamide Mononucleotide (NMN) can reverse diabetic peripheral neuropathy (DPN) by restoring NAD+ levels and activating SIRT1 protein.

Keywords:
NAD+NEDD4-1SIRT1diabetic neuropathyhigh fat dietmitochondriastreptozotocin

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Area of Science:

  • Neuroscience
  • Metabolic Disorders
  • Molecular Biology

Background:

  • Abnormal NAD+ signaling is linked to axonal degeneration in diabetic peripheral neuropathy (DPN).
  • Sirtuin-1 (SIRT1) protein plays a crucial role in neuronal health and function.
  • NAD+ precursors are potential therapeutic agents for neurological disorders.

Purpose of the Study:

  • To investigate the therapeutic potential of NAD+ precursors (Nicotinamide Riboside and Nicotinamide Mononucleotide) in alleviating DPN.
  • To determine the role of SIRT1 activation in mediating the effects of NAD+ precursors on neuronal health.
  • To evaluate the efficacy of NAD+ precursor supplementation in preclinical models of DPN.

Main Methods:

  • Cultured Dorsal Root Ganglion (DRG) neurons were treated with NR or NMN.
  • Diabetic peripheral neuropathy was induced in C57BL6 mice using streptozotocin (STZ) or a high-fat diet (HFD).
  • Mice received NR or NMN treatment for two months, followed by functional and histological assessments.

Main Results:

  • NR and NMN increased NAD+ levels, SIRT1 protein, and neurite growth in cultured neurons.
  • A SIRT1 inhibitor abolished the neurite growth-promoting effects of NR and NMN.
  • NR and NMN administration reversed neuropathy in STZ- and HFD-induced diabetic mice, improving sensory function and nerve conduction.
  • NAD+ levels and SIRT1 activity were restored in the DRGs of treated diabetic mice.
  • No additional benefit was observed in mice overexpressing SIRT1, suggesting NR/NMN act via SIRT1.

Conclusions:

  • Supplementation with NAD+ precursors (NR and NMN) shows significant therapeutic potential for diabetic peripheral neuropathy.
  • Activation of SIRT1 is a key mechanism underlying the neuroprotective effects of NAD+ precursors in DPN.
  • Targeting NAD+ metabolism and SIRT1 activation offers a promising therapeutic strategy for DPN treatment.