Zinc Regulates Glucose Metabolism of the Spinal Cord and Neurons and Promotes Functional Recovery after Spinal Cord Injury through the AMPK Signaling Pathway

Oxidative Medicine and Cellular Longevity, 2021 · DOI: https://doi.org/10.1155/2021/4331625 · Published: July 31, 2021

Spinal Cord Injury Endocrinology Nutrition & Dietetics

Simple Explanation

Spinal cord injury (SCI) often causes spinal cord mitochondrial dysfunction and produces glucose metabolism disorders, which aﬀect neuronal survival. Zinc is an essential trace element in the human body and plays multiple roles in the nervous system. Therefore, we concluded that zinc regulated the glucose metabolism of the spinal cord and neurons and promoted functional recovery after SCI through the AMPK pathway, which is expected to become a potential treatment strategy for SCI.

Study Duration

Not specified

Participants

SPF-grade C57BL/6J mice

Evidence Level

Not specified

Key Findings

1
zinc elevated the expression level of GLUT4 and promoted glucose uptake.
2
zinc enhanced the expression of proteins such as PGC-1α and NRF2, reduced oxidative stress, and promoted mitochondrial production.
3
zinc decreased neuronal apoptosis and promoted the recovery of motor function in SCI mice.

Research Summary

Our results sug- gested that zinc enhanced the glucose uptake of the injured neurons and spinal cord, reduced oxidative stress and neuro- nal apoptosis, promoted mitochondrial biogenesis, and encouraged recovery of motor function of SCI mice. After the administration of AMPK inhibitor, all the eﬀects of zinc had changed, which proved that the regulation of zinc on neuron and spinal cord glucose metabolism after SCI was mainly achieved through the AMPK signaling pathway Our current research has demonstrated that zinc regulated the glucose metabolism of the spinal cord and neurons after SCI partially through the AMPK pathway.

Practical Implications

Therapeutic Potential

Zinc therapy is expected to become a potential strategy for the treatment of SCI, addressing glucose metabolism and promoting recovery.

Target for Intervention

The AMPK pathway is identified as a key target through which zinc exerts its beneficial effects, suggesting opportunities for targeted interventions.

Mitochondrial Protection

Zinc's protective effect on mitochondria suggests a role in mitigating secondary injury mechanisms after SCI.

Zinc Regulates Glucose Metabolism of the Spinal Cord and Neurons and Promotes Functional Recovery after Spinal Cord Injury through the AMPK Signaling Pathway

Simple Explanation

Key Findings

Research Summary

Practical Implications

Therapeutic Potential

Target for Intervention

Mitochondrial Protection

Study Limitations

Your Feedback

Was this summary helpful?

Zinc Regulates Glucose Metabolism of the Spinal Cord and Neurons and Promotes Functional Recovery after Spinal Cord Injury through the AMPK Signaling Pathway

Simple Explanation

Key Findings

Research Summary

Practical Implications

Therapeutic Potential

Target for Intervention

Mitochondrial Protection

Study Limitations

Your Feedback

Was this summary helpful?