Diet could play a role in healing nerve damage after spinal cord injury

Scientists have found that regulating the hunger hormone leptin through diet can enhance nerve repair after spinal cord and sciatic injury in mice.

A study from researchers at Imperial College London has revealed that dietary interventions, specifically intermittent fasting, could play an important role in repairing nerve damage after spinal cord injuries. The scientists found that these benefits are linked to leptin, a hormone known for controlling appetite and fat storage, signals directly to nerve cells.

In a series of experiments using mouse models, the team demonstrated that intermittent fasting in mice is associated with nerve repair by improving leptin signalling in sensory neurons after sciatic and spinal nerve system injury.

"Our discovery that the hormone leptin, which is known to suppress appetite, can promote regeneration after nerve and spinal cord injuries in mice could be leveraged in humans, given that leptin is highly conserved across species." Professor Simone Di Giovanni Department of Brain Sciences

Spinal cord injuries currently have no clinically approved treatments to regenerate damaged nerves or restore lost function, and most rehabilitation currently focuses on physical therapy or managing long-term disability.

The findings therefore suggest that leveraging the hormone leptin could help to promote repair and could mean that diet plays an important role in recovery after a spinal cord injury.

Professor Simone Di Giovanni, James W Harnett Chair in Restorative Neuroscience and author of the paper said: “Our discovery that the hormone leptin, which is known to suppress appetite, can promote regeneration after nerve and spinal cord injuries in mice is a potentially important step forwards. Given that leptin is highly conserved across species, it raises the question of whether it could have a similar effect in humans.”

“It is also interesting to speculate that mammals might have developed a strategy whereby they suppress the need to eat to allow for repair in case of nervous system injuries, allowing compartmentalisation of key highly energy demanding functions that are necessary for survival.”

Diet, fasting and fat – managing leptin levels in mice

To investigate the role of leptin, the study examined how specifically intermittent fasting in mice could alter the healing of the dorsal root ganglia cells (DRG). These cells are responsible for transmitting sensory information to the spinal cord.

Intermittent fasting is an eating pattern that cycles between periods of eating and fasting on a regular schedule. The research found that intermittent fasting in mice enhanced the cells regenerative capacity by making the leptin signalling pathway more sensitive and responsive to the hormone.

In contrast having a high fat diet causes leptin resistance which means the nerve cells stop responding to leptin, which is a possible cause of nerve damage in obesity.

The findings show that the effect of leptin is independent of its role in controlling hunger and this points a new role for leptin in not just regulating appetite but also healing nerves.

Implications and future directions

While these finding are limited to animal models, the findings of this research could pave the way for using leptin and diet-based therapies to enhance nerve regeneration, especially in combination with other therapeutic and neurorehabilitation approaches.

Future research is now needed to translate these findings to humans and explore whether there are other hormones or lifestyle changes which could support neuron repair.

Dietary Dependent Sensitisation of Neuronal Leptin Signalling Promotes Neural Repair after Injury via cAMP and Gene Transcription is published in CellPress.