Intermittent fasting may help heal nerve damage – Neuroscience News

Summary: Intermittent fasting alters gut bacteria in mice, facilitating an increased ability to recover from damaged nerves.

Source: imperial college london

Intermittent fasting alters the activity of mice’s gut bacteria and increases their ability to recover from nerve damage.

The new research is published in Nature and was conducted by researchers at Imperial College London.

They observed how fasting caused gut bacteria to increase the production of a metabolite known as 3-indolepropionic acid (IPA), which is necessary for the regeneration of nerve fibers called axons – thread-like structures at the ends of nerve cells that send out electrochemical emissions. signals to other cells in the body.

This new mechanism was discovered in mice and it is hoped that it will also be valid for any future human trials. The team states that the bacterium that produces IPA, Clostridium sporogenesis, is found naturally in the intestines of humans as well as mice and that IPA is also present in the human bloodstream.

“There is currently no treatment for people with nerve damage beyond surgical reconstruction, which is only effective in a small percentage of cases, prompting us to investigate whether lifestyle changes could help with recovery,” said the study’s author, Professor Simone Di Giovanni of the Department of Imperial. Brain science.

“Intermittent fasting has already been linked by other studies to wound repair and the growth of new neurons, but our study is the first to explain exactly how fasting could help heal nerves.”

Fasting as a potential treatment

The study assessed nerve regeneration in mice where the sciatic nerve, the longest nerve running from the spine to the leg, was crushed. Half of the mice underwent intermittent fasting (eating as much as they wanted, then not eating at all on alternate days), while the other half were free to eat without any restrictions.

These diets were continued for a period of 10 days or 30 days before their operation, and the mice’s recovery was monitored 24 to 72 hours after nerve sectioning.

The length of regenerated axons was measured and was approximately 50% greater in mice that had fasted.

Professor Di Giovanni said: ‘I think the power of this is that it opens up a whole new area where we have to ask ourselves: is this the tip of an iceberg? Will there be other bacteria or metabolites of bacteria that can promote repair? »

Investigation reveals metabolic link

The researchers also studied how fasting led to this nerve regeneration. They found that there were significantly higher levels of specific metabolites, including IPA, in the blood of diet-restricted mice.

To confirm whether the IPA led to nerve repair, the mice were treated with antibiotics to clean their intestines of any bacteria. They then received genetically modified Clostridium sporogenesis strains that may or may not produce IPA.

The study assessed nerve regeneration in mice where the sciatic nerve, the longest nerve running from the spine to the leg, was crushed. Image is in public domain

“When IPA cannot be produced by these bacteria and was nearly absent from the serum, regeneration was impaired. This suggests that the IPA generated by these bacteria has the ability to heal and regenerate damaged nerves,” said Professor Di Giovanni.

Importantly, when mice were given IPA orally after sciatic nerve injury, increased regeneration and recovery were observed between two and three weeks after injury.

The next step in this research will be to test this mechanism for spinal cord injury in mice and determine if more frequent administration of IPA would maximize its effectiveness.

“One of our goals now is to systematically investigate the role of bacterial metabolite therapy.” said Professor Di Giovanni.

Further studies will need to determine whether IPA increases after fasting in humans and the effectiveness of IPA and intermittent fasting as a potential treatment in humans.

He said: “One of the issues that we haven’t fully explored is that since IPA lasts in the blood for four to six hours at high concentration, its repeated administration throughout the day or its addition to a normal diet would help maximize its therapeutic effects.

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About this neuroscience research news

Author: Press office
Source: imperial college london
Contact: Press office – Imperial College London
Image: Image is in public domain

Original research: Access closed.
“Intestinal metabolite indole-3 propionate promotes nerve regeneration and repair” by Elisabeth Serger et al. Nature


Gut metabolite indole-3 propionate promotes nerve regeneration and repair

The regenerative potential of mammalian peripheral nervous system neurons after injury is extremely limited by their low rate of axonal regeneration.

Regenerative capacity is influenced by both injury-dependent and injury-independent mechanisms. Of these, environmental factors such as exercise and environmental enrichment have been shown to affect signaling pathways that promote axonal regeneration.

Several of these pathways, including changes in gene transcription and protein synthesis, mitochondrial metabolism, and neurotrophin release, can be activated by intermittent fasting (IF). However, whether IF influences axonal regenerative capacity remains to be investigated.

Here, we show that IF promotes axonal regeneration after sciatic nerve crush in mice through an unexpected mechanism that relies on the Gram-positive gut microbiome and an increase in the derived indole-3-propionic acid (IPA) metabolite intestinal bacteria in serum.

API production by Clostridium sporogens is required for effective axonal regeneration, and administration of IPA after sciatic injury significantly enhances axonal regeneration, accelerating recovery of sensory function. Mechanistically, RNA sequencing analysis of dorsal root ganglia sciatic ganglia suggested a role for neutrophil chemotaxis in the IPA-dependent regenerative phenotype, which was confirmed by inhibition of neutrophil chemotaxis .

Our results demonstrate the ability of a microbiome-derived metabolite, such as IPA, to facilitate the regeneration and functional recovery of sensory axons through an immune-mediated mechanism.

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