Researchers at the University of Leipzig Medical Center report that Schwann cells receive crucial support with nerve repair from the fat tissue that surrounds nerves in the body. Using genetically modified mice, they have shown that the chemical messenger leptin plays a key role in this process.

The findings are published in Cell Metabolism in an article titled, “Adipo-glial signaling mediates metabolic adaptation in peripheral nerve regeneration.”

“The peripheral nervous system harbors a remarkable potential to regenerate after acute nerve trauma,” the researchers wrote. “Full functional recovery, however, is rare and critically depends on peripheral nerve Schwann cells that orchestrate breakdown and resynthesis of myelin and, at the same time, support axonal regrowth. How Schwann cells meet the high metabolic demand required for nerve repair remains poorly understood. We here report that nerve injury induces adipocyte to glial signaling and identify the adipokine leptin as an upstream regulator of glial metabolic adaptation in regeneration.”

When a nerve is crushed or severed, the individual nerve fibers affected by the damage initially die. They have the ability to grow back and regenerate completely, but this depends on the Schwann cells that surround the nerve fibers. These cells do not die after nerve damage, but instead are responsible for coordinating the breakdown and regrowth of nerve fibers in their original areas. It was previously unknown how Schwann cells cope with the metabolic load associated with the breakdown and rebuilding of nerve tissue.

The new research demonstrated that leptin signaling is also an important factor in the repair of damaged nerves by Schwann cells. “Leptin derived from fat cells stimulates the energy balance of the Schwann cells by activating their mitochondria,” explained Robert Fledrich, PhD, from the Institute of Anatomy at Leipzig University and one of the two study leaders.

“At the same time, the mitochondria of the Schwann cells use parts of the damaged nerve tissue as an energy substrate so that successful regeneration can take place,” added Ruth Stassart, MD, professor at the Paul Flechsig Institute of Neuropathology at the University of Leipzig Medical Center and co-leader of the study. “The metabolism of the Schwann cells is therefore optimized for nerve regeneration and significantly promotes the restoration of the original nerve function,” the two researchers explained.

The communication between fat cells and Schwann cells could potentially open up new treatment options that positively influence the metabolism of repair cells in the event of nerve damage. The new findings may help to improve the regeneration of damaged nerves in humans in the future.

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