Study Suggests Metabolism Issues After Spinal-Cord

Study Suggests Metabolism Issues After Spinal-Cord Injury Result from Disturbed Neuronal Activity

Researchers from The Ohio State University have found that disturbed neuronal activity may cause metabolism issues in individuals who suffer spinal-cord injuries. Findings from an animal study suggest that heart attacks, diabetes and vascular conditions that typically affect patients postspinal-cord injury are a result of neuronal activity that causes abdominal fat tissue compounds to start leaking and pooling into organs, such as the liver.

The study also pointed to common drugs that could potentially prevent some of the metabolism issues that occur after spinal-cord injuries.

The Ohio State University researchers found a connection between triglyceride breakdown in the fat tissue of mouse models and dysregulated neuron function. Furthermore, they found that a relatively small dose of gabapentin, a drug typically prescribed to alleviate nerve pain, could prevent the harmful metabolic effects seen postspinal -cord injury.

Gabapentin works by inhibiting the action of a neural protein that reacts to nervous system damage by becoming overactive and causing communication problems. In the case of spinal-cord injuries, this neural protein affects sensory neurons as well as the abdominal fat tissue they signal.

Adipose tissue and sympathetic nervous system function have been the main focus of past research related to these conditions in people afflicted with neuronal damage. The sympathetic nervous system is in charge of the infamous “fight or flight” response as well as the regulation of the adipose tissue that envelops abdominal organs.

OSU postdoctoral researcher and first study author Debasish Roy chose an unbeaten path and focused the research on sensory neurons rather than adipose tissue function. OSU College of Medicine assistant professor of neuroscience and senior study author Andrea Tedeschi says the research team believes “maladaptive reorganization” in the sensory system induces changes in abdominal fat that in turn trigger a series of reactions that result in fat breakdown.

This starts with the breakdown of triglycerides into glycerol and free fatty acids, which go into circulation and enter the heart, muscles and liver before it starts accumulating. According to Tedeschi, this accumulation also creates the ideal conditions for insulin resistance in patients postspinal-cord injury. A short gabapentin course can stabilize metabolic function and prevent abdominal fat breakdown, she adds.

Spinal-cord injuries can be quite problematic long after the physical injury is healed. Past research has shown that cardiometabolic conditions are one of the top causes of death in individuals who experienced spinal-cord injuries. The majority of these disorders can be traced back to dysregulation in the adipose tissue or visceral white fat, which is involved in storing and releasing energy as fatty acids and maintaining blood-sugar levels.

Companies such as Clene Inc. (NASDAQ: CLNN) that focus on developing pharmaceutical solutions aimed at protecting neuronal health and treating conditions arising from the degeneration of neurons could explore the suggestion that malfunctioning neurons could be behind some of the ailments that people suffer from after sustaining injuries affecting the spinal cord.

NOTE TO INVESTORS: The latest news and updates relating to Clene Inc. (NASDAQ: CLNN) are available in the company’s newsroom at https://ibn.fm/CLNN

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