The mystery on why has been found.
Individuals with spinal cord injuries often face heightened risks of developing diabetes and cardiovascular issues, and recent research offers insight into the underlying mechanisms driving these health concerns.
A new animal study suggests that post-injury neuron activity triggers the breakdown of abdominal fat into compounds that accumulate in the liver and other organs. According to senior study author Andrea Tedeschi, an assistant professor of neuroscience at Ohio State University’s College of Medicine, these changes occur rapidly following disruptions in sensory processing caused by spinal cord injury.
This breakdown of abdominal fat sets off a chain reaction, with triglycerides breaking down into glycerol and free fatty acids, which then circulate throughout the body and accumulate in organs like the liver and heart. This process ultimately leads to conditions conducive to insulin resistance, a precursor to diabetes and heart disease. However, researchers have identified a potential treatment in the form of the seizure medication gabapentin, which has shown promise in preventing these harmful metabolic effects in lab mice.
Gabapentin works by inhibiting an overactive neurotransmitter that disrupts communication within the body following nervous system damage. Through administration of gabapentin, researchers were able to normalize metabolic function in lab mice, suggesting a potential avenue for mitigating the health complications associated with spinal cord injuries.
Heart disease and type 2 diabetes are leading causes of mortality among individuals with spinal cord injuries, with researchers previously suspecting a link between these disorders and dysfunction in the regulation of abdominal fat. Adipose tissue, responsible for storing and releasing energy as needed, plays a crucial role in metabolic function.
In experiments involving lab mice, researchers induced spinal cord injuries that specifically affected sensory nerves while leaving the sympathetic nervous system intact. The results revealed abnormal activity within sensory nerves, prompting the breakdown of abdominal fat and the release of fatty acids and glycerol into the bloodstream and organs.
The administration of gabapentin effectively prevented the spillover of fatty acids into the liver, allowing for the restoration of normal metabolism. Excitingly, these benefits persisted even after discontinuation of the drug, suggesting a sustained protective effect against metabolic dysfunction.
While these findings offer promising insights, researchers emphasize the need for caution in extrapolating results from animal studies to human populations. Nevertheless, the potential of gabapentin to mitigate the health risks associated with spinal cord injuries warrants further exploration and clinical investigation.
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