Neuroendocrine and cardiac metabolic dysfunction and NLRP3 inﬂammasome activation in adipose tissue and pancreas following chronic spinal cord injury in the mouse

ASN NEURO, 2013 · DOI: 10.1042/AN20130021 · Published: August 7, 2013

Spinal Cord Injury Cardiovascular Science Endocrinology

Simple Explanation

This study investigates the link between spinal cord injury (SCI) and increased risk of cardiovascular disease (CVD). It explores how SCI affects the neuroendocrine system, heart function, and inflammation in adipose tissue and the pancreas. The researchers found that chronic SCI in mice leads to changes in the expression of key regulatory peptides in the hypothalamus, the brain region controlling metabolism and appetite. Specifically, there was a decrease in POMC and an increase in NPY. Furthermore, the study revealed increased inflammation and activation of the NLRP3 inflammasome in adipose tissue and the pancreas of mice with chronic SCI, suggesting a potential mechanism for metabolic dysfunction and increased CVD risk.

Study Duration

1-month post-SCI

Participants

Female C57 Bl/6 mice

Evidence Level

Not specified

Key Findings

1
Chronic SCI results in decreased POMC and increased NPY expression in the hypothalamic ARC and PVN.
2
Long-form leptin receptor (Ob-Rb), JAK2/STAT3/p38 and RhoA/ROCK signaling is significantly increased in the heart tissue post-SCI.
3
The formation and activation of the NLRP3 inflammasome in VAT and pancreas post-SCI.

Research Summary

This study demonstrates neuroendocrine signaling peptide alterations, associated with central inflammation and metabolic dysfunction post-SCI. The research provides evidence for the peripheral activation of signaling mechanisms involved in cardiac, VAT and pancreatic inflammation and metabolic dysfunction post-SCI. These findings demonstrate biological mechanisms related to cardiometabolic risk factors, and indicate a multi-system, chronic state of inflammation and maladaptive metabolism following SCI.

Practical Implications

Therapeutic targets

The identification of the NLRP3 inflammasome as a key player in metabolic dysfunction following SCI suggests it as a potential therapeutic target.

Rehabilitation strategies

Understanding the mechanisms contributing to cardiometabolic risk after SCI can inform the development of targeted rehabilitation strategies.

Early intervention

Early interventions aimed at mitigating inflammation and metabolic dysfunction may improve long-term outcomes and quality of life for individuals with SCI.

Study Limitations

1
The study was conducted on female C57 Bl/6 mice, and the results may not be directly applicable to humans or other populations.
2
The study focused on a 1-month post-SCI time point, and longer-term effects were not investigated.
3
The study did not explore the specific mechanisms by which SCI leads to NLRP3 inflammasome activation in VAT and pancreas.

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