Conclusion
The results show that LOI does not influence the distribution of adipose tissue, but does influence proinflammatory adipokines and cardiometabolic profiles following SCI. Further research is needed to evaluate impact of lean body mass on these findings.
Objective
Level of injury (LOI) and the role of adipose tissue and its proinflammatory adipokines in cardiometabolic dysfunction following spinal cord injury (SCI) remains poorly understood. We aim to examine the influence of LOI on adipose tissue and its relationship to proinflammatory adipokines and cardiometabolic profiles following SCI. Design: Cross sectional and correlational study. Setting: Clinical hospital and academic setting. Participants: Forty-seven individuals with chronic motor complete SCI (age 43.8±11.5 y, BMI: 27.3±5.3) were classified as having tetraplegia (TSCI; n=12) or paraplegia (PSCI; n=35). Intervention: Non applicable. Outcome measures: Visceral (VAT) and subcutaneous (SAT) adipose tissue volumes were measured using magnetic resonance imaging. Proinflammatory adipokines (tumor neurosis factor-α, interleukin-6 (IL-6), plasminogen activatable inhibitor-1, thrombin-activatable fibrinolysis inhibitor, and high-sensitivity c-reactive protein) and cardiovascular, carbohydrate, and lipid profiles were assessed according to standard techniques.
Results
VAT volume was greater in TSCI versus PSCI (p=0.042); however, after covarying for age this significance was lost (p>0.05). IL-6 was significantly elevated in TSCI (p<0.05), while other markers of inflammation generally were elevated, but did not reach statistical significance (p>0.05). Systolic blood pressure and total cholesterol were significantly lower in TSCI (p<0.05), while fasting glucose was significantly lower in PSCI (p<0.05). A number of proinflammatory adipokines and cardiometabolic markers significantly correlated with adipose tissue depots by LOI (p<0.05).