Evaluation of the Cardiometabolic Disorders after Spinal Cord Injury in Mice

Evaluation of the Cardiometabolic Disorders after Spinal Cord Injury in Mice

Changes in cardiometabolic functions contribute to increased morbidity and mortality after chronic spinal cord injury. Despite many advancements in discovering SCI-induced pathologies, the cardiometabolic risks and divergences in severity-related responses have yet to be elucidated. Here, we examine...

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Bibliographic Details
Published in:Biology (Basel, Switzerland) Vol. 11; no. 4; p. 495
Main Authors: Ghnenis, Adel B, Jones, Calvin, Sefiani, Arthur, Douthitt, Ashley J, Reyna, Andrea J, Rutkowski, Joseph M, Geoffroy, Cédric G
Format: Journal Article
Language:English
Published: Switzerland MDPI AG 24-03-2022
MDPI
Subjects:
Body composition
Body fat
Body weight
cardiometabolic disease
Cardiovascular disease
Contusions
Diabetes
Fatty acids
Fibrosis
Glucose
Heart
Hydroxylase
Inflammation
Injuries
Innervation
Insulin resistance
Lipids
Liver
liver and cardiac dysfunctions
Metabolism
Morbidity
Nervous system
Population
Quality of life
Recovery of function
Spinal cord
Spinal cord injuries
spinal cord injury severity
Therapeutic targets
Thorax
Tyrosine 3-monooxygenase
Ventricle
Vertebrae
United States > US
spinal cord injury severity
fibrosis
cardiometabolic disease
liver and cardiac dysfunctions
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Summary:Changes in cardiometabolic functions contribute to increased morbidity and mortality after chronic spinal cord injury. Despite many advancements in discovering SCI-induced pathologies, the cardiometabolic risks and divergences in severity-related responses have yet to be elucidated. Here, we examined the effects of SCI severity on functional recovery and cardiometabolic functions following moderate (50 kdyn) and severe (75 kdyn) contusions in the thoracic-8 (T8) vertebrae in mice using imaging, morphometric, and molecular analyses. Both severities reduced hindlimbs motor functions, body weight (g), and total body fat (%) at all-time points up to 20 weeks post-injury (PI), while only severe SCI reduced the total body lean (%). Severe SCI increased liver echogenicity starting from 12 weeks PI, with an increase in liver fibrosis in both moderate and severe SCI. Severe SCI mice showed a significant reduction in left ventricular internal diameters and LV volume at 20 weeks PI, associated with increased LV ejection fraction as well as cardiac fibrosis. These cardiometabolic dysfunctions were accompanied by changes in the inflammation profile, varying with the severity of the injury, but not in the lipid profile nor cardiac or hepatic tyrosine hydroxylase innervation changes, suggesting that systemic inflammation may be involved in these SCI-induced health complications.
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ISSN:2079-7737
2079-7737
DOI:10.3390/biology11040495