Gary J Farkas1, David R Gater1. 1. a Department of Physical Medicine and Rehabilitation , Penn State College of Medicine , Hershey, Pennsylvania , USA.
Abstract
CONTENT: Spinal Cord Injury (SCI) results in physiological changes that markedly reduces whole-body metabolism, resulting in neurogenic obesity via adipose tissue accumulation. Adipose tissue has been implicated in the release of proinflammatory adipokines that lead to chronic, systemic inflammation, and evidence suggests these adipokines contribute to the pathogeneses of metabolic diseases that often accompany obesity. In this review, we propose the concept of neurogenic obesity through paralysis-induced adiposity as the primary source of systemic inflammation and metabolic dysfunction reported in chronic SCI. We also briefly discuss how exercise in SCI can attenuate the negative consequences of obesity-induced inflammation and its comorbidities. METHODS: A MEDLINE, PubMed, Google Scholar, and ClinicalKey search was performed using the following search terms: obesity, adiposity, adipose tissue, proinflammatory adipokines, proinflammatory cytokines, metabolic dysfunction, exercise, physical activity, and spinal cord injury. All papers identified were full-text, English language papers. The reference list of identified papers was also searched for additional papers. RESULTS: Research suggests that obesity in SCI results in a state of chronic, systemic inflammation primarily through proinflammatory adipokines secreted from excess adipose tissue. The reduction of adipose tissue through the use of diet and exercise demonstrates promise to combat neurogenic obesity, inflammation, and cardiometabolic dysfunction in SCI. CONCLUSION: Proinflammatory adipokines may serve as biomarkers for the development of obesity-related complication in SCI. Mechanistic and interventional studies on neurogenic obesity-induced inflammation in chronic SCI are warranted.
CONTENT: Spinal Cord Injury (SCI) results in physiological changes that markedly reduces whole-body metabolism, resulting in neurogenic obesity via adipose tissue accumulation. Adipose tissue has been implicated in the release of proinflammatory adipokines that lead to chronic, systemic inflammation, and evidence suggests these adipokines contribute to the pathogeneses of metabolic diseases that often accompany obesity. In this review, we propose the concept of neurogenic obesity through paralysis-induced adiposity as the primary source of systemic inflammation and metabolic dysfunction reported in chronic SCI. We also briefly discuss how exercise in SCI can attenuate the negative consequences of obesity-induced inflammation and its comorbidities. METHODS: A MEDLINE, PubMed, Google Scholar, and ClinicalKey search was performed using the following search terms: obesity, adiposity, adipose tissue, proinflammatory adipokines, proinflammatory cytokines, metabolic dysfunction, exercise, physical activity, and spinal cord injury. All papers identified were full-text, English language papers. The reference list of identified papers was also searched for additional papers. RESULTS: Research suggests that obesity in SCI results in a state of chronic, systemic inflammation primarily through proinflammatory adipokines secreted from excess adipose tissue. The reduction of adipose tissue through the use of diet and exercise demonstrates promise to combat neurogenic obesity, inflammation, and cardiometabolic dysfunction in SCI. CONCLUSION: Proinflammatory adipokines may serve as biomarkers for the development of obesity-related complication in SCI. Mechanistic and interventional studies on neurogenic obesity-induced inflammation in chronic SCI are warranted.
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