Abstract
BACKGROUND: A spinal cord injury (SCI) from trauma or disease impairs sensorimotor pathways in somatic and autonomic divisions of the nervous system, affecting multiple body systems. Improved medical practices have increased survivability and life expectancy after SCI, allowing for the development of extensive metabolic comorbidities and profound changes in body composition that culminate in prevalent obesity. SUMMARY: Obesity is the most common cardiometabolic component risk in people living with SCI, with a diagnostic body mass index cutoff of 22 kg/m2 to account for a phenotype of high adiposity and low lean mass. The metameric organization of specific divisions of the nervous system results in level-dependent pathology, with resulting sympathetic decentralization altering physiological functions such as lipolysis, hepatic lipoprotein metabolism, dietary fat absorption, and neuroendocrine signaling. In this manner, SCI provides a unique opportunity to study in vivo the "neurogenic" components of certain pathologies that otherwise are not readily observable in other populations. We discuss the unique physiology of neurogenic obesity after SCI, including the altered functions mentioned above as well as structural changes such as reduced skeletal muscle and bone mass and increased lipid deposition in the adipose tissue, skeletal muscle, bone marrow, and liver. KEY MESSAGE: The study of neurogenic obesity after SCI gives us a unique neurological perspective on the physiology of obesity. The lessons learned from this field can guide future research and advancements to inform the study of obesity in persons with and without SCI.