Poster abstracts
Poster number 76 submitted by Anthony Alfredo
Spinal cord injury causes visceral adipose tissue inflammation and lipolysis
Anthony N. Alfredo (Neuroscience Graduate Program, The Ohio State University), Matthew T. Goodus (Department of Neuroscience, The Ohio State Universtiy), Kaitlin E. Carson (Department of Neuroscience, The Ohio State University), Richard S. Bruno (Department of Human Sciences, The Ohio State University), Dana M. McTigue (Department of Neuroscience, The Ohio State University)
Abstract:
Spinal cord injury (SCI) is a significant neurological impairment with over 18,000 new cases each year. While SCI research typically focuses on restoring mobility, few studies investigate systemic issues affecting physiological homeostasis. Individuals living with SCI are disproportionately affected by metabolic syndrome (MetS), a collection of co-morbidities including abdominal obesity and insulin resistance which increase the risk of cardiovascular disease. Previous work from our lab revealed SCI causes a novel form of “neurogenic” non-alcoholic steatohepatitis (nNASH), the hepatic manifestation of MetS. A possible driver of nNASH and MetS after SCI is the accumulation of visceral white adipose tissue (WAT). Increased WAT causes infiltration of immune cells such as macrophages, which form crown-like structures (CLS) around dying adipocytes and promote further inflammation. CLS also produce pro-inflammatory adipokines that stimulate adipocyte lipolysis via activation of hormone sensitive lipase (pHSL) by phosphorylation. Currently, no experimental studies directly assess adipose tissue pathology after SCI. Thus, we hypothesize that SCI increases adipose tissue inflammation and lipolysis in visceral WAT. To gauge the severity of adipose changes, SCI rats were compared to rats fed a high fat diet. Rats were pre-fed a high fat chow causing diet-induced obesity (DIO) or a control diet for 8w prior to injury and then given a moderate T8 contusion SCI. Animals were sacrificed at 56d post-injury (dpi) by intracardiac perfusion. Epididymal (eWAT) and retroperitoneal (rWAT) adipose tissues were collected. In support of our hypothesis, adipose histology revealed SCI and DIO+SCI animals had significantly increased CLS formation in eWAT and rWAT. In addition, pHSL was significantly elevated in eWAT and rWAT of SCI and DIO+SCI animals compared to lean and DIO naïve controls. Notably, the levels in SCI were comparable to those in the obese rats, revealing that SCI causes adipose pathology to the same extent as the “gold standard” of diet-induced obesity. Future studies will investigate mechanisms driving post-SCI WAT dysregulation in order to reduce cardiometabolic disease and improve overall health.
Keywords: Spinal Cord Injury, Inflammation, Metabolic Syndrome