Poster abstracts

Poster number 64 submitted by Anthony Alfredo

Spinal cord injury increases visceral adipose tissue inflammation and lipolysis

Anthony Alfredo (Neuroscience Graduate Program, The Ohio State University), Matthew Goodus (The Ohio State University), Kaitlin Carson (The Ohio State University), Jan Schwab (The Ohio State University), Richard Bruno (The Ohio State University), Dana McTigue (The Ohio State University)

Abstract:
Individuals with spinal cord injury (SCI) are disproportionately affected by metabolic syndrome (MetS), a collection of co-morbidities such as abdominal obesity. Our previous studies revealed SCI causes hyperlipidemia, insulin resistance, and “neurogenic” non-alcoholic steatohepatitis (nNASH), the hepatic manifestation of MetS. A possible driver of nNASH after SCI is the accumulation of visceral white adipose tissue (WAT). Excess WAT triggers macrophages to infiltrate and form crown-like structures (CLS) around dying adipocytes. CLS produce pro-inflammatory adipokines, stimulating adipocyte lipolysis via phosphorylation of hormone-sensitive lipase (pHSL). Currently, no experimental studies directly assess the relative changes in post-SCI adipose compared to obesity. Thus, we hypothesize that SCI increases inflammation and lipolysis in WAT and that this effect will be exacerbated by premorbid obesity. To test this, male rats were fed a high-fat diet causing diet-induced obesity (DIO) or low-fat (LF) diet for 8w prior to SCI and then given a moderate T8 contusion. Animals continued with their respective diets and were sacrificed at 56d post-injury (dpi). Epididymal (eWAT) and retroperitoneal (rWAT) adipose was collected. Histological analysis of eWAT and rWAT revealed LF+SCI, DIO, and DIO+SCI animals had comparably increased CLS formation versus LF controls. SCI animals had elevated pro-inflammatory adipokines TNF and IL-1b in eWAT versus LF controls. pHSL was significantly elevated in eWAT and rWAT of LF+SCI and DIO+SCI animals compared to LF and DIO controls. Thus, SCI causes visceral WAT inflammation and lipolysis independent of premorbid obesity. Identifying mechanisms driving post-SCI WAT dysregulation are therefore expected to improve cardiometabolic health following SCI.

Keywords: Spinal cord injury, Adipose tissue, Metabolic syndrome