Metabolic impairment and steatohepatitis develops after T8 contusion spinal cord injury (SCI) in non-obese male rats measured by increased insulin resistance, hyperlipidemia, endotoxemia, lipid deposition and liver inflammation, and is exacerbated by pre-morbid obesity

STUDY PURPOSE: This study is based on previous work from the McTigue lab showing spinal cord injury (SCI) causes neurogenic non-alcoholic steatohepatitis (NASH), the manifestation of metabolic syndrome (MetS) in the liver, in the absence of obesity. The purpose of this study was to compare a diet-induced obesity (DIO) model of NASH to SCI-induced NASH and determine if DIO at the time of SCI exacerbated NASH and MetS. DATA COLLECTED: 36 adult male Sprague-Dawley rats were assigned to receive one of the following nutritionally-complete purified diets: a high fat diet consisting of 60% kcal from fat causing DIO or a control low-fat diet consisting of 10% kcal from fat. Diets were maintained for 8 weeks prior to injury. Rats were then randomly assigned to the following groups: uninjured Naïve, uninjured DIO, SCI (control diet), and DIO+SCI. SCI rats received at 200 kD midline contusion injury at T8. All animals survived for an additional 8 weeks on their respective diets. Locomotor function was assessed by BBB at 1, 3, 7, 10, and 14 days post-injury (dpi) and weekly thereafter. Rats were sacrificed at 56 dpi and assessed for differences in liver and spinal cord histology as well as liver pro-inflammatory gene expression. Serum was collected weekly prior to injury and following SCI to determine changes in glucose, insulin, free fatty acids, and endotoxin. DATA USAGE NOTES: