Abstract
Within the spinal cord injured (SCI) population, metabolic dysfunction may be exacerbated. Models of cord injury coupled with metabolic stressors have translational relevance to understand disease progression in this population. In the present study, we used a rat model of thoracic SCI at level T10 (tSCI) and administered diets comprised of either 9% or 40% butterfat to create a unique model system to understand the physiology of weight regulation following cord injury. SCI rats that recovered on chow for 28 days had reduced body mass, lean mass, and reduced fat mass but no differences in percentage of lean or fat mass composition. Following 12 weeks on either low‐fat diet (LFD) or high‐fat diet (HFD), SCI rats maintained on LFD did not gain weight at the same rate as SCI animals maintained on HFD. LFD‐SCI had reduced feed conversion efficiency in comparison to Sham‐LFD whereas tSCI‐HFD were equivalent to Sham‐HFD rats. Although SCI rats still maintained lower lean body mass, by the end of the study HFD‐fed rats had higher body fat percentage than LFD‐fed rats. Macronutrient selection testing demonstrated SCI rats had a significant preference for protein over Sham rats. Analysis of metabolic cage activity showed tSCI rats had elevated energy expenditure, despite reduced locomotor activity. Muscle triglycerides and cholesterol were reduced only in LFD‐tSCI rats. These data suggest that consumption of HFD by tSCI rats alters the trajectory of metabolic dysfunction in the context of spinal cord disease progression.
Highlights
Innovations to specialized healthcare have greatly improved the longevity of persons with injury to the spinal cord (Strauss et al 2006)
Following 12 weeks on either low-fat diet (LFD) or high-fat diet (HFD), spinal cord injured (SCI) rats maintained on LFD did not gain weight at the same rate as SCI animals maintained on HFD
Muscle triglycerides and cholesterol were reduced only in LFD-thoracic spinal cord injury (tSCI) rats. These data suggest that consumption of HFD by tSCI rats alters the trajectory of metabolic dysfunction in the context of spinal cord disease progression
Summary
Innovations to specialized healthcare have greatly improved the longevity of persons with injury to the spinal cord (Strauss et al 2006). As the average age of this injured subpopulation continues to rise, the potential for the various comorbidities of Metabolic Syndrome (MetS) increases (Maruyama et al 2008). Persons with SCI are at increased risk for dyslipidemia, cardiovascular disease, and glycemic dysregulation, all contributing factors to MetS (Akkurt et al 2017; Alves et al 2017; Berg-Emons et al 2008). Understanding how and why MetS develops in this vulnerable population is important for improving quality of life for these individuals. The rate of obesity among subpopulations of SCI individuals varies from 25 to 57% (Gater 2007; Gorgey et al 2014; Gater et al 2019) which is somewhat higher than the national range 22–35% (Ogden et al 2013). Hormones, and inflammatory factors may add to this disparity, but no specific factors have been identified to-date that support the elevated risk for MetS
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