Spinal cord injury (SCI) disrupts autonomic regulation of visceral organs. As a result, a leading cause of mortality in the SCI population is metabolic dysfunction, and an organ central to metabolic control is the liver. Our recent work showed that rodent SCI promotes Kupffer cell (hepatic macrophage) activation, pro-inflammatory cytokine expression, and liver steatosis. These are symptoms of nonalcoholic steatohepatitis (NASH), the hepatic manifestation of metabolic syndrome, and these pre-clinical data replicate aspects of post-SCI human metabolic dysfunction. Because metabolic profile is highly dependent on lifestyle, including diet, it is likely that lifestyle choices prior to injury influence metabolic and hepatic outcomes after SCI. Therefore, in this study we tested if a diet rich in green tea extract (GTE), a known hepatoprotective agent, that began 3 weeks before SCI and was maintained after injury, reduced indices of liver pathology or metabolic dysfunction. GTE treatment significantly reduced post-SCI hepatic iron accumulation and blunted circulating glucose elevation compared with control-diet rats. However, GTE pre-treatment did not prevent Kupffer cell activation, hepatic lipid accumulation, increased serum alanine transaminase, or circulating non-esterified fatty acids, which were all significantly increased 6 weeks post-injury. Spinal cord pathology also was unchanged by GTE. Thus, dietary GTE prior to and after SCI had only a minor hepatoprotective effect. In general, for optimal health of SCI individuals, it will be important for future studies to evaluate how other lifestyle choices made before or after SCI positively or negatively impact systemic and intraspinal outcomes and the overall metabolic health of SCI individuals.
- fatty liver
- tumor necrosis factor