Influence of spinal cord injury in hypothalamus AMP-activated protein kinase expression and glucose level

Objective To observe the influence of spinal cord injury (SCI) in hypothalamus AMP-activated protein kinase (AMPK) expression, and explore the mechanism of SCI-induced type 2 diabetes or insulin resistance. Methods Eighteen SD rats were randomly divided into model group, High Fat/High Sucrose/High Cholesterol Diet group and SCI group (n=6). The animals in the model group and High Fat/High Sucrose/High Cholesterol Diet group underwent a T10 laminectomy without weight-drop injury, and SCI models were induced by MASCIS Impactor method. Blood glucose and glucose tolerance tests were performed before experiment and 8 weeks after the experiment. At 8 weeks, the levels of serum inflammatory factors, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6, were observed by ELISA; Western blotting was used to detect the expression of phosphorylated (p)-AMPK in the hypothalamus. Results Blood glucose levels in the rats of High Fat/High Sucrose/High Cholesterol Diet group and SCI group were significantly higher than that in the model group (P<0.05). Blood glucose levels 15 and 60 min after SCI in rats of SCI group were significantly higher than those in the model group (P<0.05); Blood glucose levels 15, 30, 60 and 120 min after SCI in rats of High Fat/High Sucrose/High Cholesterol Diet group were significantly higher than those in the model group (P<0.05). As compared with those in the model group, the expression of p-AMPK in the hypothalamus were significantly decreased, and the TNF-α, IL-1β and IL-6 levels were statistically increased in rats of High Fat/High Sucrose/High Cholesterol Diet group and SCI group (P<0.05). Conclusion SCI could inhibit AMPK expression in the hypothalamus, activate inflammatory signaling pathway and enhance chronic systemic inflammation, and therefore, insulin resistance is induced. Key words: Spinal cord injury; Hypothalamus; AMP-activated protein kinase; Insulin resistance