Resistin expression in adipose tissues and its effect on glucose metabolism in rats with brain injury

Abstract

Resistin (RSTN) expression in subcutaneous adipose tissue, and its effect on glucose metabolism in rats with traumatic brain injury, was investigated using real-time PCR, western blots, and enzyme linked immunoassays. Our results show that the expression of RSTN mRNA (3.192 ± 0.046, 4.016 ± 0.010, 6.004 ± 0.020, 8.213 ± 0.013, 11.199 ± 0.174, 15.094 ± 0.030), protein levels (1.79 ± 0.05, 1.98 ± 0.07, 2.75 ± 0.08, 3.19 ± 0.08, 4.25 ± 0.11, 4.48 ± 0.07), levels of serum insulin (512.96 ± 1.21, 580.57 ± 1.52, 769.71 ± 2.22, 826.08 ± 2.03, 1262.25 ± 3.40, 1512.80 ± 3.93), and fasting blood glucose levels (10.277 ± 0.040, 12.776 ± 0.038, 13.403 ± 0.263, 14.698 ± 0.100, 16.637 ± 0.110, 19.416 ± 0.025) were significantly higher in the traumatic rat group compared to the control group (P < 0. 05). Quantitative insulin sensitivity check index (QUICKI) was significantly lower in the traumatic group (-8.570 ± 0.005, -8.912 ± 0.004, -9.241 ± 0.022, -9.404 ± 0.007, -9.952 ± 0.007, -10.288 ± 0.002) than in the control group (-7.633 ± 0.003, -7.639 ± 0.004, -7.637 ± 0.006, -7.643 ± 0.003, -7.636 ± 0.006, -7.634 ± 0.004) (P < 0.05). Single factor linear correlation analysis showed that there was a significant negative correlation between RSTN expression and QUICKI (-0.983, P < 0.05) in the traumatic group. The increase in RSTN expression in the subcutaneous adipose tissue of rats with traumatic brain injury is likely related to the indexes of glycometabolism, including serum insulin, fasting blood glucose, and QUICKI. Our results lead us to conclude that RSTN may play an important role in the process of insulin resistance in rats with traumatic brain injury.