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

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.

H558R polymorphism in SCN5A is associated with Keshan disease and QRS prolongation in Keshan disease patients.

Keshan disease (KSD), a potentially fatal cardiomyopathy, has very high incidence in some selenium-poor regions of China. KSD may be accompanied with a variety of arrhythmia, which is associated with mutations in the gene coding for cardiac voltage-gated sodium channel (SCN5A). The molecular mechanism of KSD is still largely obscure. We aimed to determine the association between the H558R polymorphism of SCN5A and KSD. We recruited 71 patients with KSD and 80 geographical region-matched control subjects in our study. Vital sign and electrocardiographic (ECG) measurements were performed for heart rate, systolic pressure, diastolic pressure, PR interval, QT interval, QRS duration, ST-T changes and complete right bundle branch block (CRBBB), and H558R polymorphism was genotyped using the polymerase chain reaction single-strand conformation polymorphism (PCR-SSCP) method and sequencing. A significant association was found between the H558R polymorphism of exon 12 and KSD. Allele C carriers had a decreased risk for KSD with an odds ratio of 0.332 [95% confidence interval (CI), 0.160-0.692] as well as for QRS prolongation in KSD patients with an odds ratio of 0.089 (95%CI, 0.022-0.361). Our results provide support to the association between H558R polymorphism and the decreased risk for KSD. H558R polymorphism might increase susceptibility to KSD, and SCN5A containing the polymorphism might be a predisposing gene for QRS prolongation.