title: [Influence of GLP-1 on oxidative stress injury in non-alcoholic fatty liver disease rats].
abstract: OBJECTIVE
  To investigate the effects of glucagon-like peptide-1 (GLP-1) on liver oxidative stress injury using a rat model of non-alcoholic fatty liver disease.
  
  
  METHODS
  Sixty male Sprague-Dawley rats were fed 12 weeks of either a diet of normal chow (NC), for use as controls (n =15) or high-fat chow (HF), for use as models (n =45).The NC rats were administered normal saline, while the HF rats were treated with either normal saline (NS), for use as untreated model controls (n =10), low-dose GLP-1 (LG, 50 mutg/kg; n =10), mid-dose GLP-1 (MG, 100 mutg/kg; n =10), or high-dose GLP-1 (HG, 200 mug/kg; n =10); all treatments lasted for 4 weeks.The rats' weight, levels of serum biochemical markers (triglycerides, total cholesterol, high-density lipoproteincholesterol, low-density lipoprotein-cholesterol, alanine arninotransferase, and aspartate aminotransferase), levels of superoxide dismutase (SOD) and malondialdehyde (MDA), and expression of CYP2E1 mRNA and protein in liver homogenates were measured.The F test, t-test, least significant difference test and Dunnett's T3 test were used for statistical analyses.
  
  
  RESULTS
  Compared with the NC group, the rars in the NS group showed significantly lower SOD (165.81 ± 11.64 vs.192.89 ± 16.53 U/mg, P < 0.05), significantly higher MDA (7.30 ± 1.79 vs.3.10 ± 1.30 nmol/ mg, P < 0.05), and significantly higher expressions of CYP2E1 mRNA and protein (both P < 0.05).After GLP1 treatment, the rats in the LG, MG and HG groups showed increased levels of SOD (compared to the NS group; 171.44 ± 9.80 vs.177.66 ± 14.77 vs.186.17 ± 15.43 U/mg; only the HG group had P < 0.05), significantly decreased levels of MDA (compared to the NS group; 5.16 ± 1.45 vs.4.08 ± 1.22 vs.3.31 ± 1.14 nmol/mg; all P < 0.05], and decreased levels of CYP2E1 mRNA and protein expressions (CYP2E1 mRNA:only the HG group had P < 0.05; CYP2E1 protein: both the MG and HG groups had P < 0.05).
  
  
  CONCLUSIONS
  GLP-1 treatment can improve oxidative stress injury, suggesting its potential as a therapeutic agent for non-alcoholic fatty liver disease.
authors.affiliation: Department of Endocrinology and Metabolism, the First Affiliated Hospital, China Medical University, Shenyang 110001, China.
authors.forename: Xiaochen
authors.initials: X
authors.lastname: Wang
authors.forename: Na
authors.initials: N
authors.lastname: Ao
authors.forename: Jian
authors.initials: J
authors.lastname: Du
authors.forename: Jing
authors.initials: J
authors.lastname: Yang
authors.forename: Jiayu
authors.initials: J
authors.lastname: Xu
mesh_terms: D000818:Animals; D001219:Aspartate Aminotransferases; D019392:Cytochrome P-450 CYP2E1; D052216:Glucagon-Like Peptide 1 / Q000378:metabolism*; D008297:Male; D008315:Malondialdehyde; D065626:Non-alcoholic Fatty Liver Disease / Q000378:metabolism*; D018384:Oxidative Stress; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase; D014280:Triglycerides
chemical_list: D014280:Triglycerides; D008315:Malondialdehyde; D052216:Glucagon-Like Peptide 1; D019392:Cytochrome P-450 CYP2E1; D013482:Superoxide Dismutase; D001219:Aspartate Aminotransferases