title: [Expression of insulin receptor substrate-2 and its tyrosine phosphorylation in the hepatic tissue of chronic hepatitis B patients].
abstract: OBJECTIVE
  To observe the expression of insulin receptor substrate-2 (IRS-2) mRNA and protein, and its tyrosine phosphorylation in hepatic tissue of chronic hepatitis B (CHB) patients, and to explore the role of IRS-2 on insulin resistance in CHB patients.
  
  
  METHODS
  Eighteen patients with CHB were included, and 6 individuals with normal liver function were enrolled as control. Based on the insulin resistance index determined by homeostasis model assessment (HOMA), CHB patients were further divided into CHB without insulin resistance group (<2.69, n=10) and CHB with insulin resistance group (>2.69, n=8). Hepatic tissues were harvested from all patients during operation or with liver biopsy. The mRNA expression of IRS-2 in liver tissue was assessed by reverse transcription-polymerase chain reaction (RT-PCR), and the protein expression of IRS-2 was detected by Western blotting. Immunoprecipitation and enhanced chemiluminescent technique were used to measure the tyrosine phosphorylation of IRS-2.
  
  
  RESULTS
  In CHB without insulin resistance group, the mRNA expression (0.38+/-0.06), the protein expression (0.94+/-0.18) and the tyrosine phosphorylation (0.78+/-0.09) of IRS-2 in hepatic tissue were decreased, but without statistically significant difference (all P>0.05), as compared to those in control group (0.45+/-0.11, 0.99+/-0.20, 1.00+/-0.23, respectively). In CHB with insulin resistance group, the mRNA expression (0.26+/-0.08), the protein expression (0.67+/-0.11) and the tyrosine phosphorylation (0.63+/-0.14) of IRS-2 in hepatic tissue were significantly decreased compared with those of the control group with statistically significant difference (P<0.05 or P<0.01).
  
  
  CONCLUSIONS
  The decreased expression of mRNA and protein and the reduced tyrosine phosphorylation of IRS-2 in CHB patients with insulin resistance inducing impairment of the insulin signal pathway may be one of the mechanisms underlying insulin resistance.
authors.affiliation: Department of Infectious Diseases, the First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
authors.forename: Qi-Rong
authors.initials: QR
authors.lastname: Zhu
authors.forename: Bo
authors.initials: B
authors.lastname: Qin
authors.forename: Tao
authors.initials: T
authors.lastname: Huang
authors.forename: Han-Qu
authors.initials: HQ
authors.lastname: Liu
mesh_terms: D016022:Case-Control Studies; D005260:Female; D019694:Hepatitis B, Chronic / Q000378:metabolism*; D006801:Humans; D055504:Insulin Receptor Substrate Proteins / Q000378:metabolism*; D007333:Insulin Resistance; D008099:Liver / Q000378:metabolism; D008297:Male; D010766:Phosphorylation; D014443:Tyrosine / Q000378:metabolism*
chemical_list: C526297:IRS2 protein, human; D055504:Insulin Receptor Substrate Proteins; D014443:Tyrosine