title: [Role of S6K1 in the induction of SREBP1c in mouse hepatic cell by high glucose stimulation].
abstract: OBJECTIVE
  To study the role of S6K1 in the induction of SREBP1c in mouse hepatic cell by high glucose stimulation.
  
  
  METHODS
  S6K1 shRNA recombinant adenovirus (S6K1Ax) was injected into tail vein of db/db mice and then hepatic triglycerol content was analyzed. Liver specimen were stained with HE. After transfection with S6K1Ax or pU6Ax, mouse hepatic AML12 cells were treated with high glucose, insulin or glucose and insulin, the expression of mSREBP1c was detected by RT-PCR. S6K1 protein was detected by Western blot.
  
  
  RESULTS
  Hepatic S6K1 protein in db/db mice was inhibited a week after S6K1Ax injection. Compared with the control group, hepatic triglycerol content of S6K1Ax group was decreased (0.65+/-0.02) mmol/L vs (0.56+/-0.01) mmol/L (t = 4.312, P less than 0.01), hepatocyte fat droplet and vaculor generation were also decreased, fatty liver was improved. The mSREBP1c expression in S6K1Ax transfected cells was lower than that in the control cells (0.03+/-0.01 vs 0.06+/-0.01, t = 5.624, P less than 0.01). Compared with the basal state, SREBP1c expression of both groups was increased on the insulin stimulation, S6K1Ax group was 0.06+/-0.02 (t = 8.452, P less than 0.01) and control group was 0.08+/-0.02 (t = 3.591, P less than 0.05). There is no difference between control and S6K1Ax group by glucose addition (P more than 0.05).
  
  
  CONCLUSIONS
  S6K1 acts on fatty synthesis by regulating mSREBP1c expression.
authors.affiliation: Department of Dialysis, Tianjin Medical University Metabolic Diseases Hospital, Tianjin 300070, China.
authors.forename: Shu-Ying
authors.initials: SY
authors.lastname: Li
authors.forename: Rui
authors.initials: R
authors.lastname: Chen
authors.forename: Jing
authors.initials: J
authors.lastname: Li
authors.forename: Bao-Li
authors.initials: BL
authors.lastname: Wang
authors.forename: De-Min
authors.initials: DM
authors.lastname: Yu
mesh_terms: D000256:Adenoviridae / Q000235:genetics*; D000818:Animals; D002460:Cell Line; D064429:Fatty Acid Synthases / Q000235:genetics / Q000378:metabolism*; D005786:Gene Expression Regulation; D005947:Glucose / Q000008:administration & dosage; D007328:Insulin / Q000008:administration & dosage; D008099:Liver / Q000378:metabolism / Q000473:pathology; D008103:Liver Cirrhosis / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D051379:Mice; D008815:Mice, Inbred Strains; D034622:RNA Interference; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D038744:Ribosomal Protein S6 Kinases, 90-kDa / Q000235:genetics* / Q000378:metabolism; D013194:Staining and Labeling; D051780:Sterol Regulatory Element Binding Protein 1 / Q000235:genetics / Q000378:metabolism*; D014162:Transfection; D014280:Triglycerides / Q000378:metabolism
chemical_list: D007328:Insulin; D012333:RNA, Messenger; C497388:Srebf1 protein, mouse; D051780:Sterol Regulatory Element Binding Protein 1; D014280:Triglycerides; D064429:Fatty Acid Synthases; D038744:Ribosomal Protein S6 Kinases, 90-kDa; C512964:Rps6ka1 protein, mouse; D005947:Glucose