title: Puerarin improve insulin resistance of adipocyte through activating Cb1 binding protein path.
abstract: OBJECTIVE
  To explore the molecular mechanism of puerarin (Pue) in improving insulin resistance through observing its effect on the insulin resistance of 3T3-Li lipocyte induced by free fatty acid (FFA).
  
  
  METHODS
  3T3-L1 preadipocyte was induced by a culture solution containing insulin, isobutyo-menthyl-xanthine, and dexamethasone to mature lipocyte, and it was divided into six groups: the control group (normal cells), the model group (untreated model cells), and the four drug treatment group exposed to dimethyl biguanide (Met group), highdose puerarin (PueH group), low-dose puerarin (PueL group), and propylene glycol (PG group), respectively. Mature lipocytes in various groups, except those in the normal group, were established into insulin resistance model by FFA induction and treated respectively with corresponding drugs. Peroxisome proliferator-activated receptor-γ (PPAR-γ) mRNA expressions at the fourth, sixth, and eighth day were observed using reverse transcription polymerase chain reaction (RT-PCR); glucose transportation in various groups were observed by 2-deoxy-[(3)H]-D-glucose intake method; mRNA expression of Cb1 binding protein (CAP) was determined by RT-PCR; and glucose transporter-4 (Glut-4) transposition was detected by immune-fluorescence method.
  
  
  RESULTS
  PPAR-γmRNA expression increased gradually, and it showed lower levels at the fourth, sixth, and eighth day in all treatment groups than that in the model group. Glucose transportation determination showed that the transportation in the model group was 2.23±0.63, significantly lower than that in the normal group 5.05 ± 0.66 (P<0.01); as compared with the model group, they were significantly higher in the PueH and the PueL groups. In addition, the CAP mRNA expression and membranous distribution of Glut-4 were higher in the two Pue treated groups than those in the model group, respectively.
  
  
  CONCLUSIONS
  Pue could markedly improve the insulin resistance of 3T3-L1 lipocyte, which is realized possibly by way of inactivating CAP path, promoting Glut-4 transposition to cell membrane to increase the transportation of glucose.
authors.affiliation: Pharmaceutical College of Harbin Commercial University, Harbin, China. zhaoy219@163.com
authors.forename: Ying
authors.initials: Y
authors.lastname: Zhao
authors.forename: You
authors.initials: Y
authors.lastname: Zhou
mesh_terms: D041721:3T3-L1 Cells; D017667:Adipocytes / Q000187:drug effects* / Q000378:metabolism*; D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D002352:Carrier Proteins / Q000378:metabolism*; D005786:Gene Expression Regulation / Q000187:drug effects; D005947:Glucose / Q000378:metabolism; D051275:Glucose Transporter Type 4 / Q000378:metabolism; D007333:Insulin Resistance; D007529:Isoflavones / Q000494:pharmacology*; D051379:Mice; D047495:PPAR gamma / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*
chemical_list: D002352:Carrier Proteins; D051275:Glucose Transporter Type 4; D007529:Isoflavones; D047495:PPAR gamma; D012333:RNA, Messenger; C495693:Slc2a4 protein, mouse; D005947:Glucose; C033607:puerarin