title: Over-expression of AQP7 contributes to improve insulin resistance in adipocytes.
abstract: OBJECTIVE
  Aquaglyceroporin 7 (AQP7) is required for efflux of glycerol from adipocytes. In this study, we aimed to analyze expression profiles of AQP7 in the different differentiation phases of adipocytes and to investigate the role of AQP7 in the insulin resistance of adipocytes.
  
  
  METHODS
  3T3-L1 pre-adipocyte cells were induced to be fully differentiated adipocytes and then insulin resistance was induced by Dexamethasone (DXM) or TNF-α. Adenovirus vector with over-expression AQP7 (Ad-AQP7) was constructed and transfected into adipocytes. The expression level of AQP7 and phosphorylated PKB (p-PKB) were measured. The glycerol released from adipocytes and glucose consuming rate were tested too.
  
  
  RESULTS
  AQP7 expression was gradually up-regulated along with the differentiation processing of 3T3-L1 preadipocytes, which was consistent with the expression level of p-PKB. Dexamethasone down-regulated the expression of AQP7, p-PKB and the glycerol content in adipocytes. Over-expression of AQP7 by transfecting Ad-AQP7 to insulin resistant adipocytes restored the phosphorylation of PKB and attenuated the glycerol secretion and glucose consuming rate of adipocytes.
  
  
  CONCLUSIONS
  AQP7 is down-regulated in adipocytes with insulin resistance. The over-expression of AQP7 contributes to improve insulin resistance in adipocytes, which is potentially correlated with the increased phosphorylation of PKB.
authors.affiliation: Department of Endocrinology and Metabolism, The First Affiliated Hospital of Wenzhou Medical College, Wenzhou, PR China. sfx301@163.com
authors.forename: Fei-Xia
authors.initials: FX
authors.lastname: Shen
authors.forename: Xuemei
authors.initials: X
authors.lastname: Gu
authors.forename: Wei
authors.initials: W
authors.lastname: Pan
authors.forename: Wei-Ping
authors.initials: WP
authors.lastname: Li
authors.forename: Wei
authors.initials: W
authors.lastname: Li
authors.forename: Jing
authors.initials: J
authors.lastname: Ye
authors.forename: Li-Juan
authors.initials: LJ
authors.lastname: Yang
authors.forename: Xue-Jiang
authors.initials: XJ
authors.lastname: Gu
authors.forename: Lian-Song
authors.initials: LS
authors.lastname: Ni
mesh_terms: D064413:3-Phosphoinositide-Dependent Protein Kinases; D041721:3T3-L1 Cells; D017667:Adipocytes / Q000166:cytology* / Q000378:metabolism; D000818:Animals; D020346:Aquaporins / Q000235:genetics* / Q000378:metabolism; D002454:Cell Differentiation; D003907:Dexamethasone / Q000494:pharmacology; D015536:Down-Regulation; D007333:Insulin Resistance / Q000235:genetics*; D051379:Mice; D010766:Phosphorylation; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: C491927:Aqp7 protein, mouse; D020346:Aquaporins; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D003907:Dexamethasone; D064413:3-Phosphoinositide-Dependent Protein Kinases; D017346:Protein Serine-Threonine Kinases