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Publication : Over-expression of AQP7 contributes to improve insulin resistance in adipocytes.

First Author  Shen FX Year  2012
Journal  Exp Cell Res Volume  318
Issue  18 Pages  2377-84
PubMed ID  22877989 Mgi Jnum  J:187152
Mgi Id  MGI:5435613 Doi  10.1016/j.yexcr.2012.07.016
Citation  Shen FX, et al. (2012) Over-expression of AQP7 contributes to improve insulin resistance in adipocytes. Exp Cell Res 318(18):2377-84
abstractText  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-alpha. 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.
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