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

• Published in: Experimental cell research Vol. 318; no. 18; pp. 2377 - 2384
• Main Authors: Shen, Fei-Xia, Gu, Xuemei, Pan, Wei, Li, Wei-Ping, Li, Wei, Ye, Jing, Yang, Li-Juan, Gu, Xue-Jiang, Ni, Lian-Song
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.11.2012; Elsevier BV
• Subjects: 3-Phosphoinositide-Dependent Protein Kinases; 3T3-L1 adipocytes; 3T3-L1 Cells; Adipocytes - cytology; Adipocytes - metabolism; Animals; Aquaglyceroporin 7 (AQP7); Aquaporins - genetics; Aquaporins - metabolism; Cell Differentiation; Cellular biology; Dexamethasone - pharmacology; Down-Regulation; Gene expression; Insulin resistance; Insulin Resistance - genetics; Mice; Phosphorylation; PKB; Protein-Serine-Threonine Kinases - genetics; Protein-Serine-Threonine Kinases - metabolism; Proteins; RNA, Messenger - metabolism; Tumor Necrosis Factor-alpha - metabolism; Insulin resistance; 3T3-L1 adipocytes; PKB; Aquaglyceroporin 7 (AQP7)
• ISSN: 0014-4827; 1090-2422
• DOI: 10.1016/j.yexcr.2012.07.016

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. ► The level of AQP7 and p-PKB were gradually up-regulated during differentiation. ► Dexamethasone down-regulated the expression level of AQP7. ► Overexpression of AQP7 by transfecting Ad-AQP7 could attenuate glycerol secretion. ► Overexpression of AQP7 by transfecting Ad-AQP7 could restore PKB phosphorylation.