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Functional role of aquaglyceroporin 7 expression in the pancreatic beta‐cell line BRIN‐BD11
Author(s) -
Delporte C.,
Virreira M.,
Crutzen R.,
Louchami K.,
Sener A.,
Malaisse W.J.,
Beauwens R.
Publication year - 2009
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.21872
Subject(s) - tonicity , glycerol , urea , isotonic , extracellular , chemistry , biochemistry , chromatography , medicine
Both mouse and rat pancreatic islet β‐cells were recently found to express aquaglyceroporin 7 (AQP7). In the present study, the expression and role of AQP7 in the function of BRIN‐BD11 cells were investigated. AQP7 mRNA and protein were detected by RT‐PCR and Western blot analysis, respectively. In an isoosmolar medium, the net uptake of [2‐ 3 H]glycerol displayed an exponential time course reaching an equilibrium plateau value close to its extracellular concentration. Within 2 min of incubation in a hypotonic medium (caused by a 50 mM decrease in NaCl concentration), the [2‐ 3 H]glycerol uptake averaged 143.2 ± 3.8% (n = 24; P  < 0.001) of its control value in isotonic medium, declining thereafter consistently with previously demonstrated volume regulatory decrease. When isoosmolarity was restored by the addition of 100 mM urea to the hypotonic medium, [2‐ 3 H]glycerol uptake remained higher (112.1 ± 2.8%, n = 24; P  < 0.001) than its matched control under isotonic conditions, indicating rapid entry of urea and water. Insulin release by BRIN‐BD11 cells was 3 times higher in hypotonic than in isotonic medium. When glycerol (100 mM) or urea (100 mM) were incorporated in the hypotonic medium, the insulin release remained significantly higher than that found in the control isotonic medium, averaging respectively 120.2 ± 4.2 and 107.0 ± 3.8% of the paired value recorded in the hypotonic medium. These findings document the rapid entry of glycerol and urea in BRIN‐BD11 cells, likely mediated by AQP7. J. Cell. Physiol. 221: 424–429, 2009. © 2009 Wiley‐Liss, Inc.

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