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Role of aquaporin‐7 in the pathophysiological control of fat accumulation in mice
Author(s) -
Rodríguez Amaia,
Catalán Victoria,
Gómez-Ambrosi Javier,
Frühbeck Gema
Publication year - 2006
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2006.07.080
Subject(s) - aquaporin , glycerol , insulin resistance , adipocyte , endocrinology , glucose transporter , triglyceride , medicine , chemistry , carbohydrate metabolism , biology , obesity , microbiology and biotechnology , insulin , biochemistry , adipose tissue , cholesterol
Aquaporins are channels that allow the movement of water across the cell membrane. Some members of the aquaporin family, the aquaglyceroporins, also allow the transport of glycerol, which is involved in the biosynthesis of triglycerides and the maintenance of fasting glucose levels. Aquaporin‐7 (AQP7) is a glycerol channel mainly expressed in adipocytes. The deletion of AQP7 gene in mice leads to obesity and type 2 diabetes. AQP7 modulates adipocyte glycerol permeability thereby controlling triglyceride accumulation and fat cell size. Furthermore, the coordinated regulation of fat‐specific AQP7 and liver‐specific AQP9 may be key to determine glucose metabolism in insulin resistance.