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The guanine nucleotide exchange factor FLJ00068 activates Rac1 in adipocyte insulin signaling
Author(s) -
Takenaka Nobuyuki,
Nakao Mika,
Hasegawa Kiko,
Chan Man Piu,
Satoh Takaya
Publication year - 2020
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 - 10.1002/1873-3468.13939
Subject(s) - glut4 , guanine nucleotide exchange factor , rac1 , glucose transporter , insulin receptor , glucose uptake , insulin , adipocyte , chemistry , microbiology and biotechnology , medicine , biology , gtpase , signal transduction , endocrinology , biochemistry , insulin resistance , adipose tissue
Insulin stimulates glucose uptake via the translocation of the glucose transporter GLUT4 to the plasma membrane in adipocytes. Several lines of evidence suggest that the small GTPase Rac1 plays an important role in insulin‐stimulated glucose uptake in skeletal muscle and adipocytes. The purpose of this study is to investigate the mechanisms whereby Rac1 is regulated in adipocyte insulin signaling. Here, we show that knockdown of the guanine nucleotide exchange factor FLJ00068 inhibits Rac1 activation and GLUT4 translocation by insulin and a constitutively activated form of the protein kinase Akt2. Furthermore, constitutively activated FLJ00068 induced Rac1 activation and Rac1‐dependent GLUT4 translocation. Collectively, these results suggest the involvement of FLJ00068 downstream of Akt2 in insulin‐stimulated glucose uptake signaling in adipocytes.