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In vitro silencing of a putative phospholipid translocase results in an increase in glucose uptake in 3T3 L1 adipocytes
Author(s) -
Hurst Sarah Elizabeth,
Peretich Amanda,
Minkin Steven,
Dunlap John,
Biggerstaff John
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.505.2
Subject(s) - glut4 , glucose uptake , glucose transporter , gene silencing , translocase , biology , endocytic cycle , microbiology and biotechnology , adipocyte , glut1 , insulin resistance , medicine , endocrinology , insulin , gene , cell , biochemistry , endocytosis , adipose tissue , chromosomal translocation
Atp10c is a putative phospholipid translocase which encodes for a type IV P‐type ATPase. Atp10c gene, located on mouse chromosome 7, appears to be a strong candidate for diet‐induced obesity and diabetes mellitus type II. Our in vitro studies using a 3T3‐L1 murine adipocyte cell line revealed that when Atp10c expression was silenced or knocked down using siRNA, glucose uptake and fat accumulation increased, while insulin resistance decreased. Furthermore, the silencing effect of Atp10c caused an increase in Glut 1 and CEBP‐α gene expression and a decrease in Glut 4 and PPAR‐γ gene expression. To further investigate the role of Atp10c in insulin resistance and glucose uptake, immunolocalization of Atp10 c by fluorescence microscopy was employed. Data from these experiments suggest that Atp10c not only co‐localizes with caveolin‐1 and GLUT4 at the nuclear membrane, but also can be visualized as a punctate pattern in and around the nucleus. This finding suggests that Atp10c additionally may localize to the trans‐Golgi network or endosome, strengthening its biological role in protein trafficking in the exocytic and endocytic pathways.