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Regulation of Atp10c mRNA expression in mouse 3T3‐L1 adipocytes
Author(s) -
Peretich Amanda Lynn,
Pineda A' Drian,
Neilsen Nancy,
Graham Todd,
Dhar Madhu
Publication year - 2007
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.21.5.a294-c
Subject(s) - endocrinology , medicine , adipogenesis , adipocyte , biology , 3t3 l1 , adipose tissue , insulin , gene expression , insulin resistance , gene , genetics
Atp10c is a putative phospholipid translocase on mouse chromosome 7 that encodes a type IV P‐type ATPase. Heterozygous mice inheriting a maternal deletion of the Atp10c gene represent a novel genetic model of diet‐induced obesity and type 2 diabetes. High fat diet studies have shown that the mutants are hyperinsulinemic, insulin‐resistant and have an altered insulin‐stimulated response in the peripheral tissues. Adipose tissue is the primary target associated with Atp10c deletion. In view of a potential role for Atp10c in control of adiposity, we determined whether hormonal and nutritional factors known to regulate adipocyte metabolism also affected Atp10c expression in mouse adipocytes. In this study, we have used the 3T3‐L1 murine adipocyte cell line as an “ in vitro ” model with resistin and pref 1 serving as key markers for adipogenesis. Relative to a β‐ actin internal control, Atp10c mRNA was highly expressed in the preadipocytes and was downregulated about 3 fold during differentiation in adipocytes. Furthermore, we found that 100nM insulin and 100nM isoproterenol both decreased Atp10c mRNA levels whereas 100nM dexamethasone increased Atp10c mRNA levels in 3T3‐L1 adipocytes. These data suggest that Atp10c gene expression is regulated in adipocytes by insulin, glucocorticoids and a β‐adrenergic receptor agonist.