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Compound C inhibition of adipocytes differentiation: The role of an increase in p21 in suppressing the clonal expansion of preadipocytes
Author(s) -
Lee Woo Hyung,
Nam Minwoo,
Kim Sang Geon
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.527.1
Subject(s) - ampk , cycloheximide , adipogenesis , 3t3 l1 , protein kinase a , chemistry , metformin , amp activated protein kinase , endocrinology , medicine , microbiology and biotechnology , kinase , adipocyte , adipose tissue , biology , protein biosynthesis , biochemistry , diabetes mellitus
AMP‐activated protein kinase (AMPK) activation inhibits adipocytes differentiation. This study investigated the effect of compound C (CC), a widely used AMPK inhibitor, on differentiation of 3T3‐L1 preadipocytes. CC treatment blocked hormone‐induced preadipocyte differentiation due to inhibition of mitotic clonal expansion, which was accompanied by the failure of degradation of p21, a cyclin‐dependent kinase inhibitor. CC increased the level of p21 protein, but not its mRNA, in preadipocytes incubated in a hormone‐free medium. Cycloheximide decreased the basal p21 level, which was inhibited by CC treatment, supporting the stabilization of p21 by CC. Treatment of AICAR or metformin, AMPK activators, failed to induce p21 or inhibit the ability of CC to increase p21 level. In conclusion, CC inhibits proliferation of preadipocytes as a consequence of an increase in p21 content, which might result from p21 stabilization, and the increase in p21 level by CC might not be associated with AMPK inhibition.