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doi: 10.1242/10.1242/jcs.00044
Research Article |
2-induced adipocytes derived from C/EBPß and C/EBP
-deficient mouse embryonic fibroblasts
1 Department of Molecular Medicine (C-4), Osaka University Graduate School of
Medicine, Suita, Osaka 565-0871, Japan
2 Department of Internal Medicine, Nishinomiya Municipal Central Hospital,
Nishinomiya, Hyogo 663-8014, Japan
* Author for correspondence (e-mail: kasayama{at}imed3.med.osaka-u.ac.jp)
Accepted 7 July 2002
In adipose tissue, the ability of cells to respond to insulin and to
express genes such as those encoding fatty-acid-binding protein (422/aP2),
lipoprotein lipase (LPL), adipsin and glucose transporter 4 (GLUT4) is
acquired during their differentiation into mature adipocytes. It has been
recognized that peroxisome proliferator-activated receptor 
(PPAR) and CCAAT/enhancer-binding proteins (C/EBPs) play critical roles
in adipocyte differentiation. However, it remained uncertain whether
PPAR or which C/EBP is involved in the acquisition of these
characteristics. We introduced PPAR2 into C/EBPß/
-double
deficient mouse embryonic fibroblasts (MEFs), followed by stimulation with its
ligands, in order to define the roles of C/EBPß and C/EBP in
phenotypic acquisition during adipocyte differentiation. This procedure
resulted in differentiation of these MEFs into mature adipocytes
morphologically similar to wild-type MEFs. However, the adipocytes derived
from the C/EBPß/-deficient MEFs showed lower expression of GLUT4
and adipsin mRNA than those derived from wild-type MEFs, although aP2 and LPL
mRNA levels were similar in both types. The C/EBPß/-deficient
adipocytes also expressed lower amounts of insulin receptor substrate 2
(IRS-2) than the adipocytes derived from wild-type MEFs, whereas the amounts
of insulin receptor and IRS-1 were similar. Finally, insulin-responsive
2-deoxyglucose uptake was lower in the C/EBPß/-deficient cells. It
could thus be demonstrated that C/EBPß and C/EBP are involved in
the acquisition of IRS-2 and GLUT4 expression as well as in insulin-sensitive
glucose uptake during adipocyte differentiation.
Key words: Insulin receptor substrate-2, Glucose transporter 4, Insulin receptor, CCAAT/enhancer-binding protein, Peroxisome proliferator-activated receptor
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