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J. Biol. Chem., Vol. 277, Issue 37, 34322-34328, September 13, 2002
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From the Resistance to the stimulatory effects of insulin
on glucose utilization is a key feature of type 2 diabetes, obesity,
and the metabolic syndrome. Recent studies suggest that insulin
resistance is primarily caused by a defect in glucose transport. GLUT4
is the main insulin-responsive glucose transporter and is expressed predominantly in muscle and adipose tissues. Whereas GLUT4 has been
shown to play a critical role in maintaining systemic glucose homeostasis, the mechanisms regulating its expression are incompletely understood. We have cloned the murine homologue of KLF15, a member of
the Krüppel-like family of transcription factors. KLF15 is highly
expressed in adipocytes and myocytes in vivo and is induced when 3T3-L1 preadipocytes are differentiated into adipocytes. Overexpression of KLF15 in adipose and muscle cell lines potently induces GLUT4 expression. This effect is specific to KLF15 as overexpression of two other Krüppel-like factors,
KLF2/LKLF and KLF4/GKLF, did not induce GLUT4 expression. Both basal
(3.3-fold, p < 0.001) and insulin-stimulated
(2.4-fold, p < 0.00001) glucose uptake are increased
in KLF15-overexpressing adipocytes. In co-transfection assays, KLF15
and MEF2A, a known activator of GLUT4, synergistically activates the
GLUT4 promoter. Promoter deletion and mutational analyses provide
evidence that this activity requires an intact KLF15-binding site
proximal to the MEF2A site. Finally, co-immunoprecipitation assays show
that KLF15 specifically interacts with MEF2A. These studies indicate
that KLF15 is an important regulator of GLUT4 in both adipose and
muscle tissues.
Cardiovascular Division, Brigham and
Women's Hospital, Boston, Massachusetts 02115 and the
§ Pritzker School of Medicine, The University of Chicago,
Chicago, Illinois 60637
The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EBI Data Bank with accession number(s) F317225.
¶ To whom correspondence should be addressed: Cardiovascular Division, Brigham and Women's Hospital, Thorn Bldg., Rm. 1123, 20 Shattuck St., Boston, MA 02115. Tel.: 617-278-0142; Fax: 617-732-5132; E-mail: mjain@rics.bwh.harvard.edu.This article has been cited by other articles:
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