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Papers In Press, published online ahead of print July 3, 2002
Cardiovascular, Brigham and Women's Hospital, Boston, MA 02115
Corresponding Author: mjain{at}rics.bwh.harvard.edu
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. While 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 Kruppel-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 Kruppel-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 activate 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.
J. Biol. Chem, 10.1074/jbc.M201304200
Submitted on February 7, 2002
Revised on July 3, 2002
Accepted on July 3, 2002
The Kruppel-like factor KLF15 regulates the insulin-sensitive glucose transporter GLUT4
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