This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Mora, S. Articles by Pessin, J. E. Search for Related Content PubMed PubMed Citation Articles by Mora, S. Articles by Pessin, J. E. Pubmed/NCBI databases Gene GEO Profiles HomoloGene UniGene Compound via MeSH Substance via MeSH Hazardous Substances DB STREPTOZOTOCIN

The MEF2A and MEF2D Isoforms Are Differentially Regulated in Muscle and Adipose Tissue during States of Insulin Deficiency¹

Department of Physiology and Biophysics, The University of Iowa, Iowa City, Iowa 52242

Address all correspondence and requests for reprints to: Jeffrey Pessin, Department of Physiology and Biophysics, The University of Iowa, 51 Newton Road, Iowa City, Iowa 52242. E-mail: Jeffrey-Pessin{at}uiowa.edu

Previously we have demonstrated that striated muscle GLUT4 gene expression decreased following streptozotocin-induced diabetes due to a loss of MEF2A transcription factor expression without any significant effect on the MEF2D isoform (Mora, S. and J. E. Pessin (2000) J Biol Chem, 275:16323–16328). In contrast to both cardiac and skeletal muscle, adipose tissue displays a selective decrease in MEF2D expression in diabetes without any significant alteration in MEF2A protein content. Adipose tissue also expresses very low levels of the MEF2 transcription factors and nuclear extracts from white adipose tissue exhibit poor in vitro binding to the MEF2 element. However, addition of in vitro synthesized MEF2A to adipose nuclear extracts results in the formation of the expected MEF2/DNA complex. More importantly, binding to the MEF2 element was also compromised in the diabetic condition. Furthermore, in vivo overexpression of MEF2A selectively in adipose tissue did not affect GLUT4 or MEF2D expression and was not sufficient to prevent GLUT4 down-regulation that occurred in insulin-deficient states.

This article has been cited by other articles:

				D. P. Sparling, B. A. Griesel, J. Weems, and A. L. Olson GLUT4 Enhancer Factor (GEF) Interacts with MEF2A and HDAC5 to Regulate the GLUT4 Promoter in Adipocytes J. Biol. Chem., March 21, 2008; 283(12): 7429 - 7437. [Abstract] [Full Text] [PDF]

				D. P. Sparling, B. A. Griesel, and A. L. Olson Hyperphosphorylation of MEF2A in primary adipocytes correlates with downregulation of human GLUT4 gene promoter activity Am J Physiol Endocrinol Metab, April 1, 2007; 292(4): E1149 - E1156. [Abstract] [Full Text] [PDF]

				J. B. Knight, C. A. Eyster, B. A. Griesel, and A. L. Olson Regulation of the human GLUT4 gene promoter: Interaction between a transcriptional activator and myocyte enhancer factor 2A PNAS, December 9, 2003; 100(25): 14725 - 14730. [Abstract] [Full Text] [PDF]