AJP - Endo AJP: Endocrinology and Metabolism
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 QUICK SEARCH:   [advanced]


     


Am J Physiol Endocrinol Metab (June 15, 2004). doi:10.1152/ajpendo.00155.2004
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
287/4/E799    most recent
00155.2004v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Di Gregorio, G. B.
Right arrow Articles by Kern, P. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Di Gregorio, G. B.
Right arrow Articles by Kern, P. A.
Submitted on April 2, 2004
Accepted on June 9, 2004

Expression of FOXC2 in Adipose and Muscle and its Association with Whole-Body Insulin Sensitivity

Gina B. Di Gregorio1*, Rickard Westergren2, Sven Enerback2, Tong Lu1, and Philip A. Kern1

1 The Central Arkansas Veterans Healthcare System, Department of Medicine, Division of Endocrinology, University of Arkansas for Medical Sciences, Little Rock, AR, USA
2 Medical Genetics, Department of Medical Biochemistry, Goteborg University, Goteborg, Sweden

* To whom correspondence should be addressed. E-mail: Digregorioginab{at}uams.edu.

FOXC2 is a winged helix/forkhead transcription factor involved in PKA signaling. Overexpression of FOXC2 in the adipose tissue of transgenic mice protected against diet-induced obesity and insulin resistance. We examined the expression of FOXC2 in fat and muscle of non-diabetic humans with varying obesity and insulin sensitivity. There was no relation between BMI and FOXC2 mRNA in either adipose or muscle. There was a strong inverse relation between adipose FOXC2 mRNA and insulin sensitivity, using the frequently sampled IV glucose tolerance test (r=-0.78, P<0.001). However, there was no relationship between muscle FOXC2 and any measure of insulin sensitivity. To separate insulin resistance from obesity, we examined FOXC2 expression in pairs of subjects who were matched for BMI, but who were discordant for SI. When compared to the insulin sensitive subjects, the insulin resistant subjects had 3-fold higher levels of adipose FOXC2 mRNA (p=0.03). In contrast, muscle FOXC2 mRNA expression was no different between insulin resistant and insulin sensitive subjects. There was no association of adipose or muscle FOXC2 mRNA with either circulating or adipose-secreted TNF{alpha}, IL6, leptin, adiponectin, or non-esterified fatty acids. Thus, adipose FOXC2 is more highly expressed in insulin resistant subjects, and this effect is independent of obesity. This association between FOXC2 and insulin resistance may be related to the role of FOXC2 in PKA signaling.




This article has been cited by other articles:


Home page
Am. J. Pathol.Home page
A. De Pauw, S. Tejerina, M. Raes, J. Keijer, and T. Arnould
Mitochondrial (Dys)function in Adipocyte (De)differentiation and Systemic Metabolic Alterations
Am. J. Pathol., September 1, 2009; 175(3): 927 - 939.
[Abstract] [Full Text] [PDF]


Home page
Arterioscler. Thromb. Vasc. Bio.Home page
M.-C. Alessi and I. Juhan-Vague
PAI-1 and the Metabolic Syndrome: Links, Causes, and Consequences
Arterioscler Thromb Vasc Biol, October 1, 2006; 26(10): 2200 - 2207.
[Abstract] [Full Text] [PDF]


Home page
Circ. Res.Home page
N. R. Madamanchi and M. S. Runge
Five Easy Pieces: The Obesity Paradigm
Circ. Res., March 17, 2006; 98(5): 576 - 578.
[Full Text] [PDF]


Home page
Circ. Res.Home page
H. Fujita, M. Kang, M. Eren, L. A. Gleaves, D. E. Vaughan, and T. Kume
Foxc2 Is a Common Mediator of Insulin and Transforming Growth Factor {beta} Signaling to Regulate Plasminogen Activator Inhibitor Type I Gene Expression
Circ. Res., March 17, 2006; 98(5): 626 - 634.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 2004 by the American Physiological Society.