AJP - Regu Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Regul Integr Comp Physiol 282: R1429-R1435, 2002; doi:10.1152/ajpregu.00569.2001
0363-6119/02 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
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 ISI Web of Science (7)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Finck, B. N.
Right arrow Articles by Johnson, R. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Finck, B. N.
Right arrow Articles by Johnson, R. W.
Vol. 282, Issue 5, R1429-R1435, May 2002

Anti-inflammatory agents inhibit the induction of leptin by tumor necrosis factor-alpha

Brian N. Finck and Rodney W. Johnson

Department of Animal Sciences, University of Illinois at Urbana-Champaign, 390 Animal Sciences Laboratory, Urbana, Illinois 61801

Tumor necrosis factor (TNF)-alpha stimulates the secretion of the adipocyte-derived hormone leptin. However, the cellular mechanisms by which TNF-alpha influences leptin production are poorly understood. To examine this issue, epididymal fat pads were isolated from mice and cultured in recombinant murine TNF-alpha (100 ng/ml). Compared with medium-treated controls, steady-state leptin expression was increased in TNF-alpha -treated explants. Culture with inhibitors of translation (cycloheximide) or transcription (actinomycin-D) abrogated the induction of leptin following TNF-alpha . Explants were also cultured in the presence of the anti-inflammatory p38 mitogen-activated protein kinase inhibitor (SB-203580) or PG J2 metabolite [15-deoxy-Delta 12,14-PG J2 (PGJ)] and then exposed to TNF-alpha . Both compounds completely abolished TNF-alpha -induced increases in leptin production. To test the relevance of this in vivo, mice were pretreated with PGJ and then given TNF-alpha . PGJ treatment markedly blunted the TNF-alpha -induced increase in leptin, TNF-alpha , and interleukin-6 gene expression in epididymal adipose tissue. Collectively, these data indicate that TNF-alpha acutely activates leptin expression and that anti-inflammatory agents can abrogate TNF-alpha -induced hyperleptinemia.

endocrine-immune interaction; 15-deoxy-Delta 12,14-prostaglandin J2; SB-203580


This article has been cited by other articles:


Home page
 Rheumatology (Oxford)Home page
P. Harle, T. Bongartz, J. Scholmerich, U. Muller-Ladner, and R. H. Straub
Predictive and potentially predictive factors in early arthritis: a multidisciplinary approach
Rheumatology, April 1, 2005; 44(4): 426 - 433.
[Abstract] [Full Text] [PDF]

Home page
 J Am Coll CardiolHome page
Y. Yu, K. Ohmori, Y. Chen, C. Sato, H. Kiyomoto, K. Shinomiya, H. Takeuchi, K. Mizushige, and M. Kohno
Effects of pravastatin on progression of glucose intolerance and cardiovascular remodeling in a type II diabetes model
J. Am. Coll. Cardiol., August 18, 2004; 44(4): 904 - 913.
[Abstract] [Full Text] [PDF]

Home page
 Ann Rheum DisHome page
M Bokarewa, D Bokarew, O Hultgren, and A Tarkowski
Leptin consumption in the inflamed joints of patients with rheumatoid arthritis
Ann Rheum Dis, October 1, 2003; 62(10): 952 - 956.
[Abstract] [Full Text]

Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
H. Scholz
Prostaglandins
Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2003; 285(3): R512 - R514.
[Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online