AJP - Endo Information on EB 2010
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 QUICK SEARCH:   [advanced]


     


Am J Physiol Endocrinol Metab (May 4, 2004). doi:10.1152/ajpendo.00488.2003
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
287/3/E446    most recent
00488.2003v1
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 Delporte, M.-L.
Right arrow Articles by Brichard, S. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Delporte, M.-L.
Right arrow Articles by Brichard, S. M.
Submitted on October 30, 2003
Accepted on April 30, 2004

Leptin treatment markedly increased plasma adiponectin, but barely decreased plasma resistin of ob/ob mice

Marie-Laure Delporte1, Samira Ait El Mkadem1, Muriel Quisquater1, and Sonia M. Brichard1*

1 Faculty of Medicine, Endocrinology and Metabolism Unit, University of Louvain, Brussels, Belgium

* To whom correspondence should be addressed. E-mail: brichard{at}endo.ucl.ac.be.

Adiponectin (ApN) and leptin are two adipocytokines that control fuel homeostasis, body weight and insulin sensitivity. Their interplay is still poorly studied. These hormones are either undetectable or decreased in obese, diabetic ob/ob mice. We examined the effects of leptin treatment on ApN gene expression, protein production, secretion, and circulating levels of ob/ob mice. We also briefly tackled the influence of this treatment on resistin, another adipocytokine involved in obesity-related insulin resistance. Leptin-treated (T) obese mice (continuous sc infusion for 6 days) were compared to untreated lean (L), untreated obese (O) and untreated pair-fed obese (PF) mice. Blood was collected throughout the study. At day 3 or 6, fat pads were either directly analysed (mRNA, ApN content) or cultured for up to 24 h (ApN secretion). The direct effect of leptin was also studied in 3T3-F442A adipocytes. Compared to L mice, ApN content of visceral or subcutaneous fat and ApN secretion by adipose explants were blunted in obese mice. Accordingly, plasma ApN levels of O mice were decreased by 50%. Leptin treatment of ob/ob mice increased by 50-80% ApN mRNAs, ApN content and secretion from the visceral depot. Leptin also directly stimulated ApN mRNAs and secretion from 3T3-F442A adipocytes. After 6 days of treatment, plasma ApN of ob/ob mice increased 2.5-fold, a rise that did not occur in PF mice. Plasma resistin of T mice were barely decreased. Leptin treatment, but not mere calorie restriction, corrects plasma ApN in obese mice, by restoring adipose tissue ApN concentrations and secretion at least in part, via a direct stimulation of ApN gene expression. Such a treatment only minimally affects circulating resistin. ApN restoration could, in concert with leptin, contribute to the metabolic effects classically observed during leptin administration.




This article has been cited by other articles:


Home page
GutHome page
T Fujisawa, H Endo, A Tomimoto, M Sugiyama, H Takahashi, S Saito, M Inamori, N Nakajima, M Watanabe, N Kubota, et al.
Adiponectin suppresses colorectal carcinogenesis under the high-fat diet condition
Gut, November 1, 2008; 57(11): 1531 - 1538.
[Abstract] [Full Text] [PDF]


Home page
J. Nutr.Home page
R. S. Bruno, C. E. Dugan, J. A. Smyth, D. A. DiNatale, and S. I. Koo
Green Tea Extract Protects Leptin-Deficient, Spontaneously Obese Mice from Hepatic Steatosis and Injury
J. Nutr., February 1, 2008; 138(2): 323 - 331.
[Abstract] [Full Text] [PDF]


Home page
J. Lipid Res.Home page
A. A. Wendel, A. Purushotham, L.-F. Liu, and M. A. Belury
Conjugated linoleic acid fails to worsen insulin resistance but induces hepatic steatosis in the presence of leptin in ob/ob mice
J. Lipid Res., January 1, 2008; 49(1): 98 - 106.
[Abstract] [Full Text] [PDF]


Home page
Arterioscler. Thromb. Vasc. Bio.Home page
M. Itoh, T. Suganami, N. Satoh, K. Tanimoto-Koyama, X. Yuan, M. Tanaka, H. Kawano, T. Yano, S. Aoe, M. Takeya, et al.
Increased Adiponectin Secretion by Highly Purified Eicosapentaenoic Acid in Rodent Models of Obesity and Human Obese Subjects
Arterioscler Thromb Vasc Biol, September 1, 2007; 27(9): 1918 - 1925.
[Abstract] [Full Text] [PDF]


Home page
DiabetesHome page
E. D. Javor, E. K. Cochran, C. Musso, J. R. Young, A. M. DePaoli, and P. Gorden
Long-Term Efficacy of Leptin Replacement in Patients With Generalized Lipodystrophy
Diabetes, July 1, 2005; 54(7): 1994 - 2002.
[Abstract] [Full Text] [PDF]


Home page
J ANIM SCIHome page
E. Lord, S. Ledoux, B. D. Murphy, D. Beaudry, and M. F. Palin
Expression of adiponectin and its receptors in swine
J Anim Sci, March 1, 2005; 83(3): 565 - 578.
[Abstract] [Full Text] [PDF]




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