Advertisement
JBC

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 QUICK SEARCH:   [advanced]


     


A more recent version of this article appeared on May 12, 2006
This Article
Right arrow Full Text (Accepted Manuscript)
Right arrow All Versions of this Article:
281/19/13141    most recent
M512943200v1
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
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Leroyer, S.
Right arrow Articles by Antoine, B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Leroyer, S.
Right arrow Articles by Antoine, B.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Papers In Press, published online ahead of print March 8, 2006
J. Biol. Chem, 10.1074/jbc.M512943200
Submitted on December 5, 2005
Revised on February 27, 2006
Accepted on March 8, 2006

Rosiglitazone controls fatty acid cycling in human adipose tissue by means of glyceroneogenesis and glycerol phosphorylation

Stéphanie Leroyer, Joan Tordjman, Geneviève Chauvet, Joëlle Quette, Charles Chapron, Claude Forest, and Bénédicte Antoine

INSERM U 530 - Université Paris5, Centre universitaire - U.F.R. Biomédicale, Paris 75006

Corresponding Author: benedicte.antoine{at}biomedicale.univ-paris5.fr

Control of fatty acid homeostasis is crucial to prevent insulin resistance. During fasting, plasma fatty acid level depends on triglycerides lipolysis and fatty acid re-esterification within fat cells. In rodents, Rosiglitazone (Rosi) control fatty acid homeostasis by stimulating two pathways in the adipocytes, glyceroneogenesis and glycerol phosphorylation that provide the glycerol-3-phosphate necessary for fatty acid re-esterification. Here, we analysed the functionality of both pathways for controlling fatty acid release in subcutaneous adipose tissue samples from lean and obese women before and after Rosi ex vivo treatment. In controls, pyruvate, used as a substrate of glyceroneogenesis, could contribute up to 65% of the fatty acid reesterified after basal lipolysis whereas glycerol phosphorylation account for only 14 +/- 9 %. However, efficiency of glyceroneogenesis is diminishing when women body mass index (BMI) increase. After Rosi treatment, increase of either pyruvate- or glycerol- dependent fatty acid re-esterification is strictly correlated to that of Phosphoenolpyruvate carboxykinase and Glycerolkinase, the key-enzymes of each pathway but depends on women BMI. While the rosi-responsiveness of glyceroneogenesis is rather constant according to women BMI, glycerol phosphorylation is mostly enhanced in lean women (BMI<27). Overall, these data indicate that, whereas glyceroneogenesis is more utilized than glycerol phosphorylation for fatty acid re-esterification in human subcutaneous adipose tissue in physiological situation, both are sollicited in response to Rosi but with lower efficiency when BMI increased.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
J. Clin. Endocrinol. Metab.Home page
G. D. Tan, D. B. Savage, B. A. Fielding, J. Collins, L. Hodson, S. M. Humphreys, S. O'Rahilly, K. Chatterjee, K. N. Frayn, and F. Karpe
Fatty Acid Metabolism in Patients with PPAR{gamma} Mutations
J. Clin. Endocrinol. Metab., November 1, 2008; 93(11): 4462 - 4470.
[Abstract] [Full Text] [PDF]


Home page
Endocr. Rev.Home page
M. Prentki and S. R. M. Madiraju
Glycerolipid Metabolism and Signaling in Health and Disease
Endocr. Rev., October 1, 2008; 29(6): 647 - 676.
[Abstract] [Full Text] [PDF]


Home page
DiabetesHome page
T. Cadoudal, E. Distel, S. Durant, F. Fouque, J.-M. Blouin, M. Collinet, S. Bortoli, C. Forest, and C. Benelli
Pyruvate Dehydrogenase Kinase 4: Regulation by Thiazolidinediones and Implication in Glyceroneogenesis in Adipose Tissue
Diabetes, September 1, 2008; 57(9): 2272 - 2279.
[Abstract] [Full Text] [PDF]


Home page
J. Nutr.Home page
T. Cadoudal, M. Glorian, A. Massias, F. Fouque, C. Forest, and C. Benelli
Retinoids Upregulate Phosphoenolpyruvate Carboxykinase and Glyceroneogenesis in Human and Rodent Adipocytes
J. Nutr., June 1, 2008; 138(6): 1004 - 1009.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
J. Tordjman, S. Leroyer, G. Chauvet, J. Quette, C. Chauvet, C. Tomkiewicz, C. Chapron, R. Barouki, C. Forest, M. Aggerbeck, et al.
Cytosolic Aspartate Aminotransferase, a New Partner in Adipocyte Glyceroneogenesis and an Atypical Target of Thiazolidinedione
J. Biol. Chem., August 10, 2007; 282(32): 23591 - 23602.
[Abstract] [Full Text] [PDF]


Home page
EndocrinologyHome page
W. Khazen, E. Distel, M. Collinet, V. E. Chaves, J.-P. M'Bika, C. Chany, A. Achour, C. Benelli, and C. Forest
Acute and Selective Inhibition of Adipocyte Glyceroneogenesis and Cytosolic Phosphoenolpyruvate Carboxykinase by Interferon {gamma}
Endocrinology, August 1, 2007; 148(8): 4007 - 4014.
[Abstract] [Full Text] [PDF]


Home page
Endocr. Rev.Home page
M. E. Trujillo and P. E. Scherer
Adipose Tissue-Derived Factors: Impact on Health and Disease
Endocr. Rev., December 1, 2006; 27(7): 762 - 778.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 All ASBMB Journals   Molecular and Cellular Proteomics 
 Journal of Lipid Research   ASBMB Today 
Copyright © 2006 by the American Society for Biochemistry and Molecular Biology.
Advertisement
spacer
Advertisement
Advertisement