Advertisement
J. Lipid Res.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 QUICK SEARCH:   [advanced]


     


A more recent version of this article appeared on May 1, 2004

Papers In Press, published online ahead of print February 16, 2004
J. Lipid Res., doi:10.1194/jlr.M300435-JLR200
This Article
Right arrow Full Text (Accepted Manuscript)
Right arrow All Versions of this Article:
M300435-JLR200v1
45/5/859    most recent
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 Pruneta-Deloche, V.
Right arrow Articles by Moulin, P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Pruneta-Deloche, V.
Right arrow Articles by Moulin, P.
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?

Submitted on October 22, 2003
Revised on February 2, 2004
Accepted on February 10, 2004

Alteration in lipoprotein lipase activity bound to triglyceride-rich lipoproteins in the postprandial state in type 2 diabetes

Valérie Pruneta-Deloche, Agnès Sassolas, Geesje M. Dallinga-Thie, François Berthezène, Gabriel Ponsin, and Philippe Moulin

UMR 585 Inserm/Insa, Villeurbanne 69100

Corresponding Author: valerie.pruneta-deloche{at}insa-lyon.fr

Postprandial hyperlipidemia is considered to be proatherogenic in type 2 diabetes. An important determinant of postprandial lipid metabolism is the activity of lipoprotein lipase (LPL) which is responsible for hydrolysis of triglycerides. The time-course of LPL activity in the postprandial state following one single meal has never been studied since the determination of lipoprotein lipase activity requires heparin injection. Recently, we have shown that LPL activity could be accurately measured in non-heparinized VLDL using a new assay that we developed to determine the LPL-dependent VLDL-triglyceride (TG) hydrolysis (LVTH). Based on the same principle, we used in the present study a TG-rich lipoprotein (TRL)-bound LPL-dependent TRL-TG hydrolysis (LTTH) to compare the time-course of LPL activity of 10 patients with type 2 diabetes to that of 10 healthy subjects, following the ingestion of a lipid-rich test meal. In both groups, the peak triglyceride concentration was reached after 4 h and was 67% higher in type 2 diabetics (P < 0.005). Fasting LTTH were 91.3 +/- 15.6 in controls vs 70.1 +/- 4.8 nmol NEFA/ml.h in type 2 diabetics (P < 0.001). LTTH was increased 2 h postprandially by 190% in controls and by only 89% in diabetic patients, finally resulting in a 35% lowering of LTTH area under the curve in diabetics as compared to controls. Postprandial LTTH was inversely correlated to either triglyceride or remnant concentrations in controls but not in diabetics, while LTTH was inversely correlated to insulin resistance in both groups. These data provide evidence that TRL-bound LPL activity increases in human subjects in the postprandial state and is strongly reduced in type 2 diabetes, thereby contributing to the observed postprandial hypertriglyceridemia.


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
Arterioscler. Thromb. Vasc. Bio.Home page
T. Kawai, T. Ito, K. Ohwada, Y. Mera, M. Matsushita, and H. Tomoike
Hereditary Postprandial Hypertriglyceridemic Rabbit Exhibits Insulin Resistance and Central Obesity: A Novel Model of Metabolic Syndrome
Arterioscler Thromb Vasc Biol, December 1, 2006; 26(12): 2752 - 2757.
[Abstract] [Full Text] [PDF]


Home page
J. Lipid Res.Home page
S. D. Tetali, M. S. Budamagunta, J. C. Voss, and J. C. Rutledge
C-terminal interactions of apolipoprotein E4 respond to the postprandial state
J. Lipid Res., July 1, 2006; 47(7): 1358 - 1365.
[Abstract] [Full Text] [PDF]


Home page
J. Lipid Res.Home page
S. Ibrahim, A. Djimet-Baboun, V. Pruneta-Deloche, C. Calzada, M. Lagarde, and G. Ponsin
Transfer of very low density lipoprotein-associated phospholipids to activated human platelets
J. Lipid Res., February 1, 2006; 47(2): 341 - 348.
[Abstract] [Full Text] [PDF]


Home page
ANGIOLOGYHome page
A. Veiraiah
Hyperglycemia, Lipoprotein Glycation, and Vascular Disease
Angiology, July 1, 2005; 56(4): 431 - 438.
[Abstract] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 All ASBMB Journals   Journal of Biological Chemistry 
 Molecular and Cellular Proteomics   ASBMB Today 
Copyright © 2004 by the American Society for Biochemistry and Molecular Biology.
Advertisement
spacer
Advertisement
Advertisement