|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Journal of Lipid Research, Vol. 45, 859-865, May 2004
Copyright © 2004 by American Society for Biochemistry and Molecular Biology


* UMR 585 INSERM/INSA Physiopathologie des Lipides et Membranes, Villeurbanne, France
Laboratoire de Biochimie, Hôpital Neurologique, Lyon-Bron, France
Department of Internal Medicine, University Medical Center Utrecht, Utrecht, The Netherlands
** Unité 11, Hôpital Cardiovasculaire et Pneumologique Louis Pradel, Lyon-Bron, France
1 To whom correspondence should be addressed. e-mail: valerie.pruneta-deloche{at}insa-lyon.fr
Postprandial lipid metabolism is largely dependent upon lipoprotein lipase (LPL), which hydrolyses triglycerides (TGs). The time course of LPL activity in the postprandial state following a single meal has never been studied, because its determination required heparin injection. Recently, we have shown that LPL activity could be accurately measured in nonheparinized VLDL using a new assay aiming to determine the LPL-dependent VLDL-TG hydrolysis. Based on the same principle, we used in this study TG-rich lipoprotein (TRL)-bound LPL-dependent TRL-TG hydrolysis (LTTH) to compare the time course of LPL activity of 10 type 2 diabetics to that of 10 controls, following the ingestion of a lipid-rich meal. The peak TG concentration, reached after 4 h, was 67% higher in diabetics than in controls (P < 0.005). Fasting LTTHs were 91.3 ± 15.6 in controls versus 70.1 ± 4.8 nmol NEFA/ml/h in diabetics (P < 0.001). LTTH was increased 2 h postprandially by 190% in controls and by only 89% in diabetics, resulting in a 35% lowering of the LTTH area under the curve in diabetics. Postprandial LTTH was inversely correlated with TG or remnant concentrations in controls but not in diabetics, and with insulin resistance in both groups.
These data show that TRL-bound LPL activity increases in the postprandial state and is strongly reduced in type 2 diabetes, contributing to postprandial hypertriglyceridemia.
Abbreviations: FPLC, fast-protein liquid chromatography; HOMA, homeostasis model assessment; LPL, lipoprotein lipase; RLP, remnant-like lipoprotein particle; TG, triglyceride; TRL, triglyceride-rich lipoprotein
Supplementary key words lipoprotein lipase type 2 diabetes postprandial period triglyceride-rich lipoprotein remnant
![]()
CiteULike
Complore
Connotea
Del.icio.us
Digg
Reddit
Technorati What's this?
This article has been cited by other articles:
![]() |
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] |
||||
![]() |
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] |
||||
![]() |
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] |
||||
![]() |
A. Veiraiah Hyperglycemia, Lipoprotein Glycation, and Vascular Disease Angiology, July 1, 2005; 56(4): 431 - 438. [Abstract] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| All ASBMB Journals | Journal of Biological Chemistry |
| Molecular and Cellular Proteomics | ASBMB Today |