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


     

Am J Physiol Gastrointest Liver Physiol 238: G453-G457, 1980;
0193-1857/80 $5.00
This Article
Right arrow Full Text (PDF)
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 Holt, P. R.
Right arrow Articles by Dominguez, A. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Holt, P. R.
Right arrow Articles by Dominguez, A. A.

AJP - Gastrointestinal and Liver Physiology, Vol 238, Issue 5 453-G457, Copyright © 1980 by American Physiological Society

ARTICLES

Triton-induced hyperlipidemia: a model for studies of intestinal lipoprotein production

P. R. Holt and A. A. Dominguez

To estimate intestinal very low-density lipoprotein (VLDL) contribution to the circulating plasma triglyceride (TG) pool, mesenteric, hepatic, and total TG production rates were measured in mesenteric lymph-cannulated male rats after Triton WR-1339 blockage of systemic VLDL metabolism. The intestinal contribution (4.92 +/- 0.5 mg TG/h) was calculated to be 19% of total TG production rate. Triton WR-1339 administration caused profound hyperlipoproteinemia but did not alter total lymph TG or VLDL apoprotein output. The percent of lymph VLDL apoprotein present as apo A-I and apo A-IV fell dramatically after Triton with a concomitant increase in apo E and apo C peptides. Studies in this Triton-treated rat model suggest that the intestinal contribution to systemic TG formation is small but that changes in circulating apolipoproteins may alter the composition of intestinal VLDL.


This article has been cited by other articles:


Home page
 J. Biol. Chem.Home page
M. Haidari, N. Leung, F. Mahbub, K. D. Uffelman, R. Kohen-Avramoglu, G. F. Lewis, and K. Adeli
Fasting and Postprandial Overproduction of Intestinally Derived Lipoproteins in an Animal Model of Insulin Resistance. EVIDENCE THAT CHRONIC FRUCTOSE FEEDING IN THE HAMSTER IS ACCOMPANIED BY ENHANCED INTESTINAL DE NOVO LIPOGENESIS AND ApoB48-CONTAINING LIPOPROTEIN OVERPRODUCTION
J. Biol. Chem., August 23, 2002; 277(35): 31646 - 31655.
[Abstract] [Full Text] [PDF]

Home page
 J. Lipid Res.Home page
C. L. Bisgaier, A. D. Essenburg, B. C. Barnett, B. J. Auerbach, S. Haubenwallner, T. Leff, A. D. White, P. Creger, M. E. Pape, T. J. Rea, et al.
A novel compound that elevates high density lipoprotein and activates the peroxisome proliferator activated receptor
J. Lipid Res., January 1, 1998; 39(1): 17 - 30.
[Abstract] [Full Text]


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