Clinical Chemistry AACC Online Job Center
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Clinical Chemistry 43: 2379-2383, 1997;
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit an electronic Letter to
the Editor about this paper
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (5)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ribalta, J.
Right arrow Articles by Masana, L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ribalta, J.
Right arrow Articles by Masana, L.
Related Collections
Right arrow Nutrition
Right arrow Lipids, Lipoproteins, and Cardiovascular Risk Factors
(Clinical Chemistry. 1997;43:2379-2383.)
© 1997 American Association for Clinical Chemistry, Inc.


Articles

Low plasma vitamin A concentrations in familial combined hyperlipidemia

Josep Ribalta, Agnes E. LaVille, Josefa Girona, Joan C. Vallvé and Lluís Masanaa

Unitat de Recerca de Lípids, Facultat de Medicina, Hospital Universitari de Sant Joan, Universitat Rovira i Virgili, Sant Llorenç 21, 43201 Reus, Spain.
a Author for correspondence. Fax (+34-77) 75 93 22; e-mail jrv{at}fmcs.urv.es

As many as 20% of the survivors of acute myocardial infarction present with the heritable form of hyperlipidemia, termed familial combined hyperlipidemia (FCHL). Some of the genes reported to be involved in this disorder, such as those for lipoprotein lipase (LPL) and apolipoprotein (apo) C-III, are controlled by a peroxisome proliferator-activated receptor (PPAR)/retinoic acid receptor X (RXR) regulatory system, which is retinoic acid dependent. If, as we hypothesized, the availability of retinoic acid or its precursor retinol (vitamin A) could be altered in FCHL, this could help explain some aspects of the phenotypic expression of the disease. We therefore measured plasma retinol concentrations in 30 FCHL subjects and 56 controls. Plasma retinol concentrations in FCHL subjects were significantly lower than that of control subjects (1.96 ± 0.83 µmol/L vs 2.91 ± 1.23 µmol/L, respectively; P <0.0001). This novel finding of significantly decreased concentrations of plasma retinol in FCHL relative to control subjects gives support to the hypothesis that vitamin A might be involved in the expression of this disorder.




The following articles in journals at HighWire Press have cited this article:


Home page
J. Lipid Res.Home page
J. Ribalta, J. Girona, J. C. Vallvé, A. E. La Ville, M. Heras, and L. Masana
Vitamin A is linked to the expression of the AI-CIII-AIV gene cluster in familial combined hyperlipidemia
J. Lipid Res., March 1, 1999; 40(3): 426 - 431.
[Abstract] [Full Text]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1997 by the American Association for Clinical Chemistry.