HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: M600098-JLR200v1 47/11/2551    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Magnusson-Olsson, A. L. Articles by Powell, T. L. Search for Related Content PubMed PubMed Citation Articles by Magnusson-Olsson, A. L. Articles by Powell, T. L. Social Bookmarking                      What's this?

Journal of Lipid Research, Vol. 47, 2551-2561, November 2006
Copyright © 2006 by American Society for Biochemistry and Molecular Biology

Patient-Oriented Research

Gestational and hormonal regulation of human placental lipoprotein lipase

A. L. Magnusson-Olsson^1,*, B. Hamark, A. Ericsson^*, M. Wennergren, T. Jansson^*, and T. L. Powell^*,

^* Perinatal Center, Institute of Neuroscience and Physiology, Göteborg University, Göteborg, Sweden
Department of Obstetrics and Gynecology, Göteborg University, Göteborg, Sweden
Department of Obstetrics and Gynecology, University of Cincinnati, Cincinnati, OH

Published, JLR Papers in Press, August 22, 2006.

¹ To whom correspondence should be addressed. e-mail: anneliese.olsson{at}fysiologi.gu.se

ABSTRACT

The fetal demand for FFA increases as gestation proceeds, and LPL represents one potential mechanism for increasing placental lipid transport. We examined LPL activity and protein expression in first trimester and term human placenta. The LPL activity was 3-fold higher in term (n = 7; P < 0.05) compared with first trimester (n = 6) placentas. The LPL expression appeared lower in microvillous membrane from first trimester (n = 2) compared with term (n = 2) placentas. We incubated isolated placental villous fragments with a variety of effectors [GW 1929, estradiol, insulin, cortisol, epinephrine, insulin-like growth factor-1 (IGF-1), and tumor necrosis factor-] for 1, 3, and 24 h to investigate potential regulatory mechanisms. Decreased LPL activity was observed after 24 h of incubation with estradiol (1 µg/ml), insulin, cortisol, and IGF-1 (n = 12; P < 0.05). We observed an increase in LPL activity after 3 h of incubation with estradiol (20 ng/ml) or hyperglycemic medium plus insulin (n = 7; P < 0.05). To conclude, we suggest that the gestational increase in placental LPL activity represents an important mechanism to enhance placental FFA transport in late pregnancy. Hormonal regulation of placental LPL activity by insulin, cortisol, IGF-1, and estradiol may be involved in gestational changes and in alterations in LPL activity in pregnancies complicated by altered fetal growth.

Supplementary key words fetus • fatty acid transfer • fatty acid metabolism

Abbreviations: ARA, arachidonic acid; C-FABP, cardiac fatty acid binding protein; DHA, docosahexaonic acid; EFA, essential fatty acid; FABP, fatty acid binding protein; hCG, human chorionic gonadotropin; IDDM, insulin-dependent diabetes mellitus; IGF, insulin-like growth factor; IUGR, intrauterine growth restriction; L-FABP, liver fatty acid binding protein; MVM, microvillous membrane; PPAR, peroxisome proliferator-activated receptor; TBP, TATA box binding protein; TG, triglyceride; TNF, tumor necrosis factor

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

This article has been cited by other articles:

				A. L. Magnusson-Olsson, S. Lager, B. Jacobsson, T. Jansson, and T. L. Powell Effect of maternal triglycerides and free fatty acids on placental LPL in cultured primary trophoblast cells and in a case of maternal LPL deficiency Am J Physiol Endocrinol Metab, July 1, 2007; 293(1): E24 - E30. [Abstract] [Full Text] [PDF]