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This Article Full Text Full Text (PDF) All Versions of this Article: 293/1/E24    most recent 00571.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles 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.

Effect of maternal triglycerides and free fatty acids on placental LPL in cultured primary trophoblast cells and in a case of maternal LPL deficiency

¹Perinatal Center, Institute of Neuroscience and Physiology, ²Department of Obstetrics and Gynecology, Göteborg University, Gothenburg, Sweden, ³Department of Epidemiology, Institute of Public Health, University of Aarhus, Aarhus, Denmark and ⁴Department of Obstetrics and Gynecology, University of Cincinnati, Cincinnati, Ohio

Submitted 24 October 2006 ; accepted in final form 2 February 2007

Maternal hypertriglyceridemia is a normal condition in late gestation and is an adaptation to ensure an adequate nutrient supply to the fetus. Placental lipoprotein lipase (LPL) is involved in the initial step in transplacental fatty acid transport as it hydrolyzes maternal triglycerides (TG) to release free fatty acids (FFA). We investigated LPL activity and protein (Western blot) and mRNA expression (real-time RT-PCR) in the placenta of an LPL-deficient mother with marked hypertriglyceridemia. The LPL activity was fourfold lower, LPL protein expression 50% lower, and mRNA expression threefold higher than that of normal, healthy placentas at term (n = 4–7). To further investigate the role of maternal lipids in placental LPL regulation, we isolated placental cytotrophoblasts from term placentas and studied LPL activity and protein and mRNA expression after incubation in Intralipid (as a source of TG) and oleic, linoleic, and a combination of oleic, linoleic, and arachidonic acids as well as insulin. Intralipid (40 and 400 mg/dl) decreased LPL activity by 30% (n = 10–14, P < 0.05) and 400 µM linoleic and linoleic-oleic-arachidonic acid (n = 10) decreased LPL activity by 37 and 34%, respectively. No major changes were observed in LPL protein or mRNA expression. We found no effect of insulin on LPL activity or protein expression in the cultured trophoblasts. To conclude, the activity of placental LPL is reduced by high levels of maternal TG and/or FFA. This regulatory mechanism may serve to counteract an excessive delivery of FFA to the fetus in conditions where maternal TG levels are markedly increased.

fetus; placenta; fatty acid transfer; lipoprotein lipase