Submitted on October 24, 2006
Accepted on February 2, 2007
The effect of maternal lipids on placental lipoprotein lipase in cultured primary trophoblast cells and in a case of maternal LPL deficiency
Anne Liese Magnusson-Olsson1, Susanne Lager1, Bo Jacobsson2, Thomas Jansson3, and Theresa L. Powell4*
1 Physiology, Gothenburg University, Göteborg, Sweden
2 Obstetrics and Gynecology, Gothenburg University, Göteborg, Sweden
3 Physiology, Gothenburg University, Gothenburg, Sweden; Obstetrics and Gynecology, University of Cincinnati, Cincinnati, Ohio, United States
4 Physiology, Gothenburg University, Gothenburg, Sweden
* To whom correspondence should be addressed. E-mail: theresa.powell{at}fysiologi.gu.se.
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, protein and mRNA expression in the placenta of a LPL deficient mother with marked hypertriglyceridemia. The LPL activity was fourfold lower, LPL protein expression 50% lower and mRNA expression threefold higher than normal healthy placentas at term (n=4-7). In order to further investigate the role of maternal lipids in placental LPL regulation, we isolated placental cytotrophoblasts from term placentas and studied LPL activity, protein and mRNA expression after incubation in Intralipid (as a source of TG), oleic, linoleic and a combination of oleic, linoleic and arachidonic acid as well as insulin. Intralipid (40 and 400 mg/dl) decreased LPL activity by ≈ 30% (n=10-14; p<0.05) and 400 microM linoleic and a combination of 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 FFAs. This regulatory mechanism may serve to counteract an excessive delivery of FFA to the fetus in conditions where maternal TG levels are markedly increased.
