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

Artikel i vetenskaplig tidskrift
Författare AnneLiese Magnusson-Olsson
Susanne Lager
Bo Jacobsson
Thomas Jansson
Theresa L Powell
Publicerad i Am J Physiol Endocrinol Metab
Volym 293
Nummer/häfte 1
Sidor E24-30
Publiceringsår 2007
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi
Institutionen för kliniska vetenskaper
Sidor E24-30
Språk en
Länkar ajpendo.physiology.org/cgi/content/...
Ämnesord fetus; placenta; fatty acid transfer; lipoprotein lipase
Ämneskategorier Medicin och Hälsovetenskap, Fysiologi

Sammanfattning

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 approximately 30% (n = 10-14, P < 0.05) and 400 microM 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.

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