Gestational and hormonal regulation of human placental lipoprotein lipase

Anne Liese Magnusson-Olsson, Bengt Hamark, Anette Ericsson, Margareta Wennergren, Thomas Jansson, and Theresa Powell

Neuroscience and physiology, Physiology, Gothenburg

Corresponding Author: anneliese.olsson{at}fysiologi.gu.se

The fetal demand for free fatty acids (FFA) increases markedly during human gestation as fetal fat deposition occurs primarily in late gestation. In order to address potential mechanisms for increasing placental lipid transport we examined lipoprotein lipase (LPL) activity and protein expression of LPL and two cytoplasmic fatty acid binding proteins (liver-FABP and cardiac-FABP) in 1st trimester and term human placenta. The LPL activity was three-fold higher in term (n=7, p<0.05) as compared to first trimester placentas (n=6). The LPL expression appeared lower in MVM from 1st trimester (n=2) compared to term (n=2) and no significant differences were seen in L- or C-FABP expression (n=4). We incubated isolated placental villous fragments with a variety of effectors (GW 1929, estradiol, insulin, cortisol, epinephrine, IGF-1, and TNF-a) for 1, 3 and 24 h to investigate potential regulatory mechanisms. Incubation for 1 and 3 h did not change LPL activity significantly. A decreased LPL activity was observed after 24 h incubation with estradiol (1 µg/ml), insulin, cortisol and IGF-1 (n=12, p<0.05). In further studies of LPL regulation, we observed an increase in LPL activity after 3 h incubation with physiological concentrations of estradiol (20 ng/ml) or hyperglycemic media 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.

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