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-alpha] for 1, 3, and 24 h to investigate potential regulatory mechanisms. Decreased LPL activity was observed after 24 h of incubation with estradiol (1 micro g/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.
Highlights
The fetal demand for FFA increases as gestation proceeds, and LPL represents one potential mechanism for increasing placental lipid transport
We have shown previously an increased activity of microvillous membrane (MVM) LPL in placentas from pregnancies complicated by maternal insulin-dependent diabetes mellitus (IDDM) (27) associated with accelerated fetal growth and large fat depots (28) and a decreased activity in pregnancies delivering preterm fetuses with intrauterine growth restriction (IUGR), a condition typically characterized by reduced fetal fat depots (27, 29)
To the best of our knowledge, this report represents the first study of LPL in villous explants, a model that may provide a useful procedure for the analysis of lipid metabolism in small amounts of placental villous tissue
Summary
The fetal demand for FFA increases as gestation proceeds, and LPL represents one potential mechanism for increasing placental lipid transport. We suggest that the gestational increase in placental LPL activity represents an important mechanism to enhance placental FFA transport in late pregnancy. A gestational increase in estrogen, which stimulates the production of VLDLs, together with a decreased removal of lipoprotein TGs by LPL and/or hepatic lipase, has been suggested to be responsible for this hyperlipidemia (11). It has been shown in pregnant rats that a concurrent increase in LPL activity in mammary gland and placenta (10) redistributes the utilization of TGs to milk production and supplying the fetus.
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