Characterisation of triacylglycerol hydrolase activities in human placenta

Abstract

Triacylglycerol hydrolase activities were characterised in homogenates, cytosol, and microvillous membranes (MVM) of human placenta. Homogenates of placenta exhibited three distinct triacylyglycerol hydrolase activities with pH optima 4.5, 6.0 and 8. 0. On further fractionation, placental cytosol exhibited both acid cholesterol ester hydrolase (pH 4.5) and hormone sensitive lipase (pH 6.0) activities, whereas purified placental MVM exhibited two distinct triacylyglycerol hydrolase activities; a minor activity at pH 8.0 and a second major activity at pH 6.0. Triacylglycerol hydrolase activity at pH 8.0 of MVM appeared to be lipoprotein lipase (consistent with criteria such as serum stimulation and salt inhibition), whereas at pH 6.0 the activity was unique in that it was almost abolished by serum, but was not affected by high NaCl concentrations. Our data, for the first time, demonstrate that human placental MVM, in addition to lipoprotein lipase, contain a newly identified triacylglycerol hydrolase activity at pH 6.0.

Lipoprotein metabolism of pregnant women is associated with both their genetic polymorphisms and those of their newborn children

“…In this view, the absence of association of maternal lipoproteins with APOC3*S2 is consistent with what we know about the lower expression of the APOC3 genes by the placenta (20) as opposed to the LPL and APOE genes (2,3,8,9,11). Below, we present some possible mechanisms by which these proteins may play such a role.…”

“…Although this idea is consistent with the assumption that maternal lipoproteins supply lipids to the fetus via the placenta, at present it is only supported by in vitro arguments: immunochemistry and RNA hybridization in placental tissues demonstrated the presence of some key players of lipoprotein metabolism (lipoprotein lipases, receptors, and apolipoproteins) (2)(3)(4)(5)(6)(7)(8)(9), whereas tissue cultures of placental fragments indicated the capture and hydrolysis (10)(11)(12)(13) as well as the synthesis and secretion (14) of lipoproteins. However, in vivo evidence is still lacking in humans.…”

“…First, these genes are known to be involved in the metabolism of triglyceride-rich lipoproteins, which dramatically increase in concentration during pregnancy (19). Second, two of these genes, LPL and APOE, are abundantly expressed in the placenta (2,3,11), whereas APOC3 is less expressed in placenta and in fetus (20), offering the possibility to compare the influence of genes variably expressed by the placenta. Third, their polymorphisms are well known for their associations with lipoprotein concentrations in adults (16)(17)(18), and the mechanisms by which these associations occur have been linked directly to quantitative or qualitative alterations of the proteins encoded by these genes.…”

Placental triglyceride accumulation in maternal type 1 diabetes is associated with increased lipase gene expression

“…In the cytosol of the syncytiotrophoblast, FFAs may be reesterified and deposited as TGs or phospholipids and hydrolyzed for later release into the fetal circulation (13). Lysosomal acid lipase (LAL) and hormone-sensitive lipase (HSL) are intracellular lipases that are capable of hydrolyzing TGs and cholesteryl esters; both are expressed in human placental tissue (14,15).…”

Comparison of bloodstream fatty acid composition from African-American women at gestation, delivery, and postpartum

“…Although phospholipid fatty acids represent structural lipids and are biomarkers for dietary fatty acid intake (33), this fraction may not be the best indicator of fatty acid availability for placental transfer. Transfer across the placenta is limited to nonesterified fatty acids, and the localization of lipoprotein lipase and triacylglycerol hydrolase activities (34) to the placenta has led to suggestions that triacylglycerols are the major source of maternal fatty acids (35,36), although mobilization from other circulating lipid classes is also possible (21). The selectivity of nonesterified fatty acid uptake is likely controlled by cytoplasmic fatty acid binding protein, fatty acid translocase, fatty acid transporter protein, and plasma membrane fatty acid binding protein (37).…”