Placental lipoprotein lipase activity in the rabbit, rat and sheep

Clegg, Roger A.

doi:10.1016/0305-0491(81)90353-9

Cited by 9 publications

(7 citation statements)

References 11 publications

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“…Triacylglycerol hydrolase activity at pH 8.0 was almost 84 þ 7.3% released (24.19 þ 0.26 pmol oleic acid/mg protein/min) from the membranes (initial activity 27.19 þ 4.27 pmol oleic acid/mg protein/min) by heparin treatment whereas the activity at pH 6.0 (initial activity 75.14 þ 7.6 pmol oleic acid/mg protein/min), however, was only partially (47.0 þ 19.7%) released ( Table 1). Since lipoprotein lipase is readily released from membranes by heparin [21,22], this indicates that placental MVM contain a unique non-heparinreleasable triacylglycerol hydrolase with pH optima at 6.0, in addition to heparin-releasable triacylglycerol hydrolase with pH optima 8.0.…”

Section: Di¡erentiation Of the Triacylglycerol Hydrolase Activities Imentioning

confidence: 99%

Characterisation of triacylglycerol hydrolase activities in human placenta

Waterman

Emmison

Duttaroy

1998

Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metaboli

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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.

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Section: Di¡erentiation Of the Triacylglycerol Hydrolase Activities Imentioning

confidence: 99%

Characterisation of triacylglycerol hydrolase activities in human placenta

Waterman

Emmison

Duttaroy

1998

Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metaboli

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“…Since the first report in 1966 that lipopro tein lipase (LPL) was present in human and rat placenta [38], placental LPL has been described in numerous other species [39][40][41][42], but its presence has not been confirmed in humans. For this reason, we have re examined human placental tissue for evi dence of LPL activity in the metabolism of triglycerides to FFA.…”

Section: Placental Lipoprotein Lipase Activity and The Effect Of Diabmentioning

confidence: 99%

Lipoprotein Metabolism in Pregnancy, Fat Transport to the Fetus, and the Effects of Diabetes

et al. 1986

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The objective of this paper is to review the extent and mechanisms of lipoprotein alterations in pregnancy, present new data relating to placental lipid transport in. normal humans and diabetic animals and consider possible effects on fetal growth and development in normal and diabetic pregnancy. The concentration of all lipoprotein fractions increases during pregnancy. VLDL cholesterol and triglyceride increase 2.5-fold over prepregnancy levels and LDL cholesterol increases 1.6-fold, all with peak levels at term. HDL cholesterol is maximally increased in midgestation by 1.45-fold and subsequently declines to 1.15-fold at term. The mechanisms of these lipoprotein changes have not been studied in humans but the hypertriglyceridemia in animal models is related to enhanced VLDL entry into the circulation. In addition, diminished adipose tissue lipoprotein lipase (LPL) activity in late gestation may cause a rerouting of triglyceride fatty acids to other tissues such as muscle and uterus for oxidation, rather than storage, since triglyceride transport is not reduced in pregnancy. All of these changes appear to be sex hormone mediated. In diabetic pregnancies, the available data indicate that triglyceride concentrations are increased and HDL cholesterol concentrations are decreased with reference to lipoproteins in nondiabetic pregnant women. Previously unpublished data show that a transplacental FFA gradient exists across the umbilical circulation in the direction of the fetus and is proportional to the maternal FFA concentration. No gradient is seen for triglyceride or total plasma cholesterol. However, transport of unmeasured amounts of triglyceride fatty acids may still occur via placental LPL and be exaggerated in diabetes where LPL declines in adipose tissue but not in placenta. The mechanism of transplacental cholesterol transport remains to be defined. Preliminary studies suggest that it depends on HDL as well as LDL since both can provide cholesterol for placental progesterone synthesis. In addition, fetal weight and length are associated with maternal apoproteins A-I and A-II, both major apoproteins of HDL. By lowering HDL in pregnancy, diabetes mellitus could negatively affect these relationships. In conclusion, sex hormone mediated modifications of lipoprotein physiology are described in pregnancy which may enhance triglyceride fatty acid transport to muscle for oxidation and LDL and HDL cholesterol delivery to growing maternal and fetal tissues, a process that diabetes could globally disrupt.

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“…To investigate the importance of these en zymes in providing FFA for the developing fetus we modified the lipase assay of Nilsson-Ehle and Schotz [6] to enable us to assay simultaneously placental lipase activities at pH 4 (the optimal pH for one of the intracel lular lipases [4,5]) and at pH 8 (the optimal pH for the lipoprotein lipase-like enzyme [3]). Using this method we have investigated whether growth retardation in the rat in duced either by maternal undemutrition or uterine artery ligation alters placental lipase activities as fetal body fat at birth is reduced in both situations [7,8],…”

Section: Introductionmentioning

confidence: 99%

“…Lipid may be transferred from the mother to the fetus across the placenta in the form of free fatty acids (FFA), derived either directly from maternal albumin-bound FFA [1] or from maternal very low density lipoprotein (VLDL) hydrolysed by placental lipases, with the release of fatty acids [2], The pla centa contains a lipoprotein lipase-like en zyme, which hydrolyses the maternal VLDL [3] and also intracellular lipases which hy drolyse stored placental triglyceride [4,5]. To investigate the importance of these en zymes in providing FFA for the developing fetus we modified the lipase assay of Nilsson-Ehle and Schotz [6] to enable us to assay simultaneously placental lipase activities at pH 4 (the optimal pH for one of the intracel lular lipases [4,5]) and at pH 8 (the optimal pH for the lipoprotein lipase-like enzyme [3]).…”

Section: Introductionmentioning

confidence: 99%

Effects of Maternal Undernutrition and Uterine Artery Ligation on Placental Lipase Activities in the Rat

Kaminsky¹,

D'Souza²,

Massey³

et al. 1991

Neonatology

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Lipase activities measured at pH 4 and 8 were determined in the placentas of rats subjected to undernutrition or uterine artery ligation. The fetal lipid content following maternal undernutrition was also determined. The placental lipase activity (per gram placenta) measured at pH 8 (placental lipoprotein lipase) remained unchanged, whilst the activity of the intracellular lipase (per gram placenta) measured at pH 4 was significantly less than in the control group (21 % lower in maternal undernutrition and 16 % lower after uterine artery ligation). Although placentas and fetuses were significantly lighter in both situations as compared to controls (well-nourished or sham operated, respectively), fetal lipid content in maternal undernutrition was only reduced to a degree concomitant with the decrease in fetal weight. We therefore conclude that the intracellular lipase may not have an important role in the provision of free fatty acids in undernutrition.

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Placental lipoprotein lipase activity in the rabbit, rat and sheep

Cited by 9 publications

References 11 publications

Characterisation of triacylglycerol hydrolase activities in human placenta

Characterisation of triacylglycerol hydrolase activities in human placenta

Lipoprotein Metabolism in Pregnancy, Fat Transport to the Fetus, and the Effects of Diabetes

Effects of Maternal Undernutrition and Uterine Artery Ligation on Placental Lipase Activities in the Rat

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