No abstract

No abstract

No abstract

Intracellular lipolytic activity and lipoprotein lipase activity were determined in healthy human placental tissue, in placentas obtained from patients with severe pre-eclampsia, and from cases of intra-uterine growth retardation. The level of lipoprotein lipase, which is responsible for the transfer of fatty acids across membranes, was found to be much higher compared with the intracellular lipase and had increased further during pregnancy. Lipoprotein lipase activity was significantly greater in placentas of pre-eclamptic women and in the placentas of intra-uterine growth retarded fetuses. The intracellular lipolytic activity was significantly lower, however, than in controls. The levels of triglycerides and cholesterol were significantly higher in the cord blood of newbornes of women who had pre-eclampsia and in the intra-uterine growth retarded fetuses. The present study indicates that in situations causing fetal distress there are changes in the placenta leading to an increased supply of free fatty acids to the fetus. The role of lipids in fetal metabolism and their transfer across the placenta are poorly understood. The main precursor of fetal lipids in man is believed to be either carbohydrate (5) or maternal blood lipids (10). There is no evidence for the trans-placental flow of intact triglycerides. The plasma free fatty acids (FFA) constitute the only lipid fraction known to cross the placenta and could supply a significant proportion of the fetal requirements (8, 19).

Hypertriglyceridaemia was produced in rats by the intravenous infusion of Intralipid emulsion or of very low density (d < 1.006) rabbit or human lipoproteins (VLDL). Lipoprotein lipase activity was assayed, in tissues removed at the end of infusion, on serum‐activated mono‐ and triolein emulsions at pH 8.6. Hypertriglyceridaemia resulted in a marked decrease in epididymal adipose tissue lipoprotein lipase activity and in an increase in heart enzyme activity. These changes were evident with both mono‐ and triolein substrates. The effects on adipose tissue enzyme activity seemed roughly dependent on the triglyceride (TG) level and, relative to TG elevation, were most pronounced in the case of VLDL infusion. Serum lipoprotein lipase activity, measured in the absence of heparin, was considerably increased suggesting that the TG‐rich material “leached” the adipose tissue enzyme into the circulation. Leaching of lipoprotein lipase from adipose tissue by Intralipid emulsion or VLDL was also demonstrated in an in vitro system devoid of heparin. Contact with the TG‐poor, 1.006 < d < 1.063, lipoprotein induced only a small loss in adipose tissue lipoprotein lipase activity, either in vitro or in vivo. Intracellular lipolytic activity toward mono‐ and triolein, measured in adipose tissue and heart homogenates at pH 7.2 in the absence of serum, was not significantly affected by TG elevation. Thus, the observed changes in lipoprotein lipase activity seem unrelated to the intracellular lipolytic activity. It is suggested that the low adipose tissue lipoprotein lipase activity and the retarded TG removal observed in certain hypertriglyceridaemic conditions may be secondary to the increased supply of TG‐rich lipoproteins.