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Phospholipid Metabolism in Cells from Highly Luteinized Rat Ovaries¹

Departments of Obstetrics and Gynecology and Physiology, University of Pennsylvania School of Medicine Philadelphia, Pennsylvania 19174

Abstract

Collagenase-dispersed cells from superovulated rat ovaries were studied to determine whether LH induces acute changes in ovarian polar lipid metabolism. Exposure of cell suspensions to LH (1 µg/ml) for 2 h caused no change in cell lipid phosphorus content. In vitro incorporation of ³²P, [U-¹⁴C]glucose and [l-¹⁴C]oleate into the phospholipid fractions of cells was not altered by LH, but a small, significant increase in [U-¹⁴C]acetate incorporation into total polar lipids was induced by LH. In all studies with labeled compounds, phosphatidylcholine, the predominant phospholipid in superovulated rat ovaries, was most heavily labeled. With ¹⁴C-labeled acetate, oleate and glucose, phosphatidylethanolamine, the second most prominent phospholipid, was the second most labeled class, but with ³²P, the phosphatidylinositol/phosphatidylserine fraction contained the second greatest radioactivity. LH had no effect upon distribution of ³²P, [U-¹⁴C]glucose or [l-¹⁴C]oleate into various phospholipids. LH produced small increases in [U-¹⁴C]- acetate incorporation into all phospholipid classes, but the increase was only statistically significant in sphingomyelin. Analysis of fatty acids in total phospholipid fractions of cells exposed to LH for 2 h revealed a decrease in the weight percentage of palmitate and some slight, but not statistically significant, increases in weight percentages of longchain and unsaturated fatty acids. LH caused a 3.5- fold increase in secretion of progesterone by cell suspensions and a significant reduction in [U-¹⁴C]- acetate incorporation into sterols and sterol esters. Incorporation of [l-¹⁴C]oleate into sterol esters was also reduced by LH. We conclude that LH has no striking acute effect on phospholipid metabolism and that the observed alterations in ovarian polar lipids in response to LH may reflect redistribution of acyl moieties as a result of LH regulation of sterol ester metabolism.

Footnotes

¹ Supported by a grant from the Rockefeller Foundation and by N.I.H. grant HD 10451.

Received March 7, 1977.