Accumulation and mobilization of triglycerides and cholesteryl esters in Leydig tumor cells

Incubating MA-10 Leydig tumor cells with sodium oleate led to the accumulation of triglyceride within the cells. Triglycerides were deposited in a time- and dose-dependent fashion. Cellular triglyceride promoted storage of cholesteryl ester. As much cholesteryl ester was stored in oleate-treated cells as in cells treated with saturating concentrations of low density lipoprotein. Addition of both oleate and low density lipoprotein resulted in additive accumulation of cholesteryl esters. Cholesteryl esters in cells loaded with triglyceride by oleate treatment were mobilized in response to dibutyryl-cAMP to an extent similar to that in cells containing low triglyceride concentrations. Dibutyryl-cAMP stimulated cholesteryl ester mobilization under all conditions, and stimulated triglyceride mobilization when adequate fatty acid acceptors were available. The results indicate that while triglyceride accumulation in MA-10 cells promoted cholesteryl ester deposition, it did not impair cAMP-dependent cholesteryl ester hydrolysis or steroid hormone production.