Lipid dismetabolism in Leydig and Sertoli cells isolated from streptozotocin-diabetic rats.

This work evaluates how the abnormalities in fatty acid biosynthesis, already described in diabetic rats, were extended to Sertoli and Leydig cells isolated from testes of streptozotocin-treated rats. Both kinds of cells were incubated in the presence of labeled eicosa-8,11,14-trienoic acid. The uptake of the substrate and its conversion to arachidonic acid were significantly depressed in both cell types compared to the non-diabetic controls. The indirect evidence of this inhibition was observed in the total fatty acid pattern of the cells where the 20:4 n-6/18:2 n-6 ratio was significantly decreased. The addition of insulin to the incubation medium produced no changes in the uptake of the substrate by the cells. Under similar experimental conditions the synthesis of arachidonic acid was partially recovered, however, the values obtained were still below those ones of cells isolated from control animals. These results were correlated with the fatty acid profile of different lipid fractions of plasma and with the activity of enzymes involved in polyunsaturated fatty acids biosynthesis measured in the testicular microsomes of diabetic rats. We conclude that Sertoli and Leydig cells evidenced similar lipid disorders than those observed in the whole testis or in other tissues of diabetic rats, and that the biosynthesis of arachidonic acid is under insulin regulation.