Until recently, the precursors of Leydig cells were believed to be of mesenchymal origin and derived from cells in the mesonephros (primitive kidney) (14-16). However, recent tissue recombination studies do not support the hypothesis that precursor cells migrate into the interstitium from the mesonephros, and ontogeny from the embryonic neural crest has been suggested (17). By the sixth week of gestation, seminiferous cord formation within the gonadal blastema simultaneously creates the outer interstitial compartment (18). Fetal Leydig cells become identifiable in this compartment among the undifferentiated mesenchymal cells at 8 wk of gestation (19). Then, Leydig cell numbers increase continuously and reach a maximum by 14 to 15 wk, when they fill the space between the cords and comprise more than half the volume of the fetal testis. Although testosterone is first detectable in the testis as early as 6 to 7 wk of gestation (20), the sharp increment in the numbers of fetal Leydig cells is accompanied by further rises in androgen concentrations in testicular tissue, blood, and amniotic fluid, which reach a maximum at week 15 (21). After the 16th wk of gestation, the numbers of fetal Leydig cells, serum testosterone concentrations, and testicular mRNA levels for at least two of the testosterone biosynthetic enzymes, P450scc and P45017a, decline (21-23). At birth, the total number of Leydig cells per testis is 60% lower compared to the prenatal peak, and the remaining Leydig cells are half the size (21).
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