Abstract
Previous studies in this laboratory demonstrated the presence of two populations of Leydig cells (I and II) in testes of mature rats. Leydig cells of the two populations have essentially the same number of LH receptors (as measured by [125I]hCG binding), but population II Leydig cells produce considerably more testosterone in vitro in response to hCG than do population I Leydig cells. In the present studies, we demonstrate that [125I]hCG-binding capacities of Leydig cells are essentially the same in the two populations from 25–55 days of age. Therefore, changes in [125I]hCG binding in populations I and II were used to evaluate changes in the distribution of Leydig cells between the two populations during sexual maturation. In addition, changes in basal and hCG-stimulated androgen production in vitro by Leydig cells of the two populations were studied. Early in sexual maturation, most of the Leydig cells in the rat testis are in population I, and the increase in the total number of Leydig cells results from increases in the numbers of Leydig cells in both populations. After about 40 days of age, the number of Leydig cells in population I declines while the number in population II continues to increase. Thus, during the latter part of sexual maturation, most of the Leydig cells in the rat testis are in population II. In immature rats (25 and 40 days of age), Leydig cells of both populations produce more androstanediol (5α-androstane- 3a,17β-diol) than testosterone, and population I Leydig cells produce more androstanediol and more testosterone in response to maximal hCG stimulation than do population II Leydig cells. In mature rats (55 days of age), in contrast, Leydig cells of both populations produce more testosterone than androstanediol, and population II Leydig cells produce more testosterone and more androstanediol in response to maximal hCG stimulation than do population I Leydig cells. The data demonstrate that during sexual maturation the shift in the preponderance of Leydig cells from population I to population II is accompanied by a parallel shift in the greater capacity for androgen production. These results suggest that population II Leydig cells are derived from population I Leydig cells.