BASAL TESTOSTERONE SECRETION AND RESPONSE TO HUMAN LUTEINIZING, FOLLICLE-STIMULATING, AND GROWTH-HORMONES IN CULTURE OF CELLS ISOLATED FROMTESTES OF INFANTS AND CHILDREN
E. Berensztein et al., BASAL TESTOSTERONE SECRETION AND RESPONSE TO HUMAN LUTEINIZING, FOLLICLE-STIMULATING, AND GROWTH-HORMONES IN CULTURE OF CELLS ISOLATED FROMTESTES OF INFANTS AND CHILDREN, Pediatric research, 38(4), 1995, pp. 592-597
Little is known on the hormonal regulation of the early postnatal phas
e of Leydig cell activation in the human. Testosterone secretion by pr
epubertal testicular cells in culture was studied in two different age
groups, 0-7-mo-old (group 1) and 16-36-mo-old (group 2) boys. A mixed
cell preparation was isolated from testes collected at necropsy and m
aintained in culture for 6 d. Cells were cultured in serum-free medium
in basal conditions and under the stimulation of human (h)LH, hFSH, o
r recombinant hGH, and the secretion of testosterone was determined on
d 6 by RIA. in basal conditions, cells of group 1 secreted more testo
sterone (median 5.83 pmol/10(6) cells d, it = 7) than cells of group 2
(median 1.73, n = 5), p < 0.05, reflecting the steroidogenic potentia
l of the testes in vivo. Under hLH stimulation, cells of group 1 respo
nded by increasing testosterone secretion significantly. Surprisingly,
hFSH stimulation elicited a similar response in cells of group 1. Bec
ause FSH receptors are presumably located in Sertoli cells, it is conc
luded that these cells secreted a paracrine factor that stimulated tes
tosterone secretion by Leydig cells. On the other hand, recombinant hG
H also stimulated the secretion of testosterone by cells of group 1. R
ecombinant hGH could have interacted with either GH or prolactin recep
tors of testicular cells. Cells of group 2 did not respond to any stim
ulus. Because serum levels of LII, FSH, GH, and prolactin are higher d
uring the first months of life than later in childhood, it is possible
that the early postnatal activation of the testis is under multiple p
ituitary hormone influence.