LEYDIG-CELLS INCREASE THEIR NUMBERS BUT DECLINE IN STEROIDOGENIC FUNCTION IN THE ADULT-RAT AFTER NEONATAL-HYPOTHYROIDISM

Citation
Mp. Hardy et al., LEYDIG-CELLS INCREASE THEIR NUMBERS BUT DECLINE IN STEROIDOGENIC FUNCTION IN THE ADULT-RAT AFTER NEONATAL-HYPOTHYROIDISM, Endocrinology, 132(6), 1993, pp. 2417-2420
Citations number
22
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
00137227
Volume
132
Issue
6
Year of publication
1993
Pages
2417 - 2420
Database
ISI
SICI code
0013-7227(1993)132:6<2417:LITNBD>2.0.ZU;2-T
Abstract
Administration of the goitrogen, 6-propyl-2-thiouracil (PTU), to suckl ing rat pups from birth through day 24 postpartum as a 0.1% solution i n the mother's drinking water increases adult testis size and sperm pr oduction by about 80% and 140%, respectively, without affecting periph eral testosterone levels. The objectives of this study were to determi ne whether adult Leydig cell numbers were altered in PTU-treated rats and whether the steroidogenic function of these cells was normal. The number of Leydig cells per testis at 180 days increased by 69% in PTU- treated compared to control rats, whereas the average Leydig cell volu me declined by about 20%. Steroidogenic function assessed in isolated adult Leydig cells decreased after neonatal PTU treatment. LH-stimulat ed testosterone production was reduced by 55% in Leydig cells from tre ated rats, commensurate with a 50% decline in the number of hCG-bindin g sites in these cells. The difference in steroidogenic potential was even more striking after incubations with saturating concentrations of steroid substrate, 22(R)-hydroxycholesterol; Leydig cells from treate d males produced 73% less testosterone than controls. Therefore, this decrease in testosterone production may be partially due to a reductio n in the numbers of LH receptors, but also reflects the impaired stero idogenic potential of these cells. These results clearly show that the dramatic increase in adult Leydig cell number after neonatal PTU trea tment is counterbalanced by a permanent decline in Leydig cell steroid ogenic function, producing no net change in peripheral testosterone le vels.