Evidence for a major role of inhibin in the feedback control of FSH in the male rat

Publisher Website
Google Scholar
Abstract
Adult rats (16-18/group) received a single intratesticular injection of 25, 100 or 400 .mu.l glycerol solution (7:3 in distilled water, v/v). half of the rats in each group were given implants of testosterone, a testosterone-filled Silastic capsule (1.5 cm length) to provide serum values of testosterone within the normal range. After 1 week all animals were killed by decapitation. Serum concentrations of gonadotrophins, testosterone and immunoactive inhibin as well as testicular concentrations of testosterone and bioactive inhibin determined. Testicular histology was studied in Paraplast-embedded tissue stained with PAS and haematoxylin-eosin. Glycerol treatment caused a dose-dependent ablation of spermatogenesis in a distinct area around the site of injection. Serum concentrations of FSH increased proportionally with increasing spermatogenic damage while serum LH and testosterone remained unaltered except with the highest glycerol dose. The rise in serum FSH was significantly correlated with serum (r = -0.70, P < 0.001) and testicular (r - 0.66, P < 0.001) concentrations of inhibin. A less pronounced correlation was found between LH and serum inhibin (r = 0.48). No correlation was found between the concentrations of LH and testicular inhibin or between serum concentrations of FSH and serum testosterone in the 25 and 100 .mu.l groups. Maintenance of low to normal serum testosterone concentrations by means of Silastic implants blocked the elevation of FSH in glycerol-treated animals but failed to affect significantly serum FSH in untreated rats. In all testosterone treated rats testicular inhibin concentrations were markedly reduced in the presence of lowered concentrations (7-14%) of testicular testosterone and unaltered serum FSH concentrations. These findings indicate that (i) inhibin is involved in the in-vivo regulation of FSH secretion in the adult male rat, (ii) testicular inhibin content, at least in part, may be regulated at the testicular level, and (iii) serum inhibin concentrations to some extent reflect the extent of damage to spermatogenesis and Sertoli cells.