Effects of FSH and testosterone on intratesticular insulin-like growth factor-I and specific germ cell populations in rats treated with gonadotrophin-releasing hormone antagonist.

Evidence derived predominantly from a series of in-vitro studies indicates that insulin-like growth factor-I (IGF-I) plays an important role as a paracrine and autocrine regulator within the testis. We investigated the effects of FSH substitution on spermatogenesis and testicular IGF-I content in rats treated with gonadotrophin-releasing hormone (GnRH) antagonist (ANT) and injected with ethane dimethane sulphonate (EDS), a Leydig cell toxin. FSH treatment partially prevented the marked decrease in intratesticular IGF-I in rats treated with only GnRH antagonist but not in GnRH antagonist+EDS-treated animals (controls, 191.0 +/- 4.5; ANT, 80.1 +/- 5.6; ANT+EDS, 81.6 +/- 3.4; ANT+EDS+FSH, 86.3 +/- 1.4; ANT+FSH, 137.7 + 7.3 (S.E.M.) ng/testis). Correlation analysis of testicular IGF-I content with the number of pachytene spermatocytes and round spermatids per cross-section revealed r values of 0.77 and 0.74 respectively (P < 0.001). We then analysed the same parameters in GnRH antagonist-treated rats which, in addition, received daily injections of the anti-androgen flutamide, in order to investigate the potential role of testosterone, as opposed to other Leydig cell products, in the regulation of spermatogenesis and testicular IGF-I. FSH treatment prevented regression of spermatogenesis in rats treated with GnRH antagonist alone but not in GnRH antagonist- and flutamide-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)