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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 antiandrogen 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. Testicular IGF-I content was altered in all treatment groups with the most marked changes observed in animals receiving GnRH antagonist and flutamide (FL) with or without FSH (5 or 10 IU/rat twice a day; FSH5 and FSH10) (ANT + FL, 150·32 ± 7·38; ANT + FL + FSH5, 165·28 ± 5·92; ANT + FL + FSH10, 160·17 ± 11·73 vs 464·51 ± 36·04 ng/testis for controls; P < 0·05). Those animals treated with GnRH antagonist and/or FSH had testicular IGF-I levels which were significantly lower than controls and higher than the three groups receiving flutamide and antagonist. A highly significant correlation was established between intratesticular IGF-I and the number of pachytene, round and elongated spermatids per cross-section (r = 0·8 for all three germ cell types). The data presented here provide direct in-vivo evidence for the importance of Leydig cell–Sertoli cell interactions in regulating testicular IGF-I content and spermatogenesis in the testis.

Journal of Endocrinology (1993) 137, 81–89

This article has been cited by other articles:

				L. Gnessi, A. Fabbri, and G. Spera Gonadal Peptides as Mediators of Development and Functional Control of the Testis: An Integrated System with Hormones and Local Environment Endocr. Rev., August 1, 1997; 18(4): 541 - 609. [Abstract] [Full Text] [PDF]