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There is increasing evidence implicating growth factors in the regulation of spermatogenesis and in-vitro studies have shown that epidermal growth factor (EGF) and insulin-like growth factor-I (IGF-I) interact with the gonadotrophins in regulating testicular function. In the present study, the effect of FSH, testosterone and GH treatment on serum IGF-I and intratesticular EGF and IGF-I concentrations in adult male hypophysectomized rats treated with ethane dimethane sulphonate (EDS) to destroy Leydig cells has been investigated. Hypophysectomy alone or followed by EDS treatment was associated with a significant increase in intratesticular EGF concentrations compared with normal controls (P<0·05). Treatment of hypophysectomized animals with a combination of GH, FSH and testosterone resulted in a return of intratesticular EGF concentrations to normal control levels. In a second group of animals treated with a 5 cm silicone elastomer implant of testosterone and FSH, intratesticular EGF concentrations were also not significantly different from those of normal controls. Following hypophysectomy alone or hypophysectomy and EDS treatment, a significant increase in circulating IGF-I concentrations occurred, which was only reversed following the administration of GH. In addition, increases in testicular IGF-I concentrations were evident in all treated animals compared with controls, an effect which was only partially reversed in animals treated with a combination of FSH and testosterone (1·5 or 5 cm implant). Similar results were obtained with a combination of GH and FSH or GH and testosterone, although GH alone had no effect on testicular IGF-I concentrations. A combination of GH, FSH and testosterone restored testicular IGF-I to concentrations not significantly different from controls. It is suggested that GH, FSH and testosterone can play an important role in regulating circulating and testicular IGF-I and testicular EGF in the adult rat, but the regulation of growth factor production is a complex process and a number of other factors are probably involved in vivo.
Journal of Endocrinology (1991) 129, 109–117
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