Animal experiments and clinical studies on the interactions between growth hormone (GH) and the male hypothalamic-pituitary-gonadal axis have predominantly concentrated on GH and sex steroid interactions in the regulation of growth and development, or on the metabolic effects of GH. In contrast, little attention has been paid to the possible effects of GH on spermatogenesis, although the first report dealing with this topic was published almost 30 years ago. The interactions of GH and its main mediator, insulin-like growth factor I (IGF-I), with the hypothalamic-pituitary-gonadal axis, and their role in spermatogenesis have recently been investigated using in vitro systems and different animal models (mice and rats). Using Leydig and Sertoli cell cultures, complex interactions between GH/IGF-I and the gonadotropins affecting differentiated cell functions, e.g. steroidogenesis and cell division, have been demonstrated at the cellular level. In vivo studies using immature and mature hypophysectomized rats and GH-deficient mutant male mice and rats indicate that IGF-I can play an important role in the regulation of steroidogenesis and spermatogenesis. Furthermore, although follicle-stimulating hormone and luteinizing hormone are the major regulators of testicular IGF-I production, GH may play an indirect role by potentiating the actions of the gonadotropins in regulating testicular IGF-I content. A large proportion of men presenting at male-infertility clinics are diagnosed as having idiopathic infertility. Further studies are necessary to investigate whether defects associated with GH and/or IGF-I effects in the testis are the cause of male infertility in a small group of these patients.
Scrotal temperature was monitored using a portable data recorder for periods of 24 h in six normal volunteers and 48 infertile patients with unilateral varicocele while subjects pursued their regular daily activities. Temperatures during sleep (TS) were generally higher than daytime values (TD), probably as a consequence of thermal insulation in bed. These diurnal variations were found to be less pronounced in the infertile patients than in volunteers (TS - TD = 0.29 degrees C +/- 0.06 degrees C vs 0.88 degrees C +/- 0.12 degrees C; P < 0.01). Moreover, scrotal temperatures at night of patients and volunteers were indistinguishable statistically, but were different during daytime hours. After successful ligation or embolization of the spermatic-vein in 16 patients, no change in scrotal temperature was observed. Although sperm counts were higher after treatment, this difference was not significant (67.4 +/- 17.2 x 10(6) vs 105.8 +/- 25.5 x 10(6); P > 0.05). The data support the view that varicocele-related damage to the testis results from a lack of adequate cooling, and that treatment does not normalize the temperature pattern.
Stage synchronization of seminiferous epithelium after withdrawal and replenishment of vitamin A provides a valuable and powerful approach to the investigation of paracrine interactions within the testis. However, since the discovery of this model, little attention has been given to the events surrounding the synchronous reinitiation of spermatogenesis after depletion of vitamin A. Synchronization of spermatogenesis was observed in all animals previously deficient in vitamin A. However, the degree of synchrony observed, as assessed by a ratio of synchrony, decreased markedly with time. The possibility that spermatogenic synchrony decreases with time due to variability of the temporal duration of stages of the cycle of the seminiferous epithelium is supported by this observation. However, long-term studies are required to substantiate this point. After initiation of stage synchrony of spermatogenesis, increased testicular concentrations of epidermal growth factor (EGF) were observed in testes synchronized between stages IX-II than at other stages of the cycle of the seminiferous epithelium. This elevation in testicular EGF concentrations correlated well with mitotic division of type A spermatogonia at stages IX, XII, and XIV of the cycle of the seminiferous epithelium. Previous in vitro studies have implicated an EGF-like factor in the stimulation of type A spermatogonial division in the mouse. A significant increase in testicular insulin-like growth factor I (IGF-I) concentrations was observed in control animals 14 days after the injection of retinol acetate. In vitamin A deficient animals, a marked increase in testicular IGF-I concentrations was observed as compared to age-matched controls. Maximal levels of testicular IGF-I concentrations were present 14 and 28 days and again 126 days after re-supplementation with retinol acetate. No stage dependent changes in testicular IGF-I were observed but the data provided suggest the retinol may be one of the factors involved in the regulation of testicular IGF-I.
GH plays a major role in pubertal growth, effects mainly mediated by stimulation of insulin-like growth factor-I (IGF-I) production by the liver. However, the role of GH in the regulation of pubertal onset, spermatogenesis and fertility is still under debate. GH and FSH have, in addition, been implicated in the regulation of IGF-I production by Sertoli cells in a number of studies, although conflicting results have been reported. The interpretation of studies using GH-deficient mutant mice has been complicated by the presence of additional defects in the hypothalamic-pituitary-gonadal axis of these animals. We have therefore used GH-deficient mutant male rats with no other documented hormonal deficiencies to study the effect of GH administration on somatic and testicular development, circulating and testicular IGF-I concentrations and testicular histology. Body weights in GH-deficient rats substituted with GH were not significantly different from untreated or GH-treated normal rats and were significantly higher than body weights in untreated dwarf rats. Similarly, circulating IGF-I concentrations in GH-treated GH-deficient rats were not significantly different from those in untreated or GH-treated normal rats but were significantly higher than circulating IGF-I concentrations in untreated dwarf rats. No differences in testicular IGF-I concentrations were observed in any of the groups studied. Testicular weights remained low in both untreated and GH-treated GH-deficient animals compared with control animals but spermatogenesis was qualitatively and quantitatively normal in all groups at the end of the observation period.(ABSTRACT TRUNCATED AT 250 WORDS)
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