336 



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PHYSIOLOGY OF GONADS 









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1 



Fig. 5.18. Testis of dog 60 days after hypophysectomy. (From C. Huggins and P. S. 

 Russell, Endocrinology, 39, 1, 1946.) 



(1952 ( showed that early differentiation of 

 spermatids in the rat is affected first by 

 hypophysectomy. Spermatids degenerate, 

 tubuhir fluid is lost, and atrophy of the 

 germinal epithelium finally takes place 

 (Gothie and Moricard, 1939). 



Some recent studies on comi^ensatory 

 hyi)ertrophy of the remaining testis after 

 unilateral orchiectomy have been made. 

 Old investigations showed that compensa- 

 tory hypertrophy occurs in boars, rabbits, 

 and hedgehogs. Compensatory hypertrophy 

 does not occur in mature guinea pigs or man 

 (Calzolari, Pulito and Pasquinelli, 1950; 

 Pasquinelli and Calzolari, 1951; Zide, 

 1939). In the prepubertal guinea pig and 

 rat, however, the remaining testis shows 

 accelerated development. The volume of the 

 remaining testis increases in the adult rat 

 after unilateral orchiectomy (Grant, 1956). 

 Since the compensatory hypertrophy is 

 suppressed by testosterone, it appears likely 

 that the accelerated development of the 

 remaining testis is mediated by gonado- 

 tropliins. 



The effects of gonadotrophins on testicu- 

 lar structure and function have been studied 

 in many species. Injection of anterior jHtui- 

 tary extract or implantation of fragments 

 of the anterior i)ituitary into the testis of 

 guinea pigs has residted in pronounced stim- 

 ulation and hypertr()])hy of the Leydig cells 



(Petrovitch, Weill and Deminatti, 1953; 

 Petrovic, Deminatti and Weill, 1954; Petro- 

 vic, Weill and Deminatti, 1954; Marescaux 

 and Deminatti, 1955). In hypophysecto- 

 mized mice, May (1955) found that testicu- 

 lar grafts of anterior pituitary tissue repair 

 the atrojihic tubules and the involuted Ley- 

 dig cells. 



The effects of in(li\i(lual gonadotrophins 

 of both pituitary and placental origin have 

 been reviewed by Greep (1937) and Fevold 

 (1944), and in the chapter by Greep in the 

 present volume. The established concept, 

 as worked out in the rat, is that follicle- 

 stimulating hormone (FSH) maintains and 

 repairs the tubular apparatus but does not 

 affect the function or structure of the Ley- 

 dig cells. Luteinizing hormone (LH) main- 

 tains the functional activity of the Leydig 

 cells but does not dii-ectly control tubidar 

 activity. 



Urinary gonadotrophin from menopausal 

 women stimulated the tubides (Greep, 1937) 

 and the Leydig cells (Balm. Lorenz, Ben- 

 nett and Albert, 1953a-d). Hmnan chorionic 

 gonadotropiiin (HCG) has little oi' no 

 effect on tiie tubules, hut it induces ])ro- 

 nounced stimulation of the Leydig cells. 

 Pr(>gnaiit marc sci'uni (PMS) stimulates 

 spermatogenic and endocrine activities of 

 the testis. Both LH and HCG maintain 

 spermatogcniesis after hypophysectomy. 



