67G 



PHYSIOLOGY OF GONADS 



adequate dietary protein (Friedman and 

 Friedman, 1940). 



When anterior pituitar}^ glands of 60- 

 gm. male rats were extracted and adminis- 

 tered to immature female recipients, ovarian 

 weight increased from 13.0 to 37.3 mg. 

 After feeding 20 per cent casein or fox chow 

 ad libitum for 14 days, the hypophyses of 

 male rats contained almost twice as much 

 gonadotrophin per milligram of tissue as 

 did the hypophyses of the initial controls. 

 Removal of protein from the diet for 14 

 days, however, reduced hypophyseal gona- 

 dotrophin concentration below the level 

 of the initial controls (Leathem and Fisher, 

 1959). 



Data on the hypophyseal hormone con- 

 tent as influenced by specific amino acid 

 deficiencies have not come to the author's 

 attention. Cytologically, however, Scott 

 (1956) noted that an isoleucine-deficient 

 diet depleted the pituitary gonadotrophic 

 cells of their PAS-positive material and re- 

 duced the size of acidophilic cells. Omission 

 of threonine, histidine, or tryptophan in- 

 voked similar effects. The changes prob- 

 ably represent the interference of a single 

 amino acid deficiency with protein metab- 

 olism rather than specific effects attribut- 

 able to the lack of amino acid itself. Exces- 

 sive amino acid provided by injecting 

 leucine, methionine, valine, tyrosine, or 

 glycine caused release of gonadotrophin 

 (Goth, Lengyel, Bencze, Saveley and Maj- 

 say, 1955). 



Administration of 0.1 mg. stilbestrol for 

 20 days to adult male rats eliminated de- 

 tectable hypophyseal gonadotrophins. Hor- 

 mone levels returned during the postinjec- 

 tion period provided the diet contained 

 adequate protein, whereas a protein-free diet 

 markedly hindered the recovery of hypo- 

 physeal gonadotrophins. The gonadotrophin 

 content of the pituitary gland correlated 

 well with the recovery of the reproductive 

 system, indicating that gonadotrophin pro- 

 duction was subnormal on ]irotein-free feed- 

 ing (Leathem, 1958a). 



C. CAHBOHYDR.\TE .\ND FAT 



Reproduction does not appear to be in- 

 fluenced by carbohydrates per se and hy- 

 pophyseal alterations have not been noted. 



Fat-deficient diets, however, do influence 

 reproduction and the hypophysis exhibits 

 cellular changes. Pituitary glands of fe- 

 male rats fed a fat-free diet contain a sub- 

 normal number of acidophiles and an in- 

 creased number of basophiles (Panos and 

 Finerty, 1953) . In male rats the feeding oi 

 a fat-free diet increased hypophyseal baso- 

 philes, followed progessively by more cas- 

 tration changes (Finerty, Klein and Panos, 

 1957; Panos, Klein and Finerty, 1959). 



D. VITAMINS 



Despite the many investigations relating 

 reproduction to vitamin requirements, rela- 

 tively few have involved hypophyseal hor- 

 mone estimations. Thus in 1955, Wooten, 

 Nelson, Simpson and Evans reported the 

 first definitive study which related pyri- 

 doxine deficiency to hypophyseal gonado- 

 trophin content. Using the hypophysec- 

 tomized rat for assay, pituitary glands 

 from Bo-deficient rats were shown to have 

 a 10-fold increase in FSH per milligram of 

 tissue and a slightly increased LH content. 

 Earlier studies had revealed that vitamin 

 Bi-free diets decreased pituitary gonado- 

 trophins in male rats (Evans and Simpson, 

 1930) and a similar effect of the folic acid 

 antagonist, aminopterin, in the monkey was 

 found later (Salhanick, Hisaw and Zar- 

 row, 1952). 



Male rats deficient in vitamin A exhibited 

 a 43 per cent increase, and castrated vitamin 

 A-deficient rats a 100 per cent increase in 

 hypophyseal gonadotrophin potency over 

 the normal controls (Mason and Wolfe, 

 1930). The increase of gonadotrophin was 

 more marked in vitamin A-deficient male 

 than in vitamin A-deficient female rats. 

 Associated with the increase in hormone 

 level was a significant increase in basophile 

 cells (Sutton and Brief, 1939; Hodgson, 

 Hall, Sweetman, Wiseman and Converse, 

 1946; Erb, Andrews, Hauge and King, 

 1947). 



A re\-iew of the literature up to 1944 per- 

 mitted Mason to suggest that the anterior 

 hypophysis was not the instigator of re- 

 productive disturbances in vitamin E de- 

 ficiency. Nevertheless, Griesbach, Bell and 

 Livingston (1957), in an analysis of the 

 pituitary gland during progessive stages of 



