NUTRITIONAL EFFECTS 



677 



tocopherol deprivation, observed cytologic 

 changes in the hypophysis which preceded 

 testis changes. The "peripheral or FSH 

 gonadotrophes" increased in number, size, 

 and activity. The LH cells exhibited a 

 hyperplasia of lesser extent, but possibly 

 sufficient to increase LH in circulation and 

 to cause hypertrophy of the male accessory 

 glands. Gonadotrophic hormone content of 

 pituitary glands from vitamin E-deficient 

 rats may be decreased (Rowlands and 

 Singer, 1936), unchanged (Biddulph and 

 Meyer, 1941), or increased to a level be- 

 tween normal and that of the castrate, when 

 the adult male rats were examined after 22 

 weeks on a deficient diet (Nelson, 1933; 

 Drummond, Noble and Wright, 1939). 

 Using hypophysectomized male rats as as- 

 say animals, evidence was obtained that 

 FSH was increased in the pituitary glands 

 of vitamin E-deficient male and female rats 

 (P'an, Van Dyke, Kaunitz and Slanetz, 

 1949). 



IV. Male Reproductive System 



A. TESTIS 



The two basic functions of the male 

 gonads are to produce gametes and secrete 

 steroids. Spermatogenic activity can be 

 estimated from testis morphology and ex- 

 amination of semen samples. Androgen se- 

 cretion can be estimated from urinary ster- 

 oid levels, accessorj^ gland weight, and 

 from analyses of accessory sex gland secre- 

 tions, i.e., fructose and citric acid. In nor- 

 mal maturation in the rabbit, rat, boar, 

 and bull, androgen secretion precedes sper- 

 matogenesis (Lutwak-Mann, 1958). On this 

 basis it would appear that well fed young 

 bulls may come into semen production 2 to 

 3 months sooner than poorly fed animals 

 (Brat ton, 1957). 



1. Inanition 



Complete starvation will pre^•ent matura- 

 tion of immature animals. Furthermore, 

 marked undernutrition in 700 boys, 7 to 16 

 years of age, was associated with genital 

 infantilism in 37 per cent and crypt- 

 orchidism in 27 per cent (Stephens, 1941). 

 Restriction of food intake to one-half of the 

 normal in maturing bull calves had a 



marked delaying effect on the onset of 

 seminal vesicle secretion, but a lesser de- 

 laying effect on spermatogenesis (Davies, 

 Mann and Rowson, 1957) . Limiting the food 

 intake to one-third of the normal did not 

 prevent the immature rat testis from form- 

 ing spermatozoa at the same time as their 

 controls (Talbert and Hamilton, 1955). 

 When testis maturation was prevented by 

 inanition, a rapid growth and maturation 

 occurred on refeeding (Ball, Barnes and 

 Visscher, 1947; Quimby, 1948) but Schultze 

 (1955) observed that full body size was not 

 attained. 



The reproductive organs of the adult are 

 more resistant to changes imposed by diet 

 than are those of the immature animal. 

 Thus, Mann and Walton (1953) found that 

 23 weeks of underfeeding produced little 

 change in sperm density and motility in ma- 

 ture animals although seminal vesicle func- 

 tion was reduced. Li the male rat testis 

 hypofunction follows partial or complete 

 starvation (]\Iason and Wolfe, 1930; Muli- 

 nos and Pomerantz, 1941a; Escudero, Her- 

 raiz and Mussmano, 1948), but there is no 

 reduction in testicular nitrogen (Addis, Poo 

 and Lew, 1936). Loss of Leydig cell func- 

 tion precedes cessation of spermatogenesis 

 (Moore and Samuels, 1931) and is evident 

 by the atrophy of the accessory sexual or- 

 gans (^lulinos and Pomerantz, 1941a) and 

 by an alteration in accessory gland secretion 

 (Pazos and Huggins, 1945; Lutwak-]\Iann 

 and Mann, 1950). Evidence of a tubular 

 effect is provided by the lack of motile 

 sperm (Reid, 1949). Severe dietary re- 

 striction is associated with the absence of 

 spermatozoa in the seminiferous tubules and 

 epididymis (Mason, 1933; Menze, 1941). 



The human male suffering from chronic 

 malnutrition exhibits hypogonadism. The 

 testes atrophy and exhibit a decrease in size 

 of the seminiferous tubules; basement mem- 

 brane thickening and small Leydig cells 

 are seen. These individuals excrete signifi- 

 cantly subnormal amounts of 17-ketoster- 

 oids (Zubiran and Gomez-Mont, 19531. 

 Acute starvation may also decrease urinary 

 17-ketosteroid and androgen levels as much 

 as 50 per cent, with recovery evident on re- 

 feeding (Perloff, Lasche, Nodine, Schnee- 

 berg and Vieillard. 1954). 



