NUTRITIONAL EFFECTS 



683 



in weight may be subnormal in mice and 

 rats (Goldsmith, Nigrelli and Ross, 1950; 

 Kline and Dorfman, 1951a, Grayhack and 

 Scott, 1952), or above normal in chickens 

 (Breneman, 1940). Complete deprivation 

 of food reduced the quantity of prostatic 

 fluid in the dog, but exogenous androgen re- 

 stored the volume, increased acid phospha- 

 tase, and induced tissue growth (Pazos and 

 Huggins, 1945) . 



6. Protein. The response of the seminal 

 vesicles to androgen was investigated in im- 

 mature rats, using weight and /5-glucuroni- 

 dase as end points. Castration and 10 days 

 on a protein-free diet preceded the 72-hour 

 response to 0.25 mg. testosterone propionate. 

 The lack of protein did not prevent a nor- 

 mal weight increase, and enzyme concentra- 

 tion was unchanged. If an 18 per cent diet 

 was fed during the 3-day period that the 

 androgen was acting, no improvement in 

 weight response was noted, but enzyme con- 

 centration increased 100 per cent. Thus, 

 when protein stores are depleted, the andro- 

 gen response may be incomplete in the ab- 

 sence of dietary protein (Leathern, 1959c). 

 Nevertheless, varied protein levels do not 

 influence seminal vesicle weight-response 

 when caloric intake is reduced (Rivero- 

 Fontan, Paschkis, West and Cantarow, 

 1952). 



c. Vitamins. Vitamin deficiencies do not 

 prevent the seminal vesicles from respond- 

 ing to androgen. In fact, in vitamin B de- 

 ficiency, testosterone restored fructose and 

 citric acid levels to normal despite the need 

 for thiamine in carbohydrate metabolism 

 (Lutwak-Mann and Mann, 1950). In the 

 male, unlike the female, the effects of folic 

 acid deficiency in reducing responsiveness 

 to administered androgen were largely due 

 to inanition in both mice and rats (Gold- 

 smith, Nigrelli and Ross, 1950; Kline and 

 Dorfman, 1951a) , and vitamin A deficiency 

 which leads to virtual castration does not 

 prevent an essentially normal response of 

 the accessory glands to testosterone pro- 

 pionate (Mayer and Truant, 1949). Re- 

 stricting the caloric intake of vitamin A- 

 deficient rats retarded the curative effects 

 of vitamin A in restoring the accessory sex 

 glands of the A-deficient animals (Mason, 

 1939). 



V. Female Reproductive System 



A. OVARIES 



1. Inanition 



Mammalian species generally exhibit a 

 delay in sexual maturation when food in- 

 take is subnormal before puberty, and 

 ovarian atrophy with associated changes 

 in cycles if inanition is imposed on adults. 

 In human beings a decrease in fertility and 

 a greater incidence of menstrual irregulari- 

 ties were induced by war famine (Zimmer, 

 Weill and Dubois, 1944). Ovarian atrophy 

 with associated amenorrhea and sterility 

 were invoked by chronic undernutrition 

 (Stephens, 1941). The ovarian morpliologic 

 changes were similar to those of aging. 

 Urinary estrogens were subnormal in 22 of 

 25 patients exhibiting amenorrhea associ- 

 ated with limited food intake (Zubiran and 

 (_lomcz-Mont, 1953). 



The nutritional requirements of jM'imates 

 other than man have been studied in female 

 baboons. The intake of vitamins and other 

 essential nutrients was found to be of the 

 same order as that recommended for man. 

 Caloric intake varied with the menstrual 

 cycle, being least during the follicular phase 

 and maximal during the 2 to 7 days preced- 

 ing menstruation (Gilbert and Gillman, 

 1956). Various diets were also studied to 

 assess their importance in maintaining the 

 normal menstrual rhythm. The feeding of 

 (a) maize alone, (b) assorted vegetables 

 and fruit, or (c) maize, skimmed milk, and 

 fat led to menstrual irregularities or to 

 amenorrhea. The mechanism regulating ov- 

 ulation was the first to be deranged. The 

 addition of various vitamins or of animal 

 protein did not correct the menstrual dis- 

 orders. However, inclusion of ox liver in 

 the diet did maintain the menstrual rhyth- 

 micity, but the beneficial effect could not 

 be attributed to its protein content (Gill- 

 man and Gilbert, 1956 ) . 



In lower mammals that have been studied, 

 inanition will hinder vaginal opening, and 

 delay puberty and ovarian maturation and 

 functioning. In adult rats and mice ostrous 

 cycles are interrupted and the reprorUictive 

 system becomes atrophic when body weight 

 loss exceeds 15 per cent. The ovaries be- 



