NUTRITIONAL EFFECTS 



689 



epithelium in 11 to 13 weeks, but similar 

 changes failed to develop in ovariectomized 

 rats. Vitamin A-deficient castrated rats 

 quickly developed symptoms of metaplasia 

 when estrogen alone was administered, but 

 no adverse effect followed the administra- 

 tion of estrogen combined with vitamin A 

 (Bo, 1955, 1956). The vagina is different. 

 Its epithelium becomes cornified in vitamin 

 A-deficient normal and castrated rats. The 

 cornification is histologically indistinguish- 

 able from that occurring in the estrous 

 rat and can be prevented by vitamin A. 

 In fact, vitamin A will quantitatively in- 

 hibit the effect of estrogen on the vaginal 

 mucosa when both are applied locally 

 (Kahn, 1954). Conversion of ^-carotene to 

 vitamin A is influenced by tocopherol, vita- 

 min Bi2 , insulin, and thyroid, with evidence 

 for and against a similar action by cortisone 

 (Lowe and Morton, 1956; Rice and Bo, 

 1958). An additional vitamin-hormone re- 

 lationship is suggested by the augmentation 

 of progesterone action in rabbits given vita- 

 min Do . 



3. Mammary Gland 



Inanition prevents mammary growth, but 

 feeding above recommended requirements 

 for maintenance and growth from birth 

 to the first parturition also seems to inter- 

 fere with mammary growth. Furthermore, 

 steroid stimulation of the mammary gland 

 is influenced by nutritional factors. Using 

 the male mouse, Trentin and Turner (1941) 

 showed that as food intake decreased, the 

 amount of estradiol required to produce a 

 minimal duct growth w^as proportionately 

 increased. In the immature male rat a 

 limited food intake prevented the growth of 

 the mammary gland exhibited by fully fed 

 controls. Nevertheless, the gland was com- 

 petent to respond to estrogen (Reece, 1950) . 

 Inasmuch as the glands of force-fed hy- 

 pophysectomized rats did not respond to es- 

 trogen (Samuels, Reinecke and Peterson, 

 1941; Ahren, 1959), one can assume that, 

 despite inanition, a hypophyseal factor was 

 present to permit the response of the mam- 

 mary gland to estrogen. However, inanition 

 (IMeites and Reed, 1949) , but not vitamin 

 deficiencies (Reece, Turner, Hathaway and 

 Davis, 1937), did reduce the content of 

 hypophyseal lactogen in the rat. 



Growth of the mammary gland duct in 

 the male rat in response to estradiol re- 

 quires a minimum of 6 per cent casein. Pro- 

 tein levels of 3 per cent and per cent failed 

 to support growth of the duct (Reece, 1959) . 



C. PREGNANCY 



The human male after attaining adult- 

 hood is confronted with the problem of 

 maintaining the body tissues built up during 

 the growth period. However, in the human 

 female it has been estimated that the re- 

 placement of menstrual losses may require 

 the synthesis of tissue equivalent to 100 

 per cent of her body weight (Flodin, 19531. 

 In the event of pregnancy and in all vivi- 

 parous species, the female is presented with 

 even more formidable demands and a limi- 

 tation of nutritional needs can lead to loss 

 of the embryo or fetus. The role of nutrition 

 at this point in reproduction has always re- 

 ceived considerable attention and is compli- 

 cated by the circumstance that many food 

 substances influence pregnancy (Jackson, 

 1959). However, in many instances there is 

 no evidence that fetal loss or malformation 

 induced by nutritional modifications has 

 been the consequence of an endocrine im- 

 balance and thus limitation of the immense 

 literature is permissible. 



During the first 15 days of pregnancy, a 

 rat may gain 50 gm. Since the fetuses and 

 placentas are small, most of the gain is ma- 

 ternal and is associated with an' increase 

 in food intake of as much as 100 calories 

 per kilogram of body weight (Morrison, 

 1956). During the first 2 weeks of preg- 

 nancy, marked storage of fat and water oc- 

 curs in the maternal body and the animal's 

 positive nitrogen balance is above normal. 

 Liver fat also increases (Shipley, Chudzik, 

 Curtiss and Price, 1953). The increased food 

 intake in early pregnancy may therefore 

 provide a reserve for late fetal growth, as 

 food intake may decline to 65 per cent of 

 the general pregnancy level during the last 

 7 days (Morrison, 1956). During this last 

 week, fetal growth is rapid. The rapid 

 growth has been related to (1) greater de- 

 mands of the fetus, (2) greater amounts of 

 food in the maternal blood, and (31 greater 

 permeability of the placenta. Certainly the 

 anabolic potential of fetal tissues is high 

 and the mother can lose weight while the 



