672 



PHYSIOLOGY OF GOXADS 



TABLE 12.3 



Nutritional effects on the testes of cortisone- 

 maintained adrenalectomized rats 

 (From R. C. Wolf and J. H. Leathern, 

 Endocrinology, 57, 286, 1955.) 



hypofimction. Several clinical tests per- 

 mitted the evaluation of subnormal adrenal 

 function which, however, did not reach 

 Addisonian levels. Malnutrition not only- 

 reduced hypophyseal adrenocorticotrophic 

 hormone (ACTH), but also prevented an 

 incomplete response by the adrenal glands 

 to injected ACTH. In laboratory rodents, 

 anterior hypophyseal function is also in- 

 fluenced by dietary protein and vitamin 

 levels (Ershoff, 1952). The importance of 

 dietary protein in the hypophyseal-adrenal 

 system has recently been re-emphasized 

 (Leathem, 1957; Goth, Nadashi and Slader, 

 1958). Furtiiermore, adrenal cortical func- 

 tion is affected by vitamin deficiencies 

 (Morgan, 1951), from which it appears 

 that pantothenic acid is essential for corti- 

 cal hormone elaboration (Eisenstcin, 1957). 

 Administration of excessive amounts of 

 cortical steroids can induce morphologic 

 changes which have been compared to in- 

 anition (Baker, 1952). Not only is nitrogen 

 loss enhanced, but hyperglycemia can also 

 be induced which, therefore, increases the 

 need for thiamine. Cortical steroids in- 

 fluence the metabolism of various vitamins 



(Draper and Johnson, 1953; Dhyse, Fisher, 

 Tullner and Hertz, 1953; Aceto, Li Moli 

 and Panebianco, 1956; Ginoulhiac and 

 Nani, 1956). H a vitamin deficiency already 

 exists, administration of cortisone will ag- 

 gravate the condition (Meites, Feng and 

 Wilwerth, 1957). Nevertheless, drastic ef- 

 fects of therapeutic doses of cortisone on 

 reproductive function do not occur. In rare 

 cases loss of libido has been reported in 

 the male, but mori)hologic changes in the 

 testis were not observed (JVladdock, Chase 

 and Nelson, 1953). Cortisone has little if 

 any effect on the weight of the rat testis 

 (Moore, 1953; Aschkenasy, 1957) and does 

 not influence testis cholesterol (Migeon, 

 1952). In the female, menstrual disturb- 

 ances have been noted in association with 

 cortisone therapy, with the occurrence of 

 hot flashes (Ward, Slocumb, Policy, Low- 

 man and Hench, 1951). However, cortisone 

 corrected disturbances during the follicular 

 phase, possibly by increasing FSH release 

 (Jones, Howard and Langford, 1953). Cor- 

 tisone also increased the number of follicles 

 in the ovary of the rat (Moore, 1953), but 

 not in the rabbit. Cortisone administration 

 did not prevent the enhanced ovarian re- 

 sponse to chorionic gonadotrophin seen in 

 hypothyroid rats (Leathem, 1958b) and 

 had little effect on mice in parabiosis ( Nou- 

 mura, 1956). 



In pregnant female rabbits resorption and 

 stunting of fetuses occurred during treat- 

 ment with large doses of cortisone (Courrier 

 and Collonge, 1951). Similar effects were 

 noted in mice (LcRoy and Domm, 1951 ; 

 Robson and Sharaf, 1951). 



Some of the metabolic derangements of 

 human toxemia of pregnancy have been 

 correlated with accelerated secretion of 

 adrenal steroids creating a steroid imbal- 

 ance (see chapter by Zarrow). Cortisone is 

 reported to have a beneficial effect on some 

 cases (Moore, Jessop, 'Donovan, Barry, 

 Quinn and Drury, 1951). Protein inade- 

 ({uacies may also be etiologic in toxemia and 

 further (>xamination of the possibility 

 sliould he made. 



C. DIABETES MELLITUS, NUTRITION, AND 

 REPRODUCTION 



(llycosuria can be induced experimentally 

 by starvation, overfeeding, and shifting 



