MAMMALIAN OVARY 



481 



cedurcs is not clear. Occasionally adrenal 

 tumors produce physiologically significant 

 amounts of estrogen, but normally the ad- 

 renal production of estrogen, if any, is not 

 of physiologic significance. The atrophy of 

 the female genital tract after bilateral ovar- 

 iectomy suggests strongly that this is so. 



The major hormone of the adrenal cortex, 

 hydrocortisone or corticosterone, depending 

 on the species, has a profound effect on pro- 

 tein and carbohydrate metabolism. An over- 

 production, as manifested by Cushing's dis- 

 ease, results in a wasting of body protein 

 and other metabolic disturbances which by 

 nonspecific influences tend to reduce gonadal 

 function. Similarly a loss of adrenal func- 

 tion (Addison's disease) leads to anemia, 

 electrolyte imbalance, and hypoglycemia. 

 There is usually a decrease in ovarian func- 

 tion but some Addisonian patients have 

 conceived and carried their pregnancies 

 with only sodium and fluid supplements. 



There is a hereditarv metabolic defect 



of the human adrenal which renders it de- 

 fective in i)roducing hydrocortisone. This 

 is the adrenogenital syndrome. In these 

 jiatients the adrenals produce excessive 

 amounts of intermediate products which are 

 excreted in the urine. Some of these com- 

 pounds are androgenic 17-ketosteroids and 

 may cause virilization (Bradbury, 1958). 

 These androgens tend to inhibit the gonado- 

 trophic activity of the pituitary and leave 

 the ovaries unstimulated and infantile (Fig. 

 7.13). Replacement therapy with corticoids 

 reduces the adrenocorticotrophic hormone 

 ( ACTH) activity of the pituitary and then 

 the adrenal production of androgen ceases. 

 This then permits the pituitary to stimulate 

 normal cyclic activity in the ovaries (Fig. 

 7.14). The adrenogenital syndrome thus 

 has a profound effect on ovarian function 

 which is specific through its production of 

 androgen. More complete descriptions of the 

 condition and of the rationale of treat- 

 ment have been prepared by Wilkins ( 1949) , 



CHOLESTEROL 



PREGNENOLONE 



PROGESTERONE 



HYDROXY- 

 PROGESTERONE 



Fig. 7.13. Scliematic representation of tlie interaction of tlie adrenal and tlie ovary in the 

 adrenogenital syndrome. The process of hormone biosynthesis is defective in the adrenal 

 (BLOCK) and the degraded by-products (17-ketosteroids) being androgenic suppress the 

 formation of gonadotrophins (GTH). (Courtesy of Dr. J. T. Bradbury.) 



