NUTRITIONAL EFFECTS 



673 



diet^ from one of high fat content to one 

 i; which is isocaloric but high in carbohydrate 

 (Ingle, 1948). Force feeding a high carbo- 

 hydrate diet will eventually kill a rat de- 

 spite insulin administration aimed at con- 

 trolling glycosuria (Ingle and Nezamis, 

 1947). In man excessive eating leading to 

 obesity increases insulin demand and, in 

 many diabetics of middle age, obesity pre- 

 cedes the onset of diabetes. With our present 

 knowledge we must conclude that overfeed- 

 ing is wrong when glycosuria exists and that 

 vitamin B supplements may be of value 

 in diabetes (Meites, Feng and Wilwerth, 

 1957; Salvesen, 1957). 



In man urinary 17-ketosteroids and an- 

 drogen levels are subnormal in diabetes 

 (Horstmann, 1950), and in the diabetic rat 

 pituitary gonadotrophins are reduced 

 (Shipley and Danley, 1947), but testis hy- 

 aluronidase does not change (Moore, 1948) . 

 When hyperglycemia exists in rats, semen 

 ■] carbohydrates increase (Mann and Lut- 

 wak-Mann, 1951). 



Hypoglycemia influences the male re- 

 productive organs. In rats tolbutamide or 

 insulin produce lesions of the germinal 

 epithelium which can be prevented by 

 \' simultaneous administration of glucose. 

 When 2 to 5 hypoglycemic comas are in- 

 duced, such testis injuries increase pro- 

 gressively in number and frequency, and 

 only a partial return to normal is observed 

 a month later (Mancini, Izquierdo, Hein- 

 rich, Penhos and Gerschenfeld, 1959). 



It is well known that the incidence of 

 infertility in the pre-insulin era was high 

 in young diabetic women. Fertility is also 

 reduced in diabetic experimental animals, 

 and rat estrous cycles are prolonged (Davis, 

 Fugo and Lawrence, 1947) . Insulin is cor- 

 rective (Sinden and Longwell, 1949; Ferret, 

 Lindan and Morgans, 1950). Pregnancy in 

 women with uncontrolled diabetes may 

 terminate in abortion or stillbirth, possibly 

 l)ecause toxemia of pregnancy is high (Ped- 

 ersen. 1952). In rats pancreatectomy per- 

 formed the 8th to 12th day of pregnancy 

 increased the incidence of stillbirths (Hult- 

 ciuist, 1950). In another experiment almost 

 one- fourth of 163 animals with diabetes 

 induced by alloxan on the 10th to 12th day 

 of pregnancy died before parturition and 



about 25 ])er cent of the survivors aborted 

 (Angcrvall, 1959). 



D. STERILE-OBESE SYNDROME 



A sterile-obese syndrome in one colony of 

 mice has been shown to be a recessive mono- 

 genic trait (Ingalls, Dickie and Snell, 1950). 

 Obesity was transmitted to subsequent gen- 

 erations by way of ovaries that were trans- 

 planted from obese donors to nonobese re- 

 cipients (Hummel, 1957). Obesity was 

 transmitted by obese females receiving hor- 

 monal therapy and mated to obese males 

 kept on restricted food intake (Smithberg 

 and Runner, 1957). In addition to the in- 

 vestigations of the hereditary nature of the 

 sterile-obese syndrome, the physiologic 

 basis for the sterility has been studied in 

 reference to the presence of germ cells, via- 

 bility of ova and sperm, integrity of the 

 ovary, and response of the uterus to estro- 

 gen (Drasher, Dickie and Lane, 1955). The 

 data indicate that sterility in some obese 

 males can be prevented by food restriction 

 and that sterility in certain obese females 

 can be corrected. 



E. DIET AND THE LIVER 



The concentration of hormones which 

 reaches the target organs in the blood is the 

 result of the rate of their production, me- 

 tabolism, and excretion. How hypophyseal 

 hormones are destroyed is not clear, but 

 current data make it apparent that pitui- 

 tary hormones have a short half-life in the 

 circulatory system. Exerting a major con- 

 trol over circulating estrogen levels is the 

 liver, with its steroid-inactivating systems. 

 Zondek (1934) initially demonstrated that 

 the liver could inactivate estrogens and this 

 finding has had repeated confirmation 

 (Cantarow, Paschkis, Rakoff and Hansen, 

 1943; De:\Ieio, Rakoff, Cantarow and 

 Paschkis, 1948; Vanderlinde and Wester- 

 field, 1950). Other steroids are also inac- 

 tivated by the liver with several enzyme 

 systems being involved; the relative con- 

 centration of these enzymes varies among 

 species of vertebrates (Samuels, 1949). 



The liver is a labile organ which readib.' 

 responds to nutritional modifications; the 

 induced liver changes alter the steroid-in- 

 activating systems of this organ. Thus, in- 

 anition (Drill and Pfeiffer, 1946; Jailer, 



