Failure of Gonadotropic Function of the Rat Hypophysis During Chronic Inanition. ∗

Abstract

The disease picture of anorexia nervosa with marked weight loss has many features similar to that of true hypophyseal destruction in Simmond's disease. The similarity of the syndromes raises the possibility that the reduced food intake in anorexia nervosa may cause hypophyseal failure. This is further suggested by the amenorrhea that occurs with starvation and chronic wasting disease.

To test this hypothesis, the effect of inanition on hypophyseal function has been studied in the rat during the past 2 years. Marrian and Parkes, 1 2 in investigating the anestrus of vitamin B deficiency in the rat, found that the ovaries of such rats were still responsive to hypophyseal implants, as were also the ovaries of rats on a severely diminished food intake. This latter has been recently confirmed by Mulinos, et al. 3 The presence of gonadotropic principle in the hypophysis of the vitamin B deficient rats, however, led Marrian and Parkes 1 to believe that the rôle of the hypophysis in the anestrus in this condition was not clear. The experiments described below indicate plainly that during chronic inanition, the origin of the anestrus is in the anterior hypophysis.

Adult female rats, 180-260 g in weight, with regular estrous cycles, and immature 22-day-old female rats of the Long-Evans strain, were used throughout. The rats were kept in individual cages, given water ad lib., and were fed a standard rat diet, McCollum mixture No. 1, limited only in amount. Cod liver oil and yeast supplements were given twice a week. The rats were used after 1-4 months on this regime, having lost 30%-50% of their original body weight. Swiss mice, 22 days old at weaning, were used as recipients for the hypophyseal implants, with autopsy 96 hours after a single implant, using the technic of Smith.