The production of the adiposogenital syndrome in the rat,with preliminary notes upon the effects of a replacement therapy.

Abstract

The answer to the question whether the genital atrophy, skeletal undergrowth, and excessive adiposity of the adiposogenital syndrome are due to a pituitary deficiency or to an injury of the hypothalamus without pituitary involvement has rested heretofore upon observation made in two closely allied ways, (1) the extent of the injury inflicted as determined at the time of operation, (2) the extent of the injury as determined by autopsy and a study of sections. Both of these methods are open to the objection that the most careful study may fail to reveal the extent of damage done.

Another method is available for determining the significance of the pituitary and brain injury in the genesis of this syndrome, namely, that of a replacement therapy. If we have any confidence in the functional specificity of the endocrine glands, it follows that we must admit the significance of a pituitary impairment as the causative factor if the adiposogenital syndrome or any of its components can be corrected by pituitary administration. This point has been previously discussed (Smith and Smith) in connection with reports upon a replacement therapy in the hypophysectomized tadpole, in which it was shown that the enlargement of the fat organ, and the pigmentary, growth, and endocrine disturbances which invariably follow hypophysectomy in the tadpole, can be corrected by pituitary administration. It is our intention to use this method to make an analysis of the part played by the pituitary in the adiposogenital syndrome of the mammal.