Inhibition by hypophysectomy of the hyperphagia and obesity following gold thioglucose.
The effect of hypophysectomy in mice previously treated with gold thioglucose (GTG) was studied with respect to changes in food intake and development of obesity. As expected, all mice treated with GTG alone exhibited lesions in the ventromedial hypothalamus (VMH), hyperphagia and obesity. Hypophysectomy of GTG treated mice prevented the appearance of hyperphagia and obesity. Daily administration of the adrenal corticoid, cortisone, completely restored the hyperphagia and obesity in GTG treated hypophysectomized mice. The amounts of cortisone used did not appreciably affect food intake or body weights of normal, hypophysectomized or GTG treated mice. These findings indicate that the hypothalamic hyperphagia and obesity which normally follows the administration of GTG is dependent on a functional pituitary gland. Furthermore, the specific ability of an adrenal corticoid to completely restore the hyperphagia and obesity of GTG treated hypophysectomized mice in the absence of other pituitary factors, suggests that the pituitary adrenal axis serves as an important link in the regulatory mechanism for control of feeding behavior in the mouse.
D000311:Adrenal Glands / Q000502:physiology; D000818:Animals; D006051:Aurothioglucose / Q000494:pharmacology*; D001835:Body Weight / Q000187:drug effects; D003348:Cortisone / Q000494:pharmacology; D004435:Eating / Q000187:drug effects; D005260:Female; D005938:Glucocorticoids / Q000502:physiology; D006046:Gold / Q000494:pharmacology*; D007016:Hypophysectomy; D009115:Muridae; D010902:Pituitary Gland / Q000502:physiology*; D014697:Ventromedial Hypothalamic Nucleus / Q000502:physiology
D005938:Glucocorticoids; D006051:Aurothioglucose; D006046:Gold; D003348:Cortisone