Abstract
Summary and conclusions
1, Many, but not all, pituitary preparations produce an increase in liver fat content when administered to intact mice. This response is completely abolished by adrenalectomy.
2. Neither cortisone nor any other adrenocortical steroid tested to date is able, of itself, to cause a substantial increase in liver fat level of intact or of adrenalectomized mice. In the latter, however, the usual post-adren-alectomy loss of liver fat is prevented.
3. When pre-treated with adrenocortical hormone (cortisone), the ability of adrenalectomized mice to respond to pituitary hormone by mobilization of fat to the liver is equal to or greater than that of intact mice. Pituitary substances (growth hormone; weakly potent ACTH) inactive in either intact or adrenalectomized animals, became quite effective in mobilizing fat to the liver if the animals are pre-treated with adrenocortical hormone.
4. It is concluded that to mobilize fat from the depots to the liver the animal requires at least two factors, (1) adequate supplies of adrenocortical hormone (from either endogenous or exogenous sources) plus (2) a supply, either from its own anterior hypophysis or from exogenous sources, of the “triggering” pituitary factor.
5. The “triggering” action of the unidentified pituitary factor is not mediated via the adrenal cortex since it operates in the absence of the adrenal gland provided adequate amounts of exogenous cortisone are administered.
6. The possible identity of the “triggering” pituitary factor is discussed.
The authors are indebted to Miss Ilse Bauer for her kind assistance in performing the many adrenalectomies and necropsies.
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