Curtailment of the Uterotrophic Action of Estrogen by Impaired Histamine Liberation in the Alloxan-Diabetic Rat: Reversal by Insulin and by Adrenalectomy1

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Abstract
The action of estrogen, as measured by indicators of early uterine growth including hyperemia and edema, has been demonstrated to be profoundly depressed in the alloxan-diabetic rat. Hyperglycemia induced by intravenous infusion of glucose to the unanesthetized, ovariectomized, otherwise intact rat throughout the 4-hr period between estrogen administration and sacrifice failed to inhibit estrogen function. Similarly, estrogen responsiveness was undiminished in diabetes following subtotal pancreatectomy. The release of intrinsic uterine histamine, upon which estrogenic function appears dependent, was shown to be defective in alloxandiabetic rats. Both insulin and adrenalectomy repaired the liberation mechanism. The estrogen responsiveness of this preparation was restored in large measure by insulin pretreatment; full restitution was achieved, however, only on removal of the anti-inflammatory influence of the adrenal cortices, which are hypersecretory in severe, uncompensated diabetes. These findings lend support to the essential role of histamine release in the uterine action of estrogen. In the course of these studies, it has been observed that light surgical anesthesia imposed for the duration of exposure to estrogen abolishes the hormonal response.