The Effect of Estrogenic Substances Upon the Pituitary, Adrenals and Ovaries1

Ellison, E. T.; Burch, John C.

doi:10.1210/endo-20-6-746

Cited by 31 publications

(4 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is well known that in rats the adrenals increase in size during oestrus [Andersen & Kennedy, 1932;Bourne & Zuckerman, 1941] and after oestrogen treatment [Leiby, 1933 ;Ellison & Burch, 1936 ;Bourne & Zuckerman, 1941], and that they decrease in size after ovariectomy [Blumenfeld, 1939]. In analysing this relationship it should be emphasized that a general consensus of opinion supports the present finding that oestrogens stimulate the growth of the cortex alone.…”

Section: Discussionsupporting

confidence: 80%

Stress and Epidermal Mitotic Activity

BULLOUGH¹

1952

J Endocrinol

View full text Add to dashboard Cite

An examination has been made of the actions and interactions of the androgenic, oestrogenic and glucocorticoid hormones on epidermal mitotic activity in the mouse. Testosterone, which has a moderate mitogenic action in the male, does not appear to stimulate adrenal secretion. Thus no antimitotic mechanism is brought into play, and the mitotic activity induced by testosterone continues indefinitely.Oestrogenic hormones, on the other hand, cause active growth of the adrenal cortex, and this appears to be accompanied by active glucocorticoid hormone secretion. Thus the stimulation of epidermal mitotic activity caused by oestrogens is counteracted by the antimitotic action of the glucocorticoid hormones. This reaction occurs naturally on a limited scale at each oestrous period, and it is especially obvious after repeated injections of oestrone and after oestradiol implantation.Cortisone, when given simultaneously with oestrone, largely prevents the initial rise in mitotic activity, and conversely, adrenalectomy prevents the development of the full mitotic inhibition after oestradiol implantation. A detailed consideration of these last results suggests that the glucocorticoid hormones, while playing a major role in the antimitotic mechanism, may not represent the whole of that mechanism. Evidence is reviewed to indicate that the oestrogenic stimulus to the adrenal cortex passes by way of the anterior pituitary gland, and it is possible that a pituitary hormone may itself exert an antimitotic action.

show abstract

Section: Discussionsupporting

confidence: 80%

Stress and Epidermal Mitotic Activity

BULLOUGH¹

1952

J Endocrinol

View full text Add to dashboard Cite

show abstract

“…Sex differences in HPA regulation in the rodent arise from both neuronal imprinting during early development and distinct actions of estradiol (E 2 ) and testosterone (Te) in adulthood. 93–97 In the young adult animal, exposure to E 2 typically potentiates stress-induced ACTH secretion by: (1) attenuating negative feedback in the hypothalamus, hippocampus, amygdala, and pituitary gland 98,99 ; (2) inducing AVP, CRH, and CRH-R1 gene expression in the paraventricular nucleus (PVN) 77,93,100–103 ; (3) enhancing adrenal responsiveness to ACTH 104–107 ; (4) muting hippocampal and bed nucleus of the stria terminalis–directed inhibition of PVN neurons 108 ; and (5) blunting homologous downregulation of limbic GR. 76 Conversely, Te and 5α-dihydrotestosterone (5α-DHT) generally exert opposing effects on the fore-going mechanisms, resulting in diminished stress-stimulated ACTH secretion (see Fig.…”

Section: Experimental Insights Into and Clinical Inferences Regardingmentioning

confidence: 99%

Age-Dependent and Gender-Dependent Regulation of Hypothalamic-Adrenocorticotropic-Adrenal Axis

Veldhuis

Sharma

Roelfsema

2013

Endocrinology and Metabolism Clinics of North America

View full text Add to dashboard Cite

“…These effects cannot be produced in hypophysectomized animals in which the adrenal cortex is maintained in a normal state by the administration of adrenocorticotropic hormone (22, 45,52,60). This is evidence that the effects of testosterone, progesterone, and estrogens on the adrenal cortex are brought about through the pituitary.…”

Section: Discussionmentioning

confidence: 99%

Effect of Methyl Testosterone on Urinary 17-Ketosteroids of Adrenal Origin 123

Reifenstein¹,

Forbes²,

Albright³

et al. 1945

J. Clin. Invest.

View full text Add to dashboard Cite

Urinary 17-ketosteroids or their precursors are thought to arise from the adrenal cortices and the testes (1). Testosterone propionate is partially excreted as a 17-ketosteroid (2); on the other hand, 17-methyl testosterone is not excreted as such (3 to. 5). It follows that methyl testosterone in contradistinction to testosterone propionate, may be used to study the effect of a testosterone compound on the endogenous production of urinary 17-ketosteroids. The present paper is primarily concerned with the effect of methyl testosterone on the urinary 17-ketosteroids of adrenal origin.It is essential that such studies be carried out on individuals without functioning testicular tissue, since it is highly probable from animal experiments that testosterone inhibits its own endogenous production in the testis (6 to 8). It is difficult to obtain direct data in humans on the effect of testosterone on the urinary 17-ketosteroids of testicular origin. Thus, whereas the administration of methyl testosterone to a male without disease of the adrenals and testes induced a lowered 17-ketosteroid excretion (Figure 1), the entire effect may have been mediated through

show abstract

The Effect of Estrogenic Substances Upon the Pituitary, Adrenals and Ovaries1

Cited by 31 publications

References 0 publications

Stress and Epidermal Mitotic Activity

Stress and Epidermal Mitotic Activity

Age-Dependent and Gender-Dependent Regulation of Hypothalamic-Adrenocorticotropic-Adrenal Axis

Effect of Methyl Testosterone on Urinary 17-Ketosteroids of Adrenal Origin 123

Contact Info

Product

Resources

About