THE SECRETORY CAPACITY OF THE AUTOTRANSPLANTED HYPOPHYSIS AS INDICATED BY THE EFFECTS OF STEROID HORMONES ON THE MAMMARY GLANDS

1961 ◽  
Vol 38 (3) ◽  
pp. 449-468 ◽  
Author(s):  
Kurt Ahrén

ABSTRACT In the present experiments the secretory capacity of the pituitary gland, autotransplanted to the kidney capsule, was studied with special regard to the secretion of prolactin and growth hormone, using the response of the mammary glands to oestrone (3-hydroxy-oestra-1,3,5(10)-trien-17-one) and progesterone (pregn-4-ene-3,20-dione) in castrated female and male rats as indicator. The main results were as follows: 1) Daily injections of 10 μg of oestrone + 4 mg of progesterone stimulated slight duct growth and marked but not maximal lobule-alveolar development in the mammary glands of rats with transplanted hypophysis. In rats with intact pituitary gland this treatment produced more extensive duct growth and more marked alveolar development. 2) Daily injections of 1 μg of oestrone did not stimulate mammary gland development in rats with transplanted pituitary gland. The same treatment produced slight but definite duct growth in rats with intact pituitary gland. 3) Daily injections of 10 μg of oestrone stimulated slight duct growth and restricted lobule-alveolar development in rats with transplanted hypophysis. In rats with intact pituitary gland this treatment produced more extensive growth of the duct system. 4) In hypophysectomized rats all dose levels of oestrone and progesterone were ineffective in promoting mammary gland development. Combined with prolactin these hormones stimulated, in hypophysectomized rats, a mammary gland development which, qualitatively as well as quantitatively, was very similar to that found in rats with transplanted pituitary gland. These results indicate that the transplanted pituitary gland secreted considerable amounts of prolactin but did not secrete growth hormone or secreted it in only very small amounts.

1965 ◽  
Vol 32 (1) ◽  
pp. 99-NP ◽  
Author(s):  
LIDIA RUBINSTEIN ◽  
K. AHRÉN

SUMMARY The secretion of growth hormone from anterior pituitary transplants under the kidney capsule of gonadectomized and hypophysectomized male rats was investigated with special regard to the importance of the mass of functioning pituitary tissue. Body growth and mammary gland development after testosterone stimulation were studied. In rats with the pituitary gland autotransplanted to the kidney capsule body growth was markedly reduced. After administration of testosterone a few groups of alveoli only were seen in the mammary glands. Hypophysectomized rats with four pituitary transplants (an autotransplant and three homotransplants) under the kidney capsule showed slightly better body growth than rats with an autotransplanted hypophysis. When compared with rats with intact pituitary glands body growth was markedly reduced. Mammary gland development after testosterone stimulation was as poor in rats with four pituitary transplants as in rats with an autotransplanted hypophysis. These results suggest strongly that the normal secretion of growth hormone is regulated by the hypothalamus and that the deficiency of growth hormone in rats with the pituitary gland transplanted remote from the brain is due mainly to a loss of 'specific' stimuli from the hypothalamus and not to a 'non-specific' reduction in the amount of functioning pituitary tissue.


1962 ◽  
Vol 39 (3) ◽  
pp. 338-354 ◽  
Author(s):  
Kurt Ahrén

ABSTRACT The capacity of the rat mammary gland to respond to testosterone stimulation with lobule-alveolar development only when growth hormone is present, has in these experiments been used as a method for studying whether the pituitary gland, autotransplanted into the kidney capsule, can secrete growth hormone. Injections of 0.05 or 0.25 mg of testosterone propionate daily for 14 days did not stimulate any lobule-alveolar development in the mammary glands of castrated rats with autotransplanted hypophysis. When this treatment was given for about 4 weeks, a few alveoli were seen in the mammary glands. In castrated rats with intact pituitary gland the same doses of testosterone propionate stimulated an extense lobule-alveolar development even after only 14 days of treatment. Injections of testosterone propionate together with growth hormone in rats with autotransplanted hypophysis stimulated the same degree of lobule-alveolar development as did injections of testosterone alone in rats with intact pituitary gland. These observations on the mammary glands indicate that there is a considerable deficiency of growth hormone in rats with the pituitary gland autotransplanted into the kidney capsule. These results are discussed, together with the value of the method used for estimating the presence of growth hormone.


1965 ◽  
Vol 49 (1) ◽  
pp. 17-27 ◽  
Author(s):  
Å. Hjalmarson ◽  
K. Ahrén

ABSTRACT The secretory capacity of the pituitary gland, autotransplanted to the kidney capsule, was studied with special regard to the secretion of growth hormone (GH). Body weight, body length, tibial epiphyseal width and the mammary gland development after testosterone stimulation were studied. Body growth and tibial epiphyseal width were markedly reduced in the rats with transplanted hypophysis, but not as much as in the hypophysectomized controls. After injections of 0.25 mg testosterone propionate daily for 10 days, only a few groups of alveoli were seen in the mammary glands of the transplanted rats. These observations show that there is a considerable deficiency of GH in rats with the pituitary gland autotransplanted to the kidney capsule. However, the development of a few alveoli in the mammary glands is in favour of the theory that a small amount of GH is secreted from the transplanted pituitary tissue. Injections of a purified vasopressin preparation (Pitressin) in the rats with autotransplanted hypophysis did not influence body growth, tibial epiphyseal width or mammary gland development. Further, no effect of Pitressin was seen on the tibial epiphyseal cartilage of rats with intact pituitary gland as has been reported by Del Vecchio et al. (1958) and Hiroshige & Itoh (1960). These experiments therefore do not support the view that vasopressin acts as a GH releasing factor.


1997 ◽  
Vol 77 (2) ◽  
pp. 335-338 ◽  
Author(s):  
C. Farmer ◽  
G. Pelletier ◽  
P. Brazeau ◽  
D. Petitclerc

Twenty-four gilts received s.c. injections of saline or growth hormone-releasing factor (GRF) in late gestation and(or) lactation. Sows were sacrificed on day 30 of lactation and functional mammary glands were excised for chemical analyses. Weight of parenchymal (P = 0.004) and extra-parenchymal tissues (P = 0.002) were decreased with GRF injections during lactation. Parenchymal mass per milligram of DNA also decreased (P = 0.025) with GRF in lactation while parenchymal DNA concentration increased (P = 0.03). Exogenous GRF given to sows during lactation therefore decreased total parenchymal mass, increased cell density and decreased mammary cell size. Key words: Sow, mammary gland, growth hormone-releasing factor


1962 ◽  
Vol 41 (1) ◽  
pp. 88-100 ◽  
Author(s):  
Dora Jacobsohn

ABSTRACT The investigation is concerned with the question, whether the mammary gland of the rat reacts with alveolar growth to androgens alone or to the combined actions of androgens and oestrogens. Since it is difficult to deprive a rat of oestrogens, the study was performed under conditions in which the gland itself either does or does not react to oestrogens. The results were as follows: Experiments on hypophysectomized rats treated with insulin and cortisone. – This treatment makes the glands responsive to oestrogens. Administration of oestrogens resulted in alveolar development in response to endogenously produced androgens (males injected with PMS) as well as to testosterone injections (gonadectomized rats). Experiments on hypophysectomized rats. – The glands do not react to oestrogens. – Injections of oestrogens together with PMS or testosterone resulted in the abnormal reaction known to occur in the mammary glands of hypophysectomized rats given androgens alone. Alveoli were absent. Confirming previous results with testosterone, the mammary glands of hypophysectomized males injected with PMS reacted abnormally and the reaction was not normalized by simultaneous treatment of the hypophysectomized rats with insulin and cortisone. The hitherto confusing results obtained by other workers who studied the effects of growth hormone and prolactin on the mammary glands of hypophysectomized rats are discussed, in view of the present finding that a response of the rat's mammary gland to oestrogens is a prerequisite for the production of alveolar lobule development by androgens.


2020 ◽  
Vol 103 (6) ◽  
pp. 1249-1259
Author(s):  
Globinna Kim ◽  
Jong Geol Lee ◽  
Seung-A Cheong ◽  
Jung-Min Yon ◽  
Myeong Sup Lee ◽  
...  

Abstract The physiological functions of progesterone (P4) in female reproductive organs including the mammary glands are mediated via the progesterone receptor (PR), but not all P4 functions can be explained by PR-mediated signaling. Progesterone receptor membrane component 1 (PGRMC1), a potential mediator of P4 actions, plays an important role in the ovary and uterus in maintaining female fertility and pregnancy, but its function in mammary glands has not been elucidated. This study investigated the role of PGRMC1 in mouse mammary gland development. Unlike in the uterus, exogenous estrogen (E2) and/or P4 did not alter PGRMC1 expression in the mammary gland, and Pgrmc1-knockout (KO) mice displayed reduced ductal elongation and side branching in response to hormone treatment. During pregnancy, PGRMC1 was expressed within both the luminal and basal epithelium and gradually increased with gestation and decreased rapidly after parturition. Moreover, although lactogenic capacity was normal after parturition, Pgrmc1 KO resulted in defective mammary gland development from puberty until midpregnancy, while the expression of PR and its target genes was not significantly different between wild-type and Pgrmc1-KO mammary gland. These data suggest that PGRMC1 is essential for mammary gland development during puberty and pregnancy in a PR-independent manner.


Toxicology ◽  
2020 ◽  
Vol 439 ◽  
pp. 152477
Author(s):  
Ayelen L. Gomez ◽  
Gabriela A. Altamirano ◽  
María V. Tschopp ◽  
Verónica L. Bosquiazzo ◽  
Mónica Muñoz-de-Toro ◽  
...  

2002 ◽  
Vol 197 (1-2) ◽  
pp. 127-131 ◽  
Author(s):  
Paul A Kelly ◽  
Anne Bachelot ◽  
Cécile Kedzia ◽  
Lothar Hennighausen ◽  
Christopher J Ormandy ◽  
...  

2003 ◽  
Vol 161 (3) ◽  
pp. 583-592 ◽  
Author(s):  
Rui-An Wang ◽  
Ratna K. Vadlamudi ◽  
Rozita Bagheri-Yarmand ◽  
Iwan Beuvink ◽  
Nancy E. Hynes ◽  
...  

Although growth factors have been shown to influence mammary gland development, the nature of downstream effectors remains elusive. In this study, we show that the expression of p21-activated kinase (Pak)1, a serine/threonine protein kinase, is activated in mammary glands during pregnancy and lactation. By targeting an ectopic expression of a kinase-dead Pak1 mutant under the control of ovine β-lactoglobulin promoter, we found that the mammary glands of female mice expressing kinase-dead Pak1 transgene revealed incomplete lobuloalveolar development and impaired functional differentiation. The expression of whey acidic protein and β-casein and the amount of activated Stat5 in the nuclei of epithelial cells in transgenic mice were drastically reduced. Further analysis of the underlying mechanisms revealed that Pak1 stimulated β-casein promoter activity in normal mouse mammary epithelial cells and also cooperated with Stat5a. Pak1 directly interacted with and phosphorylated Stat5a at Ser 779, and both COOH-terminal deletion containing Ser 779 of Stat5a and the Ser 779 to Ala mutation completely prevented the ability of Pak1 to stimulate β-casein promoter. Mammary glands expressing inactive Pak1 exhibited a reduction of Stat5a Ser 779 phosphorylation. These findings suggest that Pak1 is required for alveolar morphogenesis and lactation function, and thus, identify novel functions of Pak1 in the mammary gland development.


2006 ◽  
Vol 91 (1) ◽  
pp. 93-103 ◽  
Author(s):  
Xiao-Juan Wang ◽  
Erika Bartolucci-Page ◽  
Suzanne E. Fenton ◽  
Li You

Sign in / Sign up

Export Citation Format

Share Document