Mammary gland development of sows injected with growth hormone-releasing factor during gestation and(or) lactation

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

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 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.


1978 ◽  
Vol 18 (6) ◽  
pp. 1325-1331 ◽  
Author(s):  
J. FÈVRE ◽  
L.-M. HOUDEBINE ◽  
Nicole VERMEIRE ◽  
B. MORET ◽  
Claudine PUISSANT

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.


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.


Endocrinology ◽  
2010 ◽  
Vol 151 (6) ◽  
pp. 2876-2885 ◽  
Author(s):  
Sarah J. Santos ◽  
Sandra Z. Haslam ◽  
Susan E. Conrad

Signal transducer and activator of transcription (Stat)5a is a critical regulator of mammary gland development. Previous studies have focused on Stat5a’s role in the late pregnant and lactating gland, and although active Stat5a is detectable in mammary epithelial cells in virgin mice, little is known about its role during early mammary gland development. In this report, we compare mammary gland morphology in pubertal and adult nulliparous wild-type and Stat5a−/− mice. The Stat5a-null mammary glands exhibited defects in secondary and side branching, providing evidence that Stat5a regulates these processes. In addition, Stat5a−/− mammary glands displayed an attenuated proliferative response to pregnancy levels of estrogen plus progesterone (E+P), suggesting that it plays an important role in early pregnancy. Finally, we examined one potential mediator of Stat5a’s effects, receptor activator of nuclear factor-κB ligand (RANKL). Stat5a−/− mammary glands were defective in inducing RANKL in response to E+P treatment. In addition, regulation of several reported RANKL targets, including inhibitor of DNA binding 2 (Id2), cyclin D1, and the cyclin-dependent kinase inhibitor p21Waf1/Cip1, was altered in Stat5a−/− mammary cells, suggesting that one or more of these proteins mediate the effects of Stat5a in E+P-treated mammary epithelial cells.


2020 ◽  
Author(s):  
Rong Xuan ◽  
Tianle Chao ◽  
Xiaodong Zhao ◽  
Aili Wang ◽  
Yunpeng Chu ◽  
...  

Abstract Background From the late lactation to late gestation stages, the mammary gland tissue of goats undergoes a process from involution to remodeling and then to high differentiation of mammary gland tissue. From the perspective of lactation, this is a continuous development process of the goat mammary gland from the termination of lactation to the restoration of lactation. We performed transcriptome sequencing on goat mammary gland tissues at three mammary gland developmental stages to screen for differentially expressed genes that affect mammary gland development and the physiological process of lactation and mapped their expression profiles in three stages. The objective of this study is to reveal the expression characteristics of these genes and their potential function during mammary gland development and lactation. Results We identified 1,381 differentially expressed genes in the mammary gland during three stages and found that the expression level of genes encoding casein, such as alpha-s1-casein (CSN1S1), alpha-s2-casein (CSN1S2), beta-casein (CSN2), and kappa-casein (CSN3), and alpha-lactalbumin (LALBA) were higher in mammary gland tissues during the late lactation stage and late gestation stage than those during the dry period. In addition, we constructed six functional networks related to differentially expressed genes and found that these genes are closely related to mammary gland growth and development, apoptosis, immunity, substance transport, biosynthesis, and metabolism. Finally, we identified 35 differentially expressed transcription factors, which were classified into 16 families, and predicted that transcription factors of the basic leucine zipper domain (bZIP) family and basic helix-loop-helix (bHLH) family regulated the expression levels of genes related to mammary gland development and lactation. Conclusions Among the late lactation, dry period, and late gestation stages, there are differences in the expression levels of genes related to mammary gland growth and development, apoptosis, immunity, basic substance transport, biosynthesis, and metabolism in mammary gland tissues. Some genes in the same family or with similar functions have similar expression patterns. These differentially expressed genes or transcription factors work synergistically to participate in the regulation of mammary gland development and the physiological process of lactation.


2020 ◽  
Author(s):  
Yao Xiao ◽  
Jason M. Kronenfeld ◽  
Benjamin J. Renquist

ABSTRACTWith a growing population, a reliable food supply is increasingly important. Heat stress reduces livestock meat and milk production. Genetic selection of high producing animals increases endogenous heat production, while climate change increases exogenous heat exposure. Both sources of heat exacerbate the risk of heat-induced depression of production. Rodents are valuable models to understand mechanisms conserved across species. Heat exposure suppresses feed intake across homeothermic species including rodents and production animal species. We assessed the response to early-mid lactation or late gestation heat exposure on milk production and mammary gland development/function, respectively. Using pair-fed controls we experimentally isolated the food intake dependent and independent effects of heat stress on mammary function and mass. Heat exposure (35°C, relative humidity 50%) decreased daily food intake. When heat exposure occurred during lactation, hypophagia accounted for approximately 50% of the heat stress induced hypogalactia. Heat exposure during middle to late gestation suppressed food intake, which was fully responsible for the lowered mammary gland weight of dams at parturition. However, the impaired mammary gland function in heat exposed dams measured by metabolic rate and lactogenesis could not be explained by depressed food consumption. In conclusion, mice recapitulate the depressed milk production and mammary gland development observed in dairy species while providing insight regarding the role of food intake. This opens the potential to apply genetic, experimental and pharmacological models unique to mice to identify the mechanism by which heat is limiting animal production.Summary StatementsThis study demonstrates that heat stress decreases lactation and mammary development through food intake dependent and independent mechanisms.


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