scholarly journals Prolactin Gene Expression in Mouse Mammary Glands during Late Pregnancy and Lactation

1996 ◽  
Vol 67 (5) ◽  
pp. 484-485
Author(s):  
Toshio HARIGAYA ◽  
Eriko IMATA ◽  
Yuko MORI
Keyword(s):  
Gene Expression ◽  
Late Pregnancy ◽  
Mammary Glands ◽  
Prolactin Gene ◽  
Pregnancy And Lactation

ANALYSIS OF RIBOSOMES AND POLYSOMES DERIVED FROM RABBIT MAMMARY GLANDS DURING PREGNANCY AND LACTATION

1971 ◽  
Vol 49 (4) ◽  
pp. 667-NP ◽  
Author(s):  
I. D. HERRIMAN ◽  
G. D. BAIRD ◽  
JUDY M. BRUCE
Keyword(s):  
Electron Microscopy ◽  
Density Gradient ◽  
Gradient Analysis ◽  
Late Pregnancy ◽  
Sucrose Density Gradient ◽  
Mammary Glands ◽  
Pregnancy And Lactation

SUMMARY Whole-ribosome and polysome-enriched fractions were prepared from the mammary glands of rabbits during late pregnancy and lactation. The composition of the fractions was determined by sucrose density gradient analysis and electron microscopy. The range of size of polysomal aggregates was similar in the late-pregnant and lactating gland, with aggregates containing five to nine ribosomal units predominating. However, the amount of polysomes relative to monosomes was invariably found to increase after parturition. The greater portion of this increase was accounted for by the increased abundance of aggregates containing five to nine units.

scholarly journals The miR-200 family in normal mammary gland development

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Majesta J. Roth ◽  
Roger A. Moorehead
Keyword(s):  
Mammary Tumor ◽  
Mammalian Species ◽  
Late Pregnancy ◽  
Mammary Glands ◽  
Mammary Development ◽  
Normal Mammary Gland ◽  
Ductal Morphogenesis ◽  
Mammary Tumor Growth ◽  
Pregnancy And Lactation ◽  
The Impact

AbstractThe miR-200 family of microRNAs plays a significant role in inhibiting mammary tumor growth and progression, and its members are being investigated as therapeutic targets. Additionally, if future studies can prove that miR-200s prevent mammary tumor initiation, the microRNA family could also offer a preventative strategy. Before utilizing miR-200s in a therapeutic setting, understanding how they regulate normal mammary development is necessary. No studies investigating the role of miR-200s in embryonic ductal development could be found, and only two studies examined the impact of miR-200s on pubertal ductal morphogenesis. These studies showed that miR-200s are expressed at low levels in virgin mammary glands, and elevated expression of miR-200s have the potential to impair ductal morphogenesis. In contrast to virgin mammary glands, miR-200s are expressed at high levels in mammary glands during late pregnancy and lactation. miR-200s are also found in the milk of several mammalian species, including humans. However, the relevance of miR-200s in milk remains unclear. The increase in miR-200 expression in late pregnancy and lactation suggests a role for miR-200s in the development of alveoli and/or regulating milk production. Therefore, studies investigating the consequence of miR-200 overexpression or knockdown are needed to identify the function of miR-200s in alveolar development and lactation.

ENZYMES OF LACTOSE BIOSYNTHESIS IN NORMAL AND HORMONALLY STIMULATED RABBIT MAMMARY GLANDS

1968 ◽  
Vol 40 (1) ◽  
pp. 81-84 ◽  
Author(s):  
R. J. HEITZMAN
Keyword(s):  
Enzyme Activities ◽  
Deoxyribonucleic Acid ◽  
Late Pregnancy ◽  
Mammary Glands ◽  
Uridine Diphosphate ◽  
Early Lactation ◽  
Uridine Diphosphate Glucose ◽  
Pregnancy And Lactation ◽  
Diphosphate Glucose ◽  
The Difference

SUMMARY The activities of uridine diphosphate glucose (UDPG) pyrophosphorylase and UDPG-4′-epimerase in mammary glands of rabbits were determined in late pregnancy and lactation. The activities in animals during the last 4 days of pregnancy and during days 0–4, 5–9 and 11–21 of lactation increased but the difference in the activities was significant between the days 5–9 and 11–21 only and for the pyrophosphorylase activity between days for 0–4 and 5–9. Prolactin and cortisol acetate given daily for 3 or 5 days to rabbits pseudopregnant for 15 days caused increases in enzyme activities that were several times greater than those found in controls. The enzyme activities in the stimulated glands were similar to those observed in early lactation. The levels of deoxyribonucleic acid/g. wet tissue were the same in the stimulated and lactating glands.

Ultrasonographic assessment of the feline mammary gland

2008 ◽  
Vol 10 (5) ◽  
pp. 466-471 ◽  
Author(s):  
Rita Payan-Carreira ◽  
Ana C. Martins-Bessa
Keyword(s):  
Mammary Gland ◽  
Diagnostic Tool ◽  
Late Pregnancy ◽  
Mammary Glands ◽  
Mammary Tissue ◽  
Physiological Changes ◽  
Linear Transducer ◽  
Pregnancy And Lactation ◽  
Ultrasonographic Assessment ◽  
Ultrasonographic Appearance

The aim of this study is to characterise the feline mammary echotexture using B-mode ultrasonography, which is not routinely used to examine the feline mammary gland. Using a 5–9 MHz linear transducer the ultrasonographic appearance of non-stimulated and stimulated mammary glands was determined in 35 mature intact non-pregnant, pregnant and lactating queens aged from 16 months to 8 years. In intact non-pregnant queens, mammary glands are fairly underdeveloped and on the ultrasonograms they appear with a regular hypoechoic texture and generally show a thickness of less than 2.0 mm. The stimulated mammary tissue typically presents a more hyperechoic appearance compared to the non-stimulated gland and a fine granular echotexture. Maximum echogenicity of the mammary gland is reached during lactation. In late pregnancy, the mammary glands reach 6–9 mm in thickness. During lactation, the size of the glands depends on the existence of a suckling stimulus, with the suckled glands reaching about 11 mm in thickness. Ductal structures can only be imaged during late pregnancy and lactation. Ultrasonographic evaluation of the feline mammary gland can become a valuable diagnostic tool to characterise physiological changes and may further contribute to a better characterisation of diseased mammary tissue.

scholarly journals Transcriptomic analysis investigating the interaction between peripheral serotonin and high-fat diet feeding on mammary gene expression in midlactation mice

2020 ◽  
Vol 52 (1) ◽  
pp. 47-55
Author(s):  
A. A. Cheng ◽  
W. Li ◽  
L. L. Hernandez
Keyword(s):  
Gene Expression ◽  
Differentially Expressed Genes ◽  
High Fat Diet ◽  
Tryptophan Hydroxylase ◽  
Mammary Glands ◽  
Differentially Expressed ◽  
P Value ◽  
High Fat ◽  
Pregnancy And Lactation ◽  
Peak Lactation

To understand the role of peripheral serotonin and its interaction with diet in midlactation mammary gene expression, our study uses tryptophan hydroxylase 1 knockout ( Tph1-KO) mice fed a high-fat diet (HFD). It has previously been demonstrated that HFD feeding increases inflammatory and immune pathways in peak lactation mammary glands of mice and increases pup mortality in wild-type (WT) mice compared with dams fed a low-fat diet (LFD). Peripheral serotonin inhibition has been associated with resistance to obesity in male mice fed an HFD. Little is known about the function of Tph1 and how peripheral serotonin affects mammary gland function during pregnancy and lactation. In this study, WT and Tph1-KO models were used to investigate global transcriptomic changes in peak lactation mammary glands when dams were fed either an HFD or LFD. WT and Tph1-KO female mice were assigned to either an LFD or HFD beginning at 3 wk of age ( n = 4/group). Dams were euthanized on lactation day 11. Differentially expressed genes (DEGs) were first filtered by adjusted P value (cutoff ≤ 0.05) and fold-change (FC, cutoff ≥2). Genes were further filtered by mean normalized read count with a cutoff 310. We did not observe many differentially expressed genes in WT and Tph1-KO dams fed LFD. However, 3,529 DEGs were observed between WT-HFD and Tph1-KO-HFD mice, including cell cycle regulation and MAPK pathways being significantly enriched. Further research is required to completely understand the physiological significance of our results on peak lactation mammary physiology and the contribution of serotonin.

Mouse calbindin-D9k gene expression in the uterus during late pregnancy and lactation

2003 ◽  
Vol 205 (1-2) ◽  
pp. 79-88 ◽  
Author(s):  
Beum-Soo An ◽  
Kyung-Chul Choi ◽  
Sung Keun Kang ◽  
Geun-Shik Lee ◽  
Eui-Ju Hong ◽  
...  
Keyword(s):  
Gene Expression ◽  
Late Pregnancy ◽  
Calbindin D9k ◽  
Pregnancy And Lactation

Regulation of serum insulin-like growth factor-I (IGF-I), hepatic growth hormone binding and IGF-I gene expression in the rat during pregnancy and lactation

1993 ◽  
Vol 139 (1) ◽  
pp. 89-95 ◽  
Author(s):  
M. T. Travers ◽  
R. J. Madon ◽  
D. J. Flint
Keyword(s):  
Gene Expression ◽  
Late Pregnancy ◽  
Liver Weight ◽  
Steady Increase ◽  
Early Lactation ◽  
Rna Content ◽  
Igf I ◽  
Pregnancy And Lactation ◽  
I Gene ◽  
Gh Resistance

ABSTRACT An apparent GH resistance occurs in pregnancy, since GH concentrations in serum are reported to be normal or elevated, whereas serum IGF-I falls to very low levels. To determine whether this GH resistance is manifest at the level of the hepatic GH receptor or in the ability of GH to initiate IGF-I gene expression, we have determined hepatic IGF-I mRNA expression, circulating IGF-I and hepatic GH binding during various stages of pregnancy and lactation in the rat. The concentration of IGF-I in serum fell from 37 ± 5 nmol/l (means ± s.e.m.) in virgin rats to 17 ± 1 nmol/l in rats in late pregnancy, recovered in early lactation (31 ± 3 nmol/l) but was again significantly lower than in virgin animals by mid-lactation (22 ± 3 nmol/l). Hepatic GH binding did not vary significantly during pregnancy but showed a small significant decrease in early lactation when expressed per mg membrane protein. When expressed as GH binding per liver, however, there were no significant changes in GH binding at any stage. Liver weight increased significantly between virgin and early pregnant animals (7·1 ± 0·2 g compared with 9·2 ± 0·5 g respectively, P<0·01) and continued to increase up to late lactation (14·3 ± 0·4 g). Similarly, although the amount of IGF-I gene expression/unit RNA declined in late pregnant when compared with virgin animals (6·0 ± 0·6 versus 3·4 ± 0·4 arbitrary optical density units respectively, P<0·05), when the increase in liver weight and RNA content during pregnancy was taken into account there was actually a steady increase in IGF-I gene expression per total liver throughout both pregnancy and lactation, the difference becoming significant by mid-lactation (P<0·05). Thus, when the changes in liver weight which take place during pregnancy and lactation are taken into account we conclude that any hepatic resistance to GH in late pregnancy and lactation must be a post-receptor event which is mitigated in large part by increase in liver size, cell number and RNA content. Journal of Endocrinology (1993) 139, 89–95

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