THE MAMMARY FAT PAD AS A PRIVILEGED TRANSPLANTATION SITE

1967 ◽  
Vol 5 (3) ◽  
pp. 542-543 ◽  
Author(s):  
Phyllis B. Blair ◽  
R. L. Moretti
Keyword(s):  
Fat Pad ◽  
Mammary Fat Pad ◽  
Transplantation Site

scholarly journals Long Intergenic Non-Coding RNAs in the Mammary Parenchyma and Fat Pad of Pre-Weaning Heifer Calves: Identification and Functional Analysis

Animals ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 1268
Author(s):  
Shengchao Zhang ◽  
Sibtain Ahmad ◽  
Yuxia Zhang ◽  
Guohua Hua ◽  
Jianming Yi
Keyword(s):  
Mammary Gland ◽  
Crude Protein ◽  
Regulatory Mechanism ◽  
Differentially Expressed ◽  
Milk Replacer ◽  
Rna Seq ◽  
Fat Pad ◽  
Mammary Fat Pad ◽  
Non Coding Rnas ◽  
Gland Development

Enhanced plane of nutrition at pre-weaning stage can promote the development of mammary gland especially heifer calves. Although several genes are involved in this process, long intergenic non-coding RNAs (lincRNAs) are regarded as key regulators in the regulated network and are still largely unknown. We identified and characterized 534 putative lincRNAs based on the published RNA-seq data, including heifer calves in two groups: fed enhanced milk replacer (EH, 1.13 kg/day, including 28% crude protein, 25% fat) group and fed restricted milk replacer (R, 0.45 kg/day, including 20% crude protein, 20% fat) group. Sub-samples from the mammary parenchyma (PAR) and mammary fat pad (MFP) were harvested from heifer calves. According to the information of these lincRNAs’ quantitative trait loci (QTLs), the neighboring and co-expression genes were used to predict their function. By comparing EH vs R, 79 lincRNAs (61 upregulated, 18 downregulated) and 86 lincRNAs (54 upregulated, 32 downregulated) were differentially expressed in MFP and PAR, respectively. In MFP, some differentially expressed lincRNAs (DELs) are involved in lipid metabolism pathways, while, in PAR, among of DELs are involved in cell proliferation pathways. Taken together, this study explored the potential regulatory mechanism of lincRNAs in the mammary gland development of calves under different planes of nutrition.

Effects of dietary fat on the growth of normal, preneoplastic and neoplastic mammary epithelial cells in vivo and in vitro

1985 ◽  
Vol 75 (1) ◽  
pp. 269-278 ◽  
Author(s):  
C.A. Carrington ◽  
H.L. Hosick
Keyword(s):  
Mammary Epithelial Cells ◽  
Saturated Fat ◽  
Mammary Epithelium ◽  
Mammary Epithelial ◽  
Dietary Fats ◽  
Polyunsaturated Fat ◽  
Fat Pad ◽  
Mammary Fat Pad

In order to determine: (1) whether there is a growth-regulating interaction between the mammary fat pad and mammary epithelium; (2) whether this interaction could be modified by dietary fats; and (3) whether these effects could be demonstrated in vitro, the following experiments were performed. Virgin Balb/c mice had the left inguinal mammary fat pad cleared of epithelium and were then maintained on one of four fully defined diets. These diets contained the following proportions of fat by weight: 5% or 10% mixed fats; 20% saturated fat plus cholesterol; or 20% polyunsaturated fat. To test for effects in vivo, animals received subcutaneous injections into the cleared fat pad of tumorigenic mammary cells (WAZ-2T(+SA) or WAZ-2T(-SA)) or preneoplastic mammary cells (CL-S1). Dietary fat had little effect on the latent period of tumour formation, but a low-fat diet increased the invasive/metastatic potential of both tumorigenic cell lines. A high-saturated-fat diet inhibited the growth of normal and preneoplastic epithelium in vivo. To test for effects in vitro, CL-S1 cells were co-cultured with explants of cleared mammary fat pad embedded within collagen gels. CL-S1 cells co-cultured with adipose explants obtained from mice fed on a diet containing 20% polyunsaturated fat showed a threefold increase in incorporation of [3H]thymidine into trichloroacetic acid-precipitable material. These results imply that dietary fats may affect the growth of mammary epithelium in two ways: the inhibition of growth caused by the high-saturated-fat diet may be due to systemic effects as it was not apparent in vitro; the increase in growth seen in vitro and caused by a high-polyunsaturated-fat diet is due to a direct interaction between the mammary fat pad and mammary epithelial cells. This interaction may be masked by systemic effects in vivo.

Abstract A012: Mammary fat pad injections: An alternative implantation method for syngeneic tumor models

2019 ◽  
Author(s):  
Cynthia Obodozie ◽  
Susanne Ruf ◽  
Gojko Bijelic ◽  
Sandra Moor ◽  
Bianca Giesen ◽  
...  
Keyword(s):  
Fat Pad ◽  
Tumor Models ◽  
Syngeneic Tumor ◽  
Mammary Fat Pad ◽  
Implantation Method

scholarly journals Prolactin affects leptin action in the bovine mammary gland via the mammary fat pad

2006 ◽  
Vol 191 (2) ◽  
pp. 407-413 ◽  
Author(s):  
Y Feuermann ◽  
S J Mabjeesh ◽  
L Niv-Spector ◽  
D Levin ◽  
A Shamay
Keyword(s):  
Mammary Gland ◽  
Epithelial Cells ◽  
Endocrine System ◽  
Metabolic Adaptation ◽  
Bovine Mammary Gland ◽  
Fat Pad ◽  
Metabolic Hormones ◽  
Mammary Fat Pad ◽  
Nutrient Partitioning ◽  
Energy Consuming

One of the roles of the endocrine system is to synchronize mammary function. Hormones, such as estrogen, progesterone, and prolactin act directly on the mammary gland. Metabolic hormones, such as GH, glucocorticoids, insulin, and leptin are responsible for coordinating the body’s response to metabolic homeostasis. Leptin has been shown to be an important factor in regulating the metabolic adaptation of nutrient partitioning during the energy-consuming processes of lactation. In the present study, we show that leptin is secreted from the mammary fat, and is regulated by prolactin. The expression of α-casein in a co-culture of epithelial cells and fat explants was enhanced by prolactin compared with that in epithelial cells cultured alone. Leptin antagonist abolished the effect of leptin on α-casein expression in mammary gland explants when exogenous leptin was not present in the medium. This finding supports our hypothesis that the antagonist abolishes the action of endogenous leptin secreted by the mammary adipocytes. These results lead us to the hypothesis that prolactin and leptin act in the bovine mammary gland, via mammary fat pad/adipocytes.

scholarly journals Mammary Fat Can Adjust Prolactin Effect on Mammary Epithelial Cells via Leptin and Estrogen

2009 ◽  
Vol 2009 ◽  
pp. 1-8 ◽  
Author(s):  
Yonatan Feuermann ◽  
Sameer J. Mabjeesh ◽  
Avi Shamay
Keyword(s):  
Estrogen Receptor ◽  
Epithelial Cells ◽  
Estrogen Receptor Alpha ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Fat Pad ◽  
Paracrine Factors ◽  
Receptor Alpha ◽  
Mammary Fat Pad ◽  
Aromatase Mrna

Leptin, like estrogen, is one of the endo/paracrine factors, which are synthesized in and secreted from mature adipocytes. The roles of the mammary fat pad and mammary adipocytes in the initiation of lactation are not clear. In this study, we showed that combination of prolactin, leptin and estrogen elevated the expression of the milk protein beta-lactoglobulin. We also showed that after prolactin stimulate the secretion of leptin from the mammary fat, leptin upregulated the expression of estrogen receptor alpha in the mammary epithelial cells. Also, prolactin affected aromatase mRNA expression in the bovine mammary fat and we demonstrated that leptin and prolactin can affect cholesterol secretion from explants in culture to the medium. Therefore, we suggest that prolactin initiates estrogen expression (as represented by aromatase mRNA) in the mammary fat pad, whereas leptin stimulates estrogen receptor alpha expression in the mammary epithelial cells. We hypothesize that leptin and estrogen, secreted from the mammary fat regulate lactation after stimulation of prolactin.

scholarly journals Trastuzumab and docetaxel in a preclinical organotypic breast cancer model using tissue slices from mammary fat pad: Translational relevance

2015 ◽  
Vol 34 (3) ◽  
pp. 1146-1152 ◽  
Author(s):  
LOREDANA VESCI ◽  
VALERIA CAROLLO ◽  
GIUSEPPE ROSCILLI ◽  
LUIGI AURISICCHIO ◽  
FABIANA FOSCA FERRARA ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Model ◽  
Fat Pad ◽  
Tissue Slices ◽  
Breast Cancer Model ◽  
Mammary Fat Pad

Pre-pubertal mammogenesis in the sheep 3. The effects of restricted feeding or daily administration of bovine growth hormone and bromocriptine on mammary growth and morphology

1986 ◽  
Vol 42 (1) ◽  
pp. 53-63 ◽  
Author(s):  
I. D. Johnsson ◽  
I. C. Hart ◽  
A. Turvey
Keyword(s):  
Growth Hormone ◽  
Weight Gain ◽  
Live Weight ◽  
Restricted Feeding ◽  
Fat Pad ◽  
Live Weight Gain ◽  
Parenchymal Tissue ◽  
Mammary Fat Pad ◽  
Ad Libitum ◽  
Plasma Gh

ABSTRACTIn crossbred female lambs reared on a concentrate diet between 8 and 20 weeks of age, a restriction in food intake to 40 g/kg body weight per day decreased live-weight gain (155 g/day) compared with that in control lambs fed ad libitum (284 g/day) and significantly reduced final live weight and the size of the mammary fat pad (P < 0·001). However, restricted lambs at 20 weeks had more total parenchymal deoxyribonucleic acid (DNA; 54·7 v. 47·5 mg) occupying a greater mass of mammary fat pad (17·0 v. 13·2 g) than control lambs (P > 0·10). Restricted feeding had little effect on mean plasma growth hormone (GH) concentrations at 12 and 18 weeks of age, but decreased plasma insulin and prolactin concentrations.In lambs fed ad libitum, daily subcutaneous (s.c.) injections of 0·1 mg bovine pituitary GH per kg live weight between 8 and 20 weeks of age significantly increased daily live-weight gain (347 g/day; P < 0·001) and also increased total mammary parenchymal DNA (71·2 mg; P < 0·10) and the mass of fat pad occupied by parenchymal tissue (20·6 g; P < 0·05), compared with the control treatment. Daily s.c. injection of bromocriptine (1 mg/day) had no effect on either body or mammary growth, but tended to reduce the effects of bovine GH when given in combination. Secretory activity was observed in the parenchymal tissue of the eight lambs receiving bovine GH alone, and also in five control lambs and three lambs receiving bromocriptine alone. Three lambs that had attained puberty by 20 weeks of age had the poorest mammary development of their respective treatment groups.Mammary gland development at 20 weeks of age was significantly correlated across treatment means with plasma GH concentrations estimated at 18 weeks of age (r = 0·95; P < 0·05), but no correlations of similar magnitude were found between individuals within treatments at 20 weeks. Strongest correlations were found among 8-week-old lambs, where mammary parenchymal DNA was positively correlated with mean plasma GH (r = 0·62) and the GH:insulin ratio (r = 0·79) and negatively correlated with the prolactin:GH ratio (r = -0·65).

Sign in / Sign up

Export Citation Format

Share Document