Role of insulin and the insulin receptor in nutrient partitioning between the mammary gland and adipose tissue

1985 ◽  
Vol 13 (5) ◽  
pp. 828-829 ◽  
Author(s):  
DAVID J. FLINT
Keyword(s):  
Adipose Tissue ◽  
Mammary Gland ◽  
Insulin Receptor ◽  
Nutrient Partitioning

scholarly journals Role of Insulin Receptor Substrate-1 Serine 307 Phosphorylation and Adiponectin in Adipose Tissue Insulin Resistance in Late Pregnancy

Endocrinology ◽  
2007 ◽  
Vol 148 (12) ◽  
pp. 5933-5942 ◽  
Author(s):  
Julio Sevillano ◽  
Javier de Castro ◽  
Carlos Bocos ◽  
Emilio Herrera ◽  
M. Pilar Ramos
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Insulin Receptor ◽  
Tyrosine Phosphorylation ◽  
Molecular Mechanisms ◽  
Ex Vivo ◽  
Late Pregnancy ◽  
Serine Phosphorylation ◽  
Pregnant Rats

Insulin resistance is a hallmark of late pregnancy both in human and rat. Adipose tissue is one of the tissues that most actively contributes to this reduced insulin sensitivity. The aim of the present study was to characterize the molecular mechanisms of insulin resistance in adipose tissue at late pregnancy. To this end, we analyzed the insulin signaling cascade in lumbar adipose tissue of nonpregnant and pregnant (d 20) rats both under basal and insulin-stimulated conditions. We found that the levels of relevant signaling proteins, such as insulin receptor (IR), IR substrate-1 (IRS-1), phosphatidylinositol 3-kinase, 3-phosphoinositide-dependent kinase-1, ERK1/2, and phosphatase and tensin homolog (PTEN) did not change at late pregnancy. However, insulin-stimulated tyrosine phosphorylation of both IR and IRS-1 were significantly decreased, coincident with decreased IRS-1/p85 association and impaired phosphorylation of AKR mouse thymoma viral protooncogene (Akt) and ERK1/2. This impaired activation of IRS-1 occurred together with an increase of IRS-1 phosphorylation at serine 307 and a decrease in adiponectin levels. To corroborate the role of IRS-1 in adipose tissue insulin resistance during pregnancy, we treated pregnant rats with the antidiabetic drug englitazone. Englitazone improved glucose tolerance, and this pharmacological reversal of insulin resistance was paralleled by an increase of adiponectin levels in adipose tissue as well as by a reduction of IRS-1 serine phosphorylation. Furthermore, the impaired insulin-stimulated tyrosine phosphorylation of IRS-1 in adipose tissue of pregnant animals could be restored ex vivo by treating isolated adipocytes with adiponectin. Together, our findings support a role for adiponectin and serine phosphorylation of IRS-1 in the modulation of insulin resistance in adipose tissue at late pregnancy.

scholarly journals SAT-588 Role of Adipose Tissue in Reproduction, Mammary Gland Development, Function and Cancer

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Audrey Brenot ◽  
Irina Hutson ◽  
Charles Andrew Harris
Keyword(s):  
Breast Cancer ◽  
Adipose Tissue ◽  
Mammary Gland ◽  
Neutral Lipids ◽  
Milk Proteins ◽  
Direct Interaction ◽  
Fat Pad ◽  
Estradiol Treatment ◽  
Primary Tumors

Abstract To investigate the role of adipose tissue in the function of the mammary gland (MG) and reproductive system, we have examined lipodystrophic (LD) mice. LD mice of both sexes are sterile, but fertility was restored in both sexes with leptin injections. In addition, leptin was only needed for initial stages of pregnancy and not for parturition. A transplant of mouse embryonic fibroblasts (MEFs) led to the formation of an ectopic fat pad which also rescued the fertility in both sexes. However, pups born to rescued LD mothers died shortly after birth. We therefore examined the mammary glands of these mothers. MGs from LD mice were rudimentary and lacked terminal end buds. Leptin-injected and MEF rescued LD mice were able to become pregnant, showed normal pregnancy-associated glandular proliferation despite a smaller glandular area, were able to produce a small amount of milk that had grossly normal content of milk proteins and neutral lipids, but could not sustain pups to weaning. In order to separate the individual requirements for 1) adipokines such as leptin, 2) estradiol, and 3) epithelial-adipocyte interactions, we performed a series of experiments with both LD and ob (leptin-deficient) mice that received either estradiol or preadipocyte transplant. The resulting fat pad did not rescue the defect in MG development in LD mice. The defect also was not rescued with estradiol pellets. Ob/ob mice, like LD mice, lack leptin and estradiol, but retain adipose tissue. Ob mice have defective MG development. However, in striking contrast to LD mice, reconstitution of a WT fat pad in ob mice rescued the defect in MG development. Estradiol treatment did not rescue MG development in ob mice. Therefore direct interaction between mammary gland epithelia and adipocytes is a requirement for full invasion and expansion of the gland during puberty, but is not required for glandular proliferation during pregnancy and milk production. Given that excess adipose tissue is a risk factor for breast cancer we wanted to determine if breast cancer was affected by the absence of adipose tissue. LD mice were bred to MMTV-PyMT mice that develop spontaneous breast cancer. Remarkably, LD PyMT+ mice had accelerated growth of primary tumors compared to WT PyMT+ mice. Using our MEF transplant model future studies will be directed to understanding whether the accelerated breast cancer growth is due to loss of adipokines or altered epithelial-stromal interactions.

scholarly journals Alterations in the rate of lipogenesis in vivo in maternal liver and adipose tissue on premature weaning of lactating rats: a possible regulatory role of prolactin

1979 ◽  
Vol 180 (3) ◽  
pp. 689-692 ◽  
Author(s):  
L Agius ◽  
A M Robinson ◽  
J R Girard ◽  
D H Williamson
Keyword(s):  
Adipose Tissue ◽  
Mammary Gland ◽  
Plasma Insulin ◽  
Regulatory Role ◽  
Maternal Liver ◽  
Peak Lactation

Removal of pups for 24 h from rats at peak lactation decreased 3H2O incorporation into lipid in vivo in mammary gland by 95%, whereas it was increased in liver (77%) and adipose tissue (330%). These increases were prevented by administration of prolactin. Plasma insulin increased 3-fold on weaning and this was partially prevented by prolactin.

The Role of Epicardial Adipose Tissue Lymphocytes in Low-Grade Inflammation and Coronary Artery Disease

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 469-P
Author(s):  
MILOS MRAZ ◽  
ANNA CINKAJZLOVA ◽  
ZDENA LACINOVÁ ◽  
JANA KLOUCKOVA ◽  
HELENA KRATOCHVILOVA ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Adipose Tissue ◽  
Coronary Artery ◽  
Epicardial Adipose Tissue ◽  
Low Grade ◽  
Artery Disease ◽  
Low Grade Inflammation

142-OR: Unique Role of the a4 Component for S6-Kinase Activity in Metabolic Regulation and Anti-apoptotic Effect in Brown Adipose Tissue

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 142-OR
Author(s):  
MASAJI SAKAGUCHI ◽  
SHOTA OKAGAWA ◽  
SAYAKA KITANO ◽  
TATSUYA KONDO ◽  
EIICHI ARAKI
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Metabolic Regulation ◽  
Kinase Activity ◽  
S6 Kinase ◽  
Unique Role ◽  
Brown Adipose ◽  
Apoptotic Effect

2029-P: Role of Adipose Tissue Macrophage–Derived F13A1 in Regulating Preadipocyte Hyperplasia during Obesity

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 2029-P
Author(s):  
DIANA M. ELIZONDO ◽  
LYNN M. GELETKA ◽  
CARMEN G. FLESHER ◽  
CAREY N. LUMENG
Keyword(s):  
Adipose Tissue ◽  
Tissue Macrophage ◽  
Adipose Tissue Macrophage

Insulin-receptor kinase activity of adipose tissue from morbidly obese humans with and without NIDDM

Diabetes ◽  
1987 ◽  
Vol 36 (5) ◽  
pp. 620-625 ◽  
Author(s):  
M. K. Sinha ◽  
W. J. Pories ◽  
E. G. Flickinger ◽  
D. Meelheim ◽  
J. F. Caro
Keyword(s):  
Adipose Tissue ◽  
Insulin Receptor ◽  
Kinase Activity ◽  
Morbidly Obese ◽  
Receptor Kinase ◽  
Insulin Receptor Kinase ◽  
Insulin Receptor Kinase Activity

The Role of Prolactin in the Development of Mammary Gland Pathology

2018 ◽  
Vol 3 (3) ◽  
pp. 209-213
Author(s):  
O. O. Kolomiyets ◽  
◽  
O. V. Yazykov ◽  
M. S. Lyndin ◽  
R. A. Moskalenko ◽  
...  
Keyword(s):  
Mammary Gland
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