Normal and Neoplastic Cells of Brown Adipose Tissue Express the Adhesion Molecule CD31

2006 ◽  
Vol 130 (4) ◽  
pp. 480-482 ◽  
Author(s):  
Renato Rosso ◽  
Marco Lucioni
Keyword(s):  
Adipose Tissue ◽  
Adhesion Molecule ◽  
Myxoid Liposarcoma ◽  
Cell Types ◽  
Brown Fat ◽  
Fat Cells ◽  
Neoplastic Cells ◽  
Brown Adipose ◽  
Formalin Fixed Paraffin Embedded ◽  
Well Differentiated

Abstract Context.—CD31 (platelet-endothelial cell adhesion molecule-1; PECAM-1), an adhesion molecule involved in the process of angiogenesis, is used as a marker of normal and neoplastic vascularization. During the assessment of angiogenesis and vascular invasion in a thymic carcinoid tumor, we observed unexpected immunostaining for CD31 in perithymic brown fat nests. Objective.—To determine whether CD31 is expressed by normal and neoplastic cells of brown fat, a tissue whose thermogenetic activity depends heavily on high perfusion. Design.—Formalin-fixed, paraffin-embedded archival tissues were immunostained by the labeled avidin-biotin method using antibodies against CD31 (clones JC70A and 1A10) after retrieval of heat-induced epitopes. Archival tissues included perithymic, periadrenal, axillary, and neck adipose tissue in which were embedded nests of brown fat (n = 15), hibernoma (n = 3), lipoma (n = 6), well-differentiated liposarcoma (n = 4), and myxoid liposarcoma (n = 4). Results.—Invariably, multivacuolated and univacuolated adipocytes of normal brown fat and hibernomas were intensely positive for the CD31 antigen. The immunostaining “decorated” cell membranes and the membranes of intracytoplasmic vacuoles. No expression of CD31 was found in normal adipocytes of white fat, in neoplastic cells of lipomas, or in multivacuolated lipoblasts of well-differentiated and myxoid liposarcomas. Conclusions.—The spectrum of cell types that express CD31 is expanded to include normal and neoplastic brown fat cells. We speculate that the expression of CD31 may play a role in the development and maintenance of the vascular network characterizing this specialized adipose tissue. Moreover, CD31 may inhibit the Bax-mediated apoptosis of brown fat cells. For practical purposes, CD31 may be used as an immunohistochemical marker for distinguishing between white and brown fat and for diagnosing hibernoma in paraffin sections.

Cold-induced developmental changes in fat cell size and number in brown adipose tissue of the rat

1981 ◽  
Vol 240 (4) ◽  
pp. E379-E383 ◽  
Author(s):  
C. Senault ◽  
G. Cherqui ◽  
M. Cadot ◽  
R. Portet
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Acclimation ◽  
Cell Size ◽  
Brown Fat ◽  
Control Group ◽  
Fat Cells ◽  
Fat Cell ◽  
Brown Adipose ◽  
The Mean

Seven-week-old Long-Evans rats were acclimated to a constant temperature of either 28 degrees C (control group) or 5 degrees C (cold-acclimated group). Cold acclimation induced a 70% increase in the interscapular brown adipose tissue (IBAT) relative mass, a 35% increase in DNA content, and a 44% decrease in triglyceride (TG) content, which resulted in a 51% decrease of the TG/DNA ratio. A procedure is described by which brown fat cells were isolated, with a yield of 21% from the IBAT of the control group and of 38% in the cold-acclimated group. In both groups, the brown fat cells accounted for 35-37% of the total cells in the tissue. Cold acclimation induced decreases in the mean fat cell diameter (about 20%), the mean fat cell TG content (50%), and the fat cell TG/DNA ratio (50%). The total number of IBAT fat cells was significantly increased in cold-acclimated rats. It is concluded that cold acclimation involves a hyperplasia of the IBAT, associated with a decrease of fat cell size without any alteration of the fat cell-to-nonfat cell ratio.

scholarly journals Apelin, a Newly Identified Adipokine Up-Regulated by Insulin and Obesity

Endocrinology ◽  
2005 ◽  
Vol 146 (4) ◽  
pp. 1764-1771 ◽  
Author(s):  
Jérémie Boucher ◽  
Bernard Masri ◽  
Danièle Daviaud ◽  
Stéphane Gesta ◽  
Charlotte Guigné ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Cell Types ◽  
Fat Cells ◽  
Mrna Levels ◽  
Blood Concentrations ◽  
Brown Adipose ◽  
Main Determinants ◽  
Differentiation Stage ◽  
Mouse Adipocytes ◽  
Human And Mouse

Abstract The results presented herein demonstrate that apelin is expressed and secreted by both human and mouse adipocytes. Apelin mRNA levels in isolated adipocytes are close to other cell types present in white adipose tissue or other organs known to express apelin such as kidney, heart, and to a lesser extent brown adipose tissue. Apelin expression is increased during adipocyte differentiation stage. A comparison of four different models of obesity in mice showed a large increase in both apelin expression in fat cells and apelin plasma levels in all the hyperinsulinemia-associated obesities and clearly demonstrated that obesity or high-fat feeding are not the main determinants of the rise of apelin expression. The lack of insulin in streptozotocin-treated mice is associated with a decreased expression of apelin in adipocytes. Furthermore, apelin expression in fat cells is strongly inhibited by fasting and recovered after refeeding, in a similar way to insulin. A direct regulation of apelin expression by insulin is observed in both human and mouse adipocytes and clearly associated with the stimulation of phosphatidylinositol 3-kinase, protein kinase C, and MAPK. These data provide evidence that insulin exerts a direct control on apelin gene expression in adipocytes. In obese patients, both plasma apelin and insulin levels were significantly higher, suggesting that the regulation of apelin by insulin could influence blood concentrations of apelin. The present work identifies apelin as a novel adipocyte endocrine secretion and focuses on its potential link with obesity-associated variations of insulin sensitivity status.

Apparent thermogenic effect of injected glucagon is not due to a direct effect on brown fat cells

1998 ◽  
Vol 275 (5) ◽  
pp. R1674-R1682 ◽  
Author(s):  
Andrea Dicker ◽  
Jin Zhao ◽  
Barbara Cannon ◽  
Jan Nedergaard
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Brown Fat ◽  
Fat Cells ◽  
Brown Adipose ◽  
Adrenergic Blocker ◽  
Vehicle Injection ◽  
Alternative Means ◽  
Glucagon Injection ◽  
Thermogenic Response

To examine the significance of brown adipose tissue for the thermogenic response to glucagon, we injected glucagon intraperitoneally into rats (that have glucagon-sensitive brown fat cells) and into hamsters (that have glucagon-insensitive brown fat cells). Although a thermogenic response to glucagon injection was apparently observed in rats, this response was not augmented by cold acclimation and was not dose dependent. Similar observations were made in hamsters. The thermogenic response could be fully blocked by prior injection of the β-adrenergic blocker propranolol. Thus no direct thermogenic response to injected glucagon could be demonstrated, and the thermogenic response observed was fully due to vehicle injection. However, glucagon injection was able to unmask mitochondrial [3H]GDP binding. As expected, isolated brown fat cells from rats and mice responded thermogenically to glucagon but brown fat cells from hamsters were unresponsive. The EC50 of the rat brown fat cells was high (5 nM); these cells also responded to secretin, with an EC50 of 22 nM. It was concluded that, in contrast to earlier observations, no thermogenic response to injected glucagon could be observed; this may be related to differences in glucagon preparations. Brown fat cells from certain species are, however, glucagon sensitive. It is uncertain whether glucagon is the endogenous agonist for these receptors, but the presence of the glucagon-responsive receptor indicates alternative means to norepinephrine for stimulation of brown adipose tissue thermogenesis and, probably, of recruitment.

Arotinolol is a weak partial agonist on β3-adrenergic receptors in brown adipocytes

2001 ◽  
Vol 79 (7) ◽  
pp. 585-593 ◽  
Author(s):  
Jin Zhao ◽  
Valeria Golozoubova ◽  
Barbara Cannon ◽  
Jan Nedergaard
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Adrenergic Receptor ◽  
Partial Agonist ◽  
Brown Fat ◽  
Fat Cells ◽  
Direct Stimulation ◽  
Brown Adipose ◽  
Adrenergic Antagonist ◽  
Low Sensitivity

Arotinolol, a clinically used α/β-adrenergic blocker, has been demonstrated to be an anti-obesity agent. The anti-obesity effect of arotinolol was suggested to be the result of direct activation of thermogenesis in brown-fat cells. We tested the ability of arotinolol to stimulate thermogenesis (oxygen consumption) in isolated brown-fat cells and in intact animals. Arotinolol stimulated thermogenesis in brown-fat cells isolated from mouse and hamster. A relatively low sensitivity to the β-adrenergic antagonist propranolol (pKB [Formula: see text] 6) indicated that arotinolol interacted with the β3-adrenergic receptor. On the β3-receptor, arotinolol was a very weak (EC50 [Formula: see text] 20 µM) and only partial ([Formula: see text]50 %) agonist, but arotinolol also demonstrated the properties of being a β3-receptor antagonist with a pKB of 5.7. In intact animals, only the antagonistic action of arotinolol could be observed. Because arotinolol is only a very weak and partial agonist on the β3-receptors, direct stimulation of thermogenesis in brown adipose tissue is unlikely to be sufficient to cause significant weight loss. It may be necessary to invoke additional pathways to explain the anti-obesity effects of chronic treatment with arotinolol.Key words: arotinolol, β3-adrenergic receptor, brown adipose tissue, thermogenesis, mouse, hamster, rat.

scholarly journals Adipose Tissue in Calves and Lambs

1968 ◽  
Vol 5 (3) ◽  
pp. 270-281 ◽  
Author(s):  
P. Wensvoort
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cell Types ◽  
Full Term ◽  
Fat Cells ◽  
Brown Adipose

The nature and localization of the brown adipose in young calves, lambs, and in practically full-term foetuses of cows and sheep has been examined. It was found that brown adipose tissue could be composed of types of fat cells greatly differing mutually and that, in lambs, a greater variety of cell-types is to be found than in calves. These types of fat cells, or the types of adipose tissue consisting of them, may transmute into one another. As a rule, these transformations begin to take place in the adipose tissue of the thorax, the more peripheral adipose tissue gradually being involved.

scholarly journals Emerging Roles for Browning of White Adipose Tissue in Prostate Cancer Malignant Behaviour

2021 ◽  
Vol 22 (11) ◽  
pp. 5560
Author(s):  
Alejandro Álvarez-Artime ◽  
Belén García-Soler ◽  
Rosa María Sainz ◽  
Juan Carlos Mayo
Keyword(s):  
Prostate Cancer ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Tumor Development ◽  
Cell Types ◽  
Protective Role ◽  
Bioactive Molecules ◽  
Brown Adipose ◽  
Endocrine Organs

In addition to its well-known role as an energy repository, adipose tissue is one of the largest endocrine organs in the organism due to its ability to synthesize and release different bioactive molecules. Two main types of adipose tissue have been described, namely white adipose tissue (WAT) with a classical energy storage function, and brown adipose tissue (BAT) with thermogenic activity. The prostate, an exocrine gland present in the reproductive system of most mammals, is surrounded by periprostatic adipose tissue (PPAT) that contributes to maintaining glandular homeostasis in conjunction with other cell types of the microenvironment. In pathological conditions such as the development and progression of prostate cancer, adipose tissue plays a key role through paracrine and endocrine signaling. In this context, the role of WAT has been thoroughly studied. However, the influence of BAT on prostate tumor development and progression is unclear and has received much less attention. This review tries to bring an update on the role of different factors released by WAT which may participate in the initiation, progression and metastasis, as well as to compile the available information on BAT to discuss and open a new field of knowledge about the possible protective role of BAT in prostate cancer.

Adrenergic modulation of intracellular pH in isolated brown fat cells from hamster and rat

1994 ◽  
Vol 267 (2) ◽  
pp. C349-C356 ◽  
Author(s):  
S. C. Lee ◽  
J. S. Hamilton ◽  
T. Trammell ◽  
B. A. Horwitz ◽  
P. A. Pappone
Keyword(s):  
Intracellular Ph ◽  
Uncoupling Protein ◽  
Cell Types ◽  
Brown Fat ◽  
Neonatal Rat ◽  
Fat Cells ◽  
Adrenergic Stimulation ◽  
Regulatory Systems ◽  
Ratio Imaging ◽  
Free Media

The activity of the uncoupling protein in brown fat mitochondria is enhanced at alkaline pH, leading to the hypothesis that changes in intracellular pH (pHi) may modulate the thermogenic response to sympathetic stimulation. We employed ratio imaging of the fluorescent dye 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein to measure pHi in acutely isolated single brown fat cells from hamster and neonatal rat and in cultured rat cells. Basal pHi averaged approximately 7.2 in HCO3- media and 0.1-0.15 pH units lower in nominally HCO3(-)-free media in all cell types. In both HCO3- and HCO3(-)-free media, stimulation with norepinephrine (NE) typically caused an alkalinization of approximately 0.05-0.1 pH units, which was followed by a smaller net acidification occurring primarily after NE was removed. Alkalinization seemed to be mediated predominantly by alpha-adrenergic stimulation, while acidification most often followed beta-adrenergic activation. Similar pHi changes were elicited by NE in rat and hamster cells, but responses were more frequent in hamster cells. Assays of recovery from ammonium prepulse-induced acid loads indicated that rat and hamster cells have both Na(+)-H+ and Na(+)- and HCO3(-)-dependent regulatory systems, while hamster cells have, in addition, a Na(+)-independent recovery mechanism activated at acid pHi. We conclude that alpha-adrenergic alkalinization of brown fat may contribute to the control of thermogenesis.

scholarly journals Anti-Obesity Effect of Galacto-Oligosaccharides in Obese Rats

2021 ◽  
Author(s):  
Shang Kong ◽  
Xingjun Huang ◽  
Hua Cao ◽  
Yan Bai ◽  
Qishi Che ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fat Body ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Protective Role ◽  
Lipoprotein Cholesterol ◽  
Fat Cells ◽  
Expression Levels ◽  
Brown Adipose ◽  
Obese Rats

Abstract Background: Galacto-oligosaccharides (GOS) is a commonly used as a prebiotic with a variety of metabolic benefits. Whether GOS plays a protective role in obesity is still unknown. Here we demonstrated that GOS possesses an anti-obesity activity by promoting adipose tissue browning and thermogenesis. Results: Our results showed that GOS effectively slow weight gain of diet-induced obese (DIO) rats without affecting energy intake. GOS significantly suppressed the hypertrophy and hyperplasia of white adipose tissue (WAT), as well as markedly lessened the ratio of fat pad to fat body. Consistently, GOS significantly improved serum total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) levels, which indicated an appropriate weight loss activity of GOS. Interestingly, GOS also significantly increased the expression levels of browning proteins (UCP1, PPARγ, PGC1α and PRMD16) both in the WAT and brown adipose tissue (BAT). We further found that GOS markedly increased the expression levels of LXRα, PPARα, LDLR and CYP7A1 proteins in the liver of obese rats. Conclusions: Taken together, we concluded that GOS inhibits obesity by accelerating the browning of white fat cells and the thermogenesis of brown fat cells, moreover GOS improves host lipid homeostasis by promoting cholesterol catabolism.

Effect of noradrenaline chronic administration on brown fat phospholipids

1988 ◽  
Vol 8 (5) ◽  
pp. 465-469 ◽  
Author(s):  
Gérard Mory ◽  
Myriam Gawer ◽  
Jean-Claude Kader
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Brown Adipose Tissue ◽  
Acid Composition ◽  
Cold Exposure ◽  
Chronic Administration ◽  
Sympathetic Tone ◽  
Brown Fat ◽  
Brown Adipose

Chronic cold exposure of rats (9 days at 5°C) induces an alteration of the fatty acid composition of phospholipids in brown adipose tissue. The alteration is due to an increase of the unsaturation degree of these lipids. The phenomenon can be reproduced by 10−7 mole. h−1 administration of noradrenaline for 9 days in rats kept at 25°C. Thus, phospholipid alteration in brown fat of cold exposed rats is most probably a consequence of the increase of sympathetic tone which occurs in this tissue during exposure to cold.

scholarly journals RalA controls glucose homeostasis by regulating glucose uptake in brown fat

2018 ◽  
Vol 115 (30) ◽  
pp. 7819-7824 ◽  
Author(s):  
Yuliya Skorobogatko ◽  
Morgan Dragan ◽  
Claudia Cordon ◽  
Shannon M. Reilly ◽  
Chao-Wei Hung ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Glucose Uptake ◽  
Glucose Transporter ◽  
Brown Fat ◽  
Specific Chemical ◽  
Diet Induced Obesity ◽  
Brown Adipose ◽  
Chemical Inhibitors ◽  
Glucose Transporter Glut4

Insulin increases glucose uptake into adipose tissue and muscle by increasing trafficking of the glucose transporter Glut4. In cultured adipocytes, the exocytosis of Glut4 relies on activation of the small G protein RalA by insulin, via inhibition of its GTPase activating complex RalGAP. Here, we evaluate the role of RalA in glucose uptake in vivo with specific chemical inhibitors and by generation of mice with adipocyte-specific knockout of RalGAPB. RalA was profoundly activated in brown adipose tissue after feeding, and its inhibition prevented Glut4 exocytosis. RalGAPB knockout mice with diet-induced obesity were protected from the development of metabolic disease due to increased glucose uptake into brown fat. Thus, RalA plays a crucial role in glucose transport in adipose tissue in vivo.

Sign in / Sign up

Export Citation Format

Share Document