scholarly journals ADRENERGIC FIBERS IN BROWN FAT OF COLD-ACCLIMATED RATS

1970 ◽  
Vol 18 (2) ◽  
pp. 116-119 ◽  
Author(s):  
MERVA K. W. COTTLE ◽  
W. H. COTTLE
Keyword(s):  
Adrenergic Innervation ◽  
Nerve Fibers ◽  
Brown Fat ◽  
Adrenergic Nerve ◽  
Fat Cells ◽  
Fat Tissue ◽  
Histochemical Technique ◽  
Small Arteries ◽  
Brown Adipose ◽  
Adrenergic Fibers

The adrenergic nerve fibers of brown adipose tissue of warm- and cold-acclimated rats were visualized using the fluorescence histochemical technique. Small arteries and arterioles evidenced by their rich adrenergic innervation appeared more abundant in tissue from cold-acclimated animals. Lengths of fine fibers between the fat cells were demonstrable in the brown fat tissue from cold-acclimated rats because of their abundant, strongly fluorescent varicosities whereas such portions of fine fibers were only occasionally seen in the tissue of warm-acclimated rats.

Adrenergic Innervation of Brown Adipose Tissue from the Ground Squirrel (Citellus richardsonii)

1974 ◽  
Vol 52 (1) ◽  
pp. 70-73 ◽  
Author(s):  
M. K. W. Cottle ◽  
W. H. Cottle ◽  
C. W. Nash
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Adrenergic Innervation ◽  
Nerve Fibers ◽  
Ground Squirrels ◽  
Brown Fat ◽  
Adrenergic Nerve ◽  
Fat Pad ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose

Determinations of noradrenaline (NA) content and observations of histochemical fluorescence were carried out on the axillary brown fat pad of ground squirrels Citellus richardsonii kept at two temperatures, 20 °C and 5 °C. For comparison, NA content of hearts and intrathoracic brown adipose tissue were also determined. Like interscapular brown adipose tissue from cold-acclimated rats, the axillary brown fat of cold-acclimated ground squirrels contained a high level of NA. The NA content of the fat pad from ground squirrels living at 20 °C, however, though somewhat lower was not statistically different from that of the fat pad from the cold-acclimated animals. Fine adrenergic nerve fibers were observed between the adipocytes and more intense and extensive networks were present around arterioles. The density of adrenergic innervation appeared similar in the axillary brown fat of the two groups. The NA content of the hearts of ground squirrels living at 5 °C was lower than that for hearts from animals at 20 °C. Intrathoracic brown fat tissue from both groups of animals showed large variation.

Degeneration and Regrowth of Adrenergic Nerve Fibers in the Rat Peripheral Tissues after 6-Hydroxydopamine

1971 ◽  
Vol 49 (4) ◽  
pp. 345-355 ◽  
Author(s):  
J. de Champlain
Keyword(s):  
Ganglion Cells ◽  
Adrenergic Innervation ◽  
Nerve Fibers ◽  
Adrenergic Nerve ◽  
High Dose ◽  
Rat Tissues ◽  
Peripheral Tissues ◽  
Endogenous Noradrenaline ◽  
6 Hydroxydopamine ◽  
Noradrenaline Levels

Histofluorescent and biochemical changes in the adrenergic nervous system were followed up in rat tissues after one single intravenous injection of a high dose of 100 mg/kg of 6-hydroxydopamine (6-OH-DA). This treatment results in the rapid disappearance of terminal and preterminal fibers in the iris, atria, and small arteries of rats, whereas endogenous noradrenaline pools of the heart are 95% depleted. The capacity of the adrenergic nerve to take up and accumulate tritiated noradrenaline is reduced proportionally to the reduction in endogenous noradrenaline levels. These changes are compatible with the concept of a complete sympathectomy induced by the specific toxic action of 6-OH-DA on the adrenergic fibers. This sympathectomy is not permanent, however, and numerous bundles of preterminal fibers start to grow in the iris and atria within 4 to 5 days following injection. Progressively, in the following weeks, these fibers distribute over the whole organ and give birth to terminal fibers which form a new adrenergic plexus in these tissues. A completely normal innervation is restored 2 to 3 months after administration of 6-OH-DA. The endogenous noradrenaline levels rise progressively in parallel to the development of the new plexus of fibers. Since a complete regeneration of the adrenergic innervation can be demonstrated in the weeks following injection of 6-OH-DA, it appears that this compound can selectively destroy the adrenergic terminal and preterminal fibers without causing a degeneration of the adrenergic ganglion cells.

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 Cold-induced reduction in Giα proteins in brown adipose tissue. Effects on the cellular hypersensitization to noradrenaline caused by pertussis-toxin treatment

1996 ◽  
Vol 314 (3) ◽  
pp. 761-768 ◽  
Author(s):  
Petr SVOBODA ◽  
Lena UNELIUS ◽  
Andrea DICKER ◽  
Barbara CANNON ◽  
Graeme MILLIGAN ◽  
...  
Keyword(s):  
Cold Acclimation ◽  
Pertussis Toxin ◽  
Fold Increase ◽  
Brown Fat ◽  
Fat Cells ◽  
Brown Adipose ◽  
Increased Sensitivity ◽  
Gi Proteins ◽  
Thermogenic Response ◽  
In Cells

The significance of Gi proteins for the physiological desensitization phenomena observed in brown-fat cells from cold-acclimated hamsters was investigated. For this purpose, pertussis toxin (the inhibitor of Gi function) was injected into control and cold-acclimated hamsters. After 3 days the thermogenic response to noradrenaline injection was monitored in the intact animals. It was found that the pertussis-toxin pretreatment did not affect the thermogenic response to noradrenaline. Nonetheless, the pertussis toxin pretreatment had a dramatic effect on the noradrenaline-sensitivity of isolated brown-fat cells (measured the following day as the respiratory response): a 250-fold-increased sensitivity to noradrenaline was observed in cells from control animals that had been pertussis-toxin pretreated. However, only a 20-fold increase was observed in cells from cold-acclimated hamsters, implying a lower complement of the Gi system in these cells. Therefore the content of Gi proteins was determined by quantitative immunoblotting of purified plasma-membrane proteins. Cold acclimation resulted in a nearly 50% reduction in the content of Gi1α and Gi2α, as well as of the β-subunit, both when expressed on a protein basis and when related to the content of forskolin-stimulated adenylyl cyclase; when expressed per unit of [3H]ouabain-binding (Na+/K+-ATPase), the reduction was even higher. In view of the magnitude of the pertussis-toxin effect, it was concluded that Gi proteins must play a substantial role in the regulation of the response of brown-fat cells to noradrenaline. As the capacity of the Gi pathway is reduced rather than augmented during cold acclimation, Gi activity cannot be responsible for the desensitization to noradrenaline observed in cells from cold-acclimated animals. However, the reduced Gi content may explain the earlier observed desensitization to adenosine that occurs after acclimation to cold.

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.

Effect of serotonin on brown adipose tissue and on its sympathetic neurons

1976 ◽  
Vol 231 (1) ◽  
pp. 34-39 ◽  
Author(s):  
G Steiner ◽  
S Evans
Keyword(s):  
Stromal Cells ◽  
Sympathetic Neurons ◽  
Metabolic Effect ◽  
Brown Fat ◽  
Fat Cells ◽  
Fat Pad ◽  
Adrenergic Neurons ◽  
Brown Adipose ◽  
Short Adrenergic Neurons ◽  
Metabolic Action

Previously we have shown that there are two types of sympathetic neurons in the rat interscapular brown fat-pad: long adrenergic neurons with cell bodies located in the paraspinal ganglia and short adrenergic neurons with cell bodies located within the pad itself. The present studies examine 1) the uptake of [3H]norepinephrine by these neurons, 2) the effect of serotonin on release of the catecholamine, and 3) the metabolic action of serotonin on brown fat. [3H]norepinephrine uptake from the medium in which brown fat slices are incubated is linear with time up to 90 min. This uptake is blocked by both cocaine and imipramine. As these drugs block uptake by sympathetic neurons, the [3H]norepinephrine is probably taken up by neurons and not by some other cell in the pad. Serotonin creatinine sulfate, but not creatinine sulfate, promotes the release of the catecholamine from these neurons. Serotonin also exerts a norepinephrine-like metabolic effect on slices of normal brown fat. It stimulates lipolysis and inhibits lipogenesis. Serotonin has no effect on isolated brown fat cells or on slices of reserpinized tissue. It also does not potentiate the action of norepinephrine on these last two preparations. Therefore serotonin's action on brown fat is mediated by norepinephrine-containing stromal cells. The data suggest that the rat brown fat-pad has sympathetic neurons that can take up norepinephrine and that serotonin exerts its metabolic effect by stimulating the release of norepinephrine from these neurons.

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.

Two sympathetic nerve supplies to brown adipose tissue of the rat

1969 ◽  
Vol 47 (1) ◽  
pp. 57-63 ◽  
Author(s):  
D. M. Derry ◽  
E. Schönbaum ◽  
G. Steiner
Keyword(s):  
Blood Vessel ◽  
Blood Vessels ◽  
Sympathetic Nerve ◽  
Nerve Fibers ◽  
Brown Fat ◽  
Adrenergic Neurons ◽  
Small Vessels ◽  
Sympathetic Nerve Fibers ◽  
Brown Adipose ◽  
Intrinsic Ganglia

The fluorescent histochemical technique of Falck for demonstrating catecholamines in sympathetic nerve fibers was modified for use in brown fat. In normal interscapular and mediastinal brown fat, the nerve fibers surrounded the arterial Mood vessels and all parenchymal cells. Both immunosympathectomy and surgical denervation gave an almost identical histological picture of massive loss of nerves from the blood vessels only. The parenchymal innervation remained intact. The blood vessels retained single isolated nerve fibers, which were relatively more numerous on the small vessels and which were connected with the parenchymal innervation. After sympathetic nerve fibers were depleted of catecholamines by treating the rat with reserpine, the parenchymal nerves reestablished catecholamine fluorescence at a faster rate than the blood vessel nerves. Intrinsic (tissue) ganglia in the brown fat were resistant to immunosympathectomy. These ganglia contained cells which were very brightly fluorescent. These results indicate that there are two anatomically, immunologically, and pharmacologically different nerve supplies to brown fat, one to the blood vessels and the other predominantly to the parenchyma. It was concluded that the parenchymal nerve supply is derived from the intrinsic ganglia via 'short' adrenergic neurons, and the blood vessel innervation is derived from the sympathetic chain via 'long' adrenergic neurons.

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