Potentiation of in vivo thermogenesis in rat brown adipose tissue by stimulation of α1-adrenoreceptors is associated with increased release of cyclic AMP

1984 ◽  
Vol 62 (8) ◽  
pp. 943-948 ◽  
Author(s):  
Stephanie W. Y. Ma ◽  
David O. Foster
Keyword(s):  
Adipose Tissue ◽  
Cyclic Amp ◽  
Brown Adipose Tissue ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
Plasma Camp ◽  
Na Release ◽  
Stimulation Of ◽  
Thermogenic Response

Release of cyclic AMP (cAMP) from the interscapular brown adipose tissue (IBAT) of barbital-anesthetized, cold-acclimated rats given activators and inhibitors of brown adipose tissue (BAT) thermogenesis was assessed by measuring IBAT blood flow (microsphere method) and the arteriovenous difference in plasma cAMP across the tissue. The release was taken as an index of the generation of cAMP in the IBAT. During thermogenesis induced by infusion of graded doses of noradrenaline (NA), release of cAMP increased from no significant release without NA to 68 pmol/min at a NA dose that effected maximal thermogenesis. The α-adrenoreceptor antagonist dihydroergotoxin inhibited NA-induced BAT thermogenesis and markedly reduced the release of cAMP. The α1-adrenoreceptor agonist phenylephrine potentiated the in vivo thermogenic response of BAT to isoproterenol or to a suboptimal dose of NA and enhanced the release of cAMP elicited by these catecholamines. But given alone, phenylephrine or dihydroergotoxin had very little or no effect on thermogenesis and cAMP release. These results suggest that stimulation of the α1-adrenoreceptors on BAT adipocytes potentiates the thermogenic response originating from stimulation of the adenylate cyclase-coupled β1-adrenoreceptors by increasing, in some indirect way, the generation of cAMP, the intracellular messenger for activation of thermogenesis. However, in the absence of proof that adipocytes are the principal source of the cAMP released from IBAT, during catecholamine-induced thermogenesis, this explanation for the effect of α1-adrenoreceptor stimulation on thermogenesis remains tentative.

Effect of norepinephrine and uncoupling agents on brown adipose tissue

1968 ◽  
Vol 46 (6) ◽  
pp. 897-902 ◽  
Author(s):  
Barbara A. Horwitz ◽  
Paul A. Herd ◽  
Robert Emrie Smith
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Brown Fat ◽  
Brown Adipose ◽  
In Vitro Response ◽  
Stimulation Of ◽  
Thermogenic Response

Examination of the in vivo effect of 2,4-dinitrophenol (DNP) on the brown adipose tissue of cold-exposed rats, as well as the in vitro response of this tissue to DNP and dicumarol, indicates that brown fat does possess a functional electron transport coupled phosphorylating system. Moreover, the fact that a norepinephrine-induced thermogenic response (in vivo) can be elicited from the brown fat after DNP administration implies that the effect of norepinephrine (NE) is not primarily due either to a physiological uncoupling by fatty acids, the level of which is increased by NE, or to stimulation of an ATP-ase system. Alternatively, our data suggest that under basal conditions (i.e. when the animal is not stimulated by cold stress or NE), the heat production (oxygen consumption) of the brown fat is limited by the availability of substrate rather than ADP. It is thus proposed that the thermogenic effect of NE results from the stimulation of lipolysis and an attendant increase of substrate available for oxidation.

Sympathetic denervation impairs responses of brown adipose tissue to VMH stimulation

1986 ◽  
Vol 251 (5) ◽  
pp. R1005-R1008 ◽  
Author(s):  
Y. Minokoshi ◽  
M. Saito ◽  
T. Shimazu
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Temperature Response ◽  
Sympathetic Denervation ◽  
Nerve Supply ◽  
Rapid Rise ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
Stimulation Of

Effects of unilateral surgical denervation of the interscapular brown adipose tissue (IBAT) on its thermogenic and lipogenic responses to electrical stimulation of the ventromedial hypothalamic (VMH) nucleus were studied in anesthetized rats. The rapid rise in IBAT temperature in response to VMH stimulation was greatly suppressed in the denervated IBAT, whereas the temperature response was not impaired in the contralateral innervated IBAT in the same animals. Similarly, the increased rates of conversion of [14C] glucose and [3H]H2O to fatty acids and glyceride glycerol in vivo in IBAT after VMH stimulation were almost completely inhibited by sympathetic denervation. These results indicate clearly that the increases in lipogenic and thermogenic activities in IBAT in response to VMH stimulation are mediated by the sympathetic nerve supply of this tissue.

Control of brown adipose tissue lipolysis and respiration by adenosine

1983 ◽  
Vol 245 (6) ◽  
pp. E555-E559 ◽  
Author(s):  
D. Szillat ◽  
L. J. Bukowiecki
Keyword(s):  
Adipose Tissue ◽  
Cyclic Amp ◽  
Palmitic Acid ◽  
Brown Adipose Tissue ◽  
Brown Adipocyte ◽  
Tissue Respiration ◽  
Dibutyryl Cyclic Amp ◽  
Response Curves ◽  
Brown Adipose ◽  
Stimulation Of

Adenosine competitively inhibited the stimulatory effects of (-)-isoproterenol on lipolysis and respiration in hamster brown adipocytes. The low value of the apparent ki for respiratory inhibition by adenosine (7 nM) indicated that the nucleoside may control brown adipocyte function under physiological concentrations. Significantly, the dose-response curves for isoproterenol stimulation of lipolysis and respiration were both shifted by adenosine to higher agonist concentrations by the same order of magnitude, providing additional evidence for a tight coupling between lipolysis and respiration. The inhibitory effects of adenosine were rapidly reversed by a) adenosine deaminase, b) agents known to increase intracellular cyclic AMP levels (isoproterenol, isobutylmethylxanthine, dibutyryl cyclic AMP), and c) direct stimulation of respiration with palmitic acid. These results, combined with the fact that adenosine failed to affect respiration evoked either by dibutyryl cyclic AMP or by palmitic acid, strongly indicate that adenosine regulates brown adipose tissue respiration at an early metabolic step of the stimulus-thermogenesis sequence, most probably at the level of the adenylate cyclase complex.

Suppression of norepinephrine-induced thermogenesis in brown adipose tissue by fasting

1983 ◽  
Vol 245 (6) ◽  
pp. E582-E586 ◽  
Author(s):  
M. Hayashi ◽  
T. Nagasaka
Keyword(s):  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Thyroid Hormones ◽  
Brown Adipose Tissue ◽  
Plasma Levels ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
Colonic Temperature ◽  
Induced Changes ◽  
Thermogenic Response

Fasting-induced changes in thermogenic responses to norepinephrine (NE, 4.0 micrograms X kg-1 X min-1 iv) were studied in anesthetized rats previously cold acclimated. The rats were divided into five groups at the end of 30–40 days of cold acclimation (5 degrees C). The five groups were kept for 5 days at 25 degrees C and fed (intact fed), fasted (intact fasted), fasted with daily treatment with thyroxine (T4, 2 micrograms/kg sc), thyroidectomized and fed, or thyroidectomized and fasted. In the intact fasted group, in which the weight of brown adipose tissue decreased, NE-induced increases in oxygen consumption, colonic temperature (T col), and temperature of the interscapular brown adipose tissue (TBAT) were markedly suppressed. The two thyroidectomized groups also showed a reduction in thermogenic response. In these three groups, TBAT was lower than Tcol throughout NE infusion. In the T4-treated fasted group, fasting-induced suppression of thermogenic response to NE was largely prevented. In the intact fed and the T4-treated fasted groups, TBAT attained higher values than Tcol during NE infusion. Plasma levels of thyroid hormones were significantly lower in the intact fasted group than in the intact fed or the T4-treated fasted group. These results suggest that fasting-induced suppression of the thermogenic response to NE is largely due to the reduced thermogenic response of brown adipose tissue to NE. The lowering of the levels of the thyroid hormones induced by fasting may be one of a number of causes of the reduction in the thermogenic response of brown adipose tissue.

Role of mast cell histamine in brown adipose tissue thermogenic response to VMH stimulation

1994 ◽  
Vol 266 (3) ◽  
pp. R831-R837 ◽  
Author(s):  
M. Desautels ◽  
A. Wollin ◽  
I. Halvorson ◽  
D. V. Muralidhara ◽  
J. Thornhill
Keyword(s):  
Adipose Tissue ◽  
Mast Cells ◽  
Brown Adipose Tissue ◽  
Receptor Antagonist ◽  
Histamine Content ◽  
Hypothalamic Area ◽  
Neural Input ◽  
Brown Adipose ◽  
Stimulation Of ◽  
Thermogenic Response

Electrical stimulation of the ventromedial hypothalamic area in rats caused a significant but transient increase in interscapular brown adipose tissue temperature. This response was markedly reduced by cimetidine, a histamine H2-receptor antagonist, but not by pyrilamine, an H1-receptor antagonist. Histamine is present in substantial amounts within mast cells in brown adipose tissue as injections of compound 48/80, which cause degranulation of connective tissue mast cells, reduced the tissue histamine content by > 85%. In contrast, histamine content in brown adipose tissue was not affected by loss of sympathetic neural input (with 6-hydroxydopamine) or sensory neural input (with capsaicin). Neither cimetidine nor histamine had any effect on basal and norepinephrine-stimulated rates of O2 consumption by isolated brown adipocytes. These results indicate that histamine released from mast cells acting on H2-receptors may play an important but indirect role in the thermogenic response of brown adipose tissue to stimulation of the ventromedial hypothalamic area.

Transient upregulation of IGF-I gene expression in brown adipose tissue of cold-exposed rats

1997 ◽  
Vol 272 (3) ◽  
pp. E453-E460 ◽  
Author(s):  
C. Duchamp ◽  
K. A. Burton ◽  
A. Geloen ◽  
M. J. Dauncey
Keyword(s):  
Adipose Tissue ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Unit Weight ◽  
Mrna Levels ◽  
Interscapular Brown Adipose Tissue ◽  
Total Rna ◽  
Brown Adipose ◽  
Igf I

The possible involvement of locally produced insulin-like growth factor I (IGF-I) in the cold-induced hyperplasia of interscapular brown adipose tissue (BAT) was investigated in 2-, 4-, and 7-day cold-exposed (CE, 4 degrees C) rats by measuring BAT IGF-I expression at a time when extensive BAT cell proliferation occurs. By comparison with thermoneutral (25 degrees C) controls, plasma IGF-I decreased in CE rats despite an increased food intake, whereas BAT IGF-I peptide increased markedly to peak after 4 days at 4 degrees C. The ratio of class 1 to class 2 IGF-I mRNA was much higher in BAT than in liver. BAT IGF-I mRNA levels per unit weight total RNA doubled after 2 days at 4 degrees C but decreased thereafter to the level in controls. Upregulation of BAT IGF-I mRNA also occurred in CE rats with a food intake restricted to the level of controls. The transient cold-induced upregulation of BAT IGF-I (per unit weight total RNA) suggests that IGF-I plays a role in the early cold-induced BAT hyperplasia that occurs in vivo.

scholarly journals Glucose utilization by interscapular brown adipose tissue in vivo during nutritional transitions in the rat

1991 ◽  
Vol 273 (1) ◽  
pp. 233-235 ◽  
Author(s):  
M J Holness ◽  
Y L Liu ◽  
J S Beech ◽  
M C Sugden
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Glucose Utilization ◽  
Fold Increase ◽  
Interscapular Brown Adipose Tissue ◽  
Overall Response ◽  
Brown Adipose ◽  
Control Post

Glucose utilization indices (GUI) of interscapular brown adipose tissue (IBAT) declined by 84% after 48 h starvation. Two-thirds of the overall response was observed within 6 h, correlating with decreased insulin concentrations. Re-feeding 48 h-starved rats restored insulin concentrations and evoked a rapid 15-fold increase in IBAT GUI. GUI values after re-feeding were markedly higher than those observed at equivalent insulin concentrations in control post-absorptive rats.

scholarly journals Evidence for a high fatty acid synthesis activity in interscapular brown adipose tissue of genetically obese Zucker rats

1982 ◽  
Vol 204 (2) ◽  
pp. 503-507 ◽  
Author(s):  
M Lavau ◽  
R Bazin ◽  
Z Karaoghlanian ◽  
C Guichard
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Brown Adipose Tissue ◽  
Fatty Acid Synthetase ◽  
High Fatty Acid ◽  
Acid Synthesis ◽  
Zucker Rats ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose

Obese (fa/fa) rats (30 days old) exhibited a 50% increase in the weight of interscapular brown adipose tissue compared with their lean (Fa/fa) littermates. The tissue weight increase was accounted for by an increased fat content. Lipogenesis in vivo, as assessed by the incorporation of 3H from 3H2O into lipid, was increased 5-fold in brown adipose tissue of obese as compared with lean rats. Accordingly, acetyl-CoA carboxylase, fatty acid synthetase, citrate-cleavage enzyme and malic enzyme in this tissue were 4-8 times more active in obese than in lean rats.

scholarly journals Stimulation of the hypothalamic arcuate nucleus increases brown adipose tissue nerve activity via hypothalamic paraventricular and dorsomedial nuclei

2016 ◽  
Vol 311 (2) ◽  
pp. H433-H444 ◽  
Author(s):  
Vineet C. Chitravanshi ◽  
Kazumi Kawabe ◽  
Hreday N. Sapru
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Arcuate Nucleus ◽  
Glutamate Transporter ◽  
Nerve Activity ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
Hypothalamic Arcuate Nucleus ◽  
Male Wistar Rats ◽  
Stimulation Of

Hypothalamic arcuate nucleus (ARCN) stimulation elicited increases in sympathetic nerve activity (IBATSNA) and temperature (TBAT) of interscapular brown adipose tissue (IBAT). The role of hypothalamic dorsomedial (DMN) and paraventricular (PVN) nuclei in mediating these responses was studied in urethane-anesthetized, artificially ventilated, male Wistar rats. In different groups of rats, inhibition of neurons in the DMN and PVN by microinjections of muscimol attenuated the increases in IBATSNA and TBAT elicited by microinjections of N-methyl-d-aspartic acid into the ipsilateral ARCN. In other groups of rats, blockade of ionotropic glutamate receptors by combined microinjections of D(-)-2-amino-7-phosphono-heptanoic acid (D-AP7) and NBQX into the DMN and PVN attenuated increases in IBATSNA and TBAT elicited by ARCN stimulation. Blockade of melanocortin 3/4 receptors in the DMN and PVN in other groups of rats resulted in attenuation of increases in IBATSNA and TBAT elicited by ipsilateral ARCN stimulation. Microinjections of Fluoro-Gold into the DMN resulted in retrograde labeling of cells in the ipsilateral ARCN, and some of these cells contained proopiomelanocortin (POMC), α-melanocyte-stimulating hormone (α-MSH), or vesicular glutamate transporter-3. Since similar projections from ARCN to the PVN have been reported by us and others, these results indicate that neurons containing POMC, α-MSH, and glutamate project from the ARCN to the DMN and PVN. Stimulation of ARCN results in the release of α-MSH and glutamate in the DMN and PVN which, in turn, cause increases in IBATSNA and TBAT.

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