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.

scholarly journals NCLX prevents cell death during adrenergic activation of the brown adipose tissue

2018 ◽  
Author(s):  
Essam A. Assali ◽  
Anthony E. Jones ◽  
Michaela Veliova ◽  
Mahmoud Taha ◽  
Nathanael Miller ◽  
...  
Keyword(s):  
Cell Death ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Mitochondrial Permeability Transition ◽  
Core Body Temperature ◽  
Adrenergic Stimulation ◽  
Brown Adipose ◽  
Stimulation Of

AbstractA sharp increase in mitochondrial Ca2+ marks the activation of the brown adipose tissue (BAT) thermogenesis, yet the mechanisms preventing Ca2+ deleterious effects are poorly understood. Here, we show that adrenergic stimulation of BAT activates a PKA-dependent mitochondrial Ca2+ extrusion via the mitochondrial Na+/Ca2+ exchanger, NCLX. Adrenergic stimulation of NCLX-ablated brown adipocytes (BA) induces a profound mitochondrial Ca2+ overload and impaired uncoupled respiration. Core body temperature, PET imaging and VO2 measurements confirm a BAT specific thermogenic defect in NCLX-null mice.We show that mitochondrial Ca2+ overload induced by adrenergic stimulation of NCLX-null BAT, triggers the opening of the mitochondrial permeability transition pore (mPTP), leading to remarkable mitochondrial swelling, Cytochrome c release and cell death in BAT. However, treatment with mPTP inhibitors rescue mitochondrial respiratory function and thermogenesis in NCLX-null BA, in vitro and in vivo.Our findings identify a novel pathway enabling non-lethal mitochondrial Ca2+ elevation during adrenergic stimulation of uncoupled respiration. Deletion of NCLX transforms the adrenergic pathway responsible for the stimulation of thermogenesis into a death pathway.

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.

scholarly journals TAF7L modulates brown adipose tissue formation

eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Haiying Zhou ◽  
Bo Wan ◽  
Ivan Grubisic ◽  
Tommy Kaplan ◽  
Robert Tjian
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Core Promoter ◽  
Uncoupling Protein ◽  
Dna Looping ◽  
Chromatin Interactions ◽  
Brown Adipose ◽  
Important Regulator

Brown adipose tissue (BAT) plays an essential role in metabolic homeostasis by dissipating energy via thermogenesis through uncoupling protein 1 (UCP1). Previously, we reported that the TATA-binding protein associated factor 7L (TAF7L) is an important regulator of white adipose tissue (WAT) differentiation. In this study, we show that TAF7L also serves as a molecular switch between brown fat and muscle lineages in vivo and in vitro. In adipose tissue, TAF7L-containing TFIID complexes associate with PPARγ to mediate DNA looping between distal enhancers and core promoter elements. Our findings suggest that the presence of the tissue-specific TAF7L subunit in TFIID functions to promote long-range chromatin interactions during BAT lineage specification.

Effect of sucrose-induced overfeeding on brown adipose tissue—With special reference to in vitro thermogenesis and fatty acids compositions

1995 ◽  
Vol 20 (6) ◽  
pp. 477-484 ◽  
Author(s):  
Akihiro Kuroshima ◽  
Tomie Ohno ◽  
Mitsuru Moriya ◽  
Hiroshi Ohinata ◽  
Takehiro Yahata ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Special Reference ◽  
Brown Adipose

scholarly journals Dopamine receptor D1- and D2-agonists do not spark brown adipose tissue thermogenesis in mice

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Francesca-Maria Raffaelli ◽  
Julia Resch ◽  
Rebecca Oelkrug ◽  
K. Alexander Iwen ◽  
Jens Mittag
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Dopamine Receptor ◽  
Ex Vivo ◽  
Potential Target ◽  
D2 Agonist ◽  
Obesity And Diabetes ◽  
Brown Adipose

AbstractBrown adipose tissue (BAT) thermogenesis is considered a potential target for treatment of obesity and diabetes. In vitro data suggest dopamine receptor signaling as a promising approach; however, the biological relevance of dopamine receptors in the direct activation of BAT thermogenesis in vivo remains unclear. We investigated BAT thermogenesis in vivo in mice using peripheral administration of D1-agonist SKF38393 or D2-agonist Sumanirole, infrared thermography, and in-depth molecular analyses of potential target tissues; and ex vivo in BAT explants to identify direct effects on key thermogenic markers. Acute in vivo treatment with the D1- or D2-agonist caused a short spike or brief decrease in BAT temperature, respectively. However, repeated daily administration did not induce lasting effects on BAT thermogenesis. Likewise, neither agonist directly affected Ucp1 or Dio2 mRNA expression in BAT explants. Taken together, the investigated agonists do not seem to exert lasting and physiologically relevant effects on BAT thermogenesis after peripheral administration, demonstrating that D1- and D2-receptors in iBAT are unlikely to constitute targets for obesity treatment via BAT activation.

EFFECT OF TEMPERATURE ON METABOLIC RATES OF LIVER AND BROWN FAT HOMOGENATES

1967 ◽  
Vol 45 (11) ◽  
pp. 1763-1771 ◽  
Author(s):  
Jane C. Roberts ◽  
Robert E. Smith
Keyword(s):  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Brown Adipose Tissue ◽  
Brown Fat ◽  
Effect Of Temperature ◽  
Metabolic Rates ◽  
Brown Adipose ◽  
Rate Of Oxygen Consumption ◽  
Effects Of Temperature

The effects of temperature in vitro upon metabolic rates of homogenates of brown fat and liver from control and cold-acclimated rats have been examined over the range 10–37 °C. At all temperatures, brown adipose tissue exhibits a higher rate of oxygen consumption [Formula: see text] than does liver, α-ketoglutarate being used as substrate. At 10 °C, brown adipose tissue retains a larger percentage (36–38%) of its 37 °C metabolic rate than does liver (22–24%).Q10 values and energies of activation (Ea) have been determined and compared with other data reported for these tissues. At 20 °C, breaks appear in the Arrhenius plots for liver from both control and cold-acclimated rats and also for brown fat from control rats, but not for the brown fat from cold-acclimated rats. Thus brown adipose tissue from cold-acclimated rats retains relatively higher levels of respiration at temperatures below the 20 °C breaking point than does brown fat from control rats.In view of previously reported cold-induced increases in mass, vascularity, and [Formula: see text] of brown fat, this decreased temperature sensitivity in the cold-acclimated rats appears wholly consonant with the adaptive behavior of brown fat in its role as a thermogenic effector.

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.

Uptake of glucose and release of fatty acids and glycerol by rat brown adipose tissue in vivo

1986 ◽  
Vol 64 (5) ◽  
pp. 609-614 ◽  
Author(s):  
Stephanie W. Y. Ma ◽  
David O. Foster
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Brown Adipose Tissue ◽  
Tissue Blood Flow ◽  
Glycerol Release ◽  
Maximal Stimulation ◽  
Brown Adipose ◽  
Lactate And Pyruvate

The net in vivo uptake or release of free fatty acids glycerol, glucose, lactate, and pyruvate by the interscapular brown adipose tissue (IBAT) of barbital-anesthetized, cold-acclimated rats was determined from measurements of plasma arteriovenous concentration differences across IBAT and tissue blood flow. Measurements were made without stimulation of the tissue and also during submaximal and maximal stimulation by infused noradrenaline (NA), the physiological activator of BAT thermogenesis. There was no appreciable uptake of glucose or release of fatty acids and glycerol by the nonstimulated tissue. At both levels of stimulation there was significant uptake of glucose (1.7 and 2.0 μmol/min) and release of glycerol (0.9 and 1.2 μmol/min), but only at maximal stimulation was there significant release of fatty acids (1.9 μmol/min). Release of lactate and pyruvate accounted for 33% of the glucose taken up at submaximal stimulation and 88% at maximal stimulation. By calculation, the remainder of the glucose taken up was sufficient to have fueled about 12% of the thermogenesis at submaximal stimulation, but only about 2% at maximal stimulation. As estimated from the rate of glycerol release, the rate of triglyceride hydrolysis was sufficient at submaximal stimulation to fuel IBAT thermogenesis entirely with the resulting fatty acids, but it was not sufficient to do so at maximal stimulation when some of the fatty acid was exported. It is suggested that at maximal NA-induced thermogenesis a portion of lipolysis proceeded only to the level of mono- and di-glycerides with the result that glycerol release did not fully reflect the rate of fatty acid formation. Both in absolute terms and in relation to the export of glycerol the in vivo export of fatty acids from the adipocytes of IBAT was much less than is observed with brown adipocytes in vitro.

Thermogenesis of brown adipose tissue in cold-acclimated rats

1964 ◽  
Vol 206 (1) ◽  
pp. 143-148 ◽  
Author(s):  
Robert E. Smith ◽  
Jane C. Roberts
Keyword(s):  
Spinal Cord ◽  
Adipose Tissue ◽  
Heat Exchange ◽  
Brown Adipose Tissue ◽  
Respiratory Rate ◽  
Cold Acclimation ◽  
Brown Fat ◽  
Brown Adipose

Multilocular brown adipose tissue in the rat is shown to increase in both mass and respiratory rate, in vitro, during cold acclimation. By vascular convection the resulting heat is directly applied to the thoracocervical regions of the spinal cord, the heart, and other thoracic organs. The vasculature is so arranged as to exercise a fine order of thermogenic control over the brown fat and temperature of the peripheral venous returns to the thorax, facilitated in part by a "reverse" type of countercurrent heat exchange apparently not previously described.

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