Adrenergic receptors mediating depolarization in brown adipose tissue

1976 ◽  
Vol 231 (3) ◽  
pp. 700-706 ◽  
Author(s):  
SA Fink ◽  
JA Williams
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Adrenergic Receptors ◽  
Neonatal Rat ◽  
Bathing Medium ◽  
Beta Adrenergic ◽  
Endogenous Catecholamine ◽  
Brown Adipose ◽  
Adrenergic Blocker

Adrenergic receptors mediating depolarization in in vitro neonatal rat brown adipose tissue (BAT) have been characterized by use of adrenergic agonists and antagonists. Releasable endogenous catecholamine was present in BAT as demonstrated by tyramine- and 1,1-dimethyl-4-phenylpiperazinium iodide- (DMPP) induced depolarization in BAT from normal rats and its absence when BAT from reserpinized rats was used. In BAT from reserpinized rats l-norepinephrine, l-phenylephrine, and l-isoproterenol all similarly depolarized the bronw adipocytes over the concentration range of 10(-8) to 10(-6) M with a maximal depolarization of about 25 mV. Dopamine and d-norepinephrine were more than 100 times less potent. The beta-adrenergic blocker propranolol competitively inhibited isoproterenol-induced depolarization, whereas the alpha-adrenergic blackers, phentolamine and phenoxybenzamine, inhibited the phenylephrine-induced depolarization with much smaller inhibitory effects on the isoproterenol-induced depolarization. Both phenylephrine and isoproterenol elicited transient depolarizations when briefly added to the bathing medium while continuously recording from the same cell. Both the agonist and antagonist studies are interpreted as indicating the presence of both alpha- and beta-adrenergic receptors on BAT cells which mediate catecholamine-induced depolarization.

Adrenergic effects on thyroxine 5'-deiodinase in brown adipose tissue of lean and ob/ob mice

1990 ◽  
Vol 258 (2) ◽  
pp. R430-R435
Author(s):  
A. L. Kates ◽  
G. Zaror-Behrens ◽  
J. Himms-Hagen
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Acute Effect ◽  
Beta Adrenergic ◽  
Brown Adipose ◽  
Adrenergic Antagonist ◽  
Secondary Objective ◽  
Adrenergic Effects

Genetically obese, ob/ob, mice have an impaired capacity to increase the level of thyroxine 5'-deiodinase (T5'D) in their brown adipose tissue (BAT) when they are exposed to cold. Yet they are able to secrete norepinephrine (NE) from the nerves of their BAT in response to cold and are apparently refractory to this action of NE. The principal objective was to find out whether injected NE could increase T5'D in BAT of the ob/ob mouse. A secondary objective was to elucidate the nature of the adrenergic receptor(s) involved in this response in lean and ob/ob mice. Injection of NE increased T5'D in BAT of lean mice within 3 h. It also increased T5'D in BAT of ob/ob mice but to a lesser extent. Basal T5'D activity in BAT of ob/ob mice was greater than that seen in BAT of lean mice because of the greater size of the tissue. Neither isopropylnorepinephrine nor phenylephrine alone could increase T5'D activity, but a combination increased it almost as well as did NE, although to a lesser extent in ob/ob mice than in lean mice. Both a beta-adrenergic antagonist (propranolol) and an alpha 1-adrenergic antagonist (prazosin) could inhibit the effect of NE. The acute effect of NE on metabolic rate of intact mice also involves an action of both beta- and alpha 1-adrenergic receptors. The beta-adrenergic component appears to be defective in the ob/ob mouse.

Increased alpha 1-adrenoceptor density in brown adipose tissue indicates recruitment drive in hypothyroid rats

1992 ◽  
Vol 263 (4) ◽  
pp. E654-E662 ◽  
Author(s):  
A. Dicker ◽  
A. Raasmaja ◽  
B. Cannon ◽  
J. Nedergaard
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Uncoupling Protein ◽  
Whole Body ◽  
Total Protein Content ◽  
Receptor Density ◽  
Beta Adrenergic ◽  
Brown Adipose

The effects of hypothyroidism on whole body thermogenesis, brown adipose tissue recruitment state, and alpha 1-adrenergic receptor density were investigated. Treatment of rats with methimazole for 4-5 wk led, as expected, to reduction of growth and resting metabolic rate. The thermogenic response to norepinephrine injection was practically abolished. Generally, only small effects of hypothyroidism on brown adipose tissue were observed: total protein content, mitochondrial GDP binding capacity, and total content of the uncoupling protein thermogenin were not altered. The density of beta-adrenergic receptors (estimated with [3H]CGP-12177 as a ligand) was also unchanged. However, the density of alpha 1-adrenergic receptors (estimated with [3H]prazosin) was markedly increased; in other physiological conditions, such an increase has been associated with an increased degree of recruitment of the tissue. These data indicate that brown adipose tissue in the subthermoneutral hypothyroid animal, probably due to homeostatic mechanisms, is exposed to an increased sympathetic stimulation, leading to an increased alpha 1-adrenoceptor density. However, other features of recruitment are only poorly induced, probably due to attenuation of the beta-adrenergic signaling mechanism. The increased alpha 1-adrenergic receptor density may be responsible for certain altered features of brown adipose tissue in hypothyroid animals, such as peroxisomal recruitment and perhaps also for maintenance of the thermogenin content. The results also indicate that the increased alpha 1-adrenergic density generally seen in recruitment would not result from chronic beta-adrenergic stimulation of the tissue but may be controlled via another regulatory pathway, e.g., via the alpha 1-adrenergic pathway itself.

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.

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