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Adenosine activates brown adipose tissue and recruits beige adipocytes via A(2A) receptors

Artikel i vetenskaplig tidskrift
Författare T. Gnad
S. Scheibler
I. von Kugelgen
C. Scheele
A. Kilic
A. Glode
L. S. Hoffmann
L. Reverte-Salisa
P. Horn
S. Mutlu
A. El-Tayeb
M. Kranz
W. Deuther-Conrad
P. Brust
Martin Lidell
Mattias J. Betz
Sven Enerbäck
J. Schrader
G. G. Yegutkin
C. E. Muller
A. Pfeifer
Publicerad i Nature
Volym 516
Nummer/häfte 7531
Sidor 395-+
ISSN 0028-0836
Publiceringsår 2014
Publicerad vid Institutionen för biomedicin, avdelningen för medicinsk genetik och klinisk genetik
Sidor 395-+
Språk en
Länkar dx.doi.org/10.1038/nature13816
Ämnesord FAT, MOUSE, NORADRENALINE, RESPIRATION, LIPOLYSIS, HUMANS, CELLS, ATP
Ämneskategorier Cell- och molekylärbiologi

Sammanfattning

Brown adipose tissue (BAT) is specialized in energy expenditure, making it a potential target for anti-obesity therapies(1-5). Following exposure to cold, BAT is activated by the sympathetic nervous system with concomitant release of catecholamines and activation of beta-adrenergic receptors(1-5). Because BAT therapies based on cold exposureor beta-adrenergic agonists are clinically not feasible, alternative strategies must be explored. Purinergic co-transmission might be involved in sympathetic control of BAT and previous studies reported inhibitory effects of the purinergic transmitter adenosine in BAT from hamster or rat(6-8). However, the role of adenosine in human BAT is unknown. Here we show that adenosine activates human and murine brown adipocytes at low nanomolar concentrations. Adenosine is released in BAT during stimulation of sympathetic nerves as well as from brown adipocytes. The adenosine A(2A) receptor is the most abundant adenosine receptor in human and murine BAT. Pharmacological blockade or genetic loss of A(2A) receptors in mice causes adecrease in BAT-dependent thermogenesis, whereas treatment with A(2A) agonists significantly increases energy expenditure. Moreover, pharmacological stimulation of A(2A) receptors or injection of lentiviral vectors expressing the A(2A) receptor into white fat induces brown-like cells-so-called beige adipocytes. Importantly, mice fed a high-fat diet and treated with an A(2A) agonist are leaner with improved glucose tolerance. Taken together, our results demonstrate that adenosine-A(2A) signalling plays an unexpected physiological role in sympathetic BAT activation and protects mice from diet-induced obesity. Those findings reveal new possibilities for developing novel obesity therapies.

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