Imperial College London
Alternate

ProfessorDavidCarling

Faculty of Medicine, Institute of Clinical Sciences

Professor of Biochemistry
 
 
 
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Contact

 

+44 (0)7590 250 559david.carling

 
 
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Location

 

2.14DLMS BuildingHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Pollard:2019:10.1038/s42255-019-0036-9,
author = {Pollard, AE and Martins, L and Muckett, PJ and Khadayate, S and Bornot, A and Clausen, M and Admyre, T and Bjursell, M and Fiadeiro, R and Wilson, L and Whilding, C and Kotiadis, VN and Duchen, MR and Sutton, D and Penfold, L and Sardini, A and Bohlooly-Y, M and Smith, DM and Read, JA and Snowden, MA and Woods, A and Carling, D},
doi = {10.1038/s42255-019-0036-9},
journal = {Nature Metabolism},
pages = {340--349},
title = {AMPK activation protects against diet induced obesity through Ucp1-independent thermogenesis in subcutaneous white adipose tissue},
url = {http://dx.doi.org/10.1038/s42255-019-0036-9},
volume = {1},
year = {2019}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Obesity results from a chronic imbalance between energy intake and energy output but remains difficult to prevent or treat in humans. Adenosine monophosphate (AMP)-activated protein kinase (AMPK) is an important regulator of energy homeostasis1,2,3 and is a molecular target of drugs used for the treatment of metabolic diseases, including obesity4,5. Here we show that mice expressing a gain-of-function AMPK mutant6 display a change in morphology of subcutaneous white adipocytes that is reminiscent of browning. However, despite a dramatic increase in mitochondrial content, Ucp1 expression is undetectable in these adipocytes. In response to a high-fat diet (HFD), expression of skeletal muscle–associated genes is induced in subcutaneous white adipocytes from the gain-of-function AMPK mutant mice. Chronic genetic AMPK activation results in protection against diet-induced obesity due to an increase in whole-body energy expenditure, most probably because of a substantial increase in the oxygen consumption rate of white adipose tissue. These results suggest that AMPK activation enriches, or leads to the emergence of, a population of subcutaneous white adipocytes that produce heat via Ucp1-independent uncoupling of adenosine triphosphate (ATP) production on a HFD. Our findings indicate that AMPK activation specifically in adipose tissue may have therapeutic potential for the treatment of obesity.
AU  - Pollard,AE
AU  - Martins,L
AU  - Muckett,PJ
AU  - Khadayate,S
AU  - Bornot,A
AU  - Clausen,M
AU  - Admyre,T
AU  - Bjursell,M
AU  - Fiadeiro,R
AU  - Wilson,L
AU  - Whilding,C
AU  - Kotiadis,VN
AU  - Duchen,MR
AU  - Sutton,D
AU  - Penfold,L
AU  - Sardini,A
AU  - Bohlooly-Y,M
AU  - Smith,DM
AU  - Read,JA
AU  - Snowden,MA
AU  - Woods,A
AU  - Carling,D
DO  - 10.1038/s42255-019-0036-9
EP  - 349
PY  - 2019///
SN  - 2522-5812
SP  - 340
TI  - AMPK activation protects against diet induced obesity through Ucp1-independent thermogenesis in subcutaneous white adipose tissue
T2  - Nature Metabolism
UR  - http://dx.doi.org/10.1038/s42255-019-0036-9
UR  - https://www.ncbi.nlm.nih.gov/pubmed/30887000
UR  - http://hdl.handle.net/10044/1/69486
VL  - 1
ER  -
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