BibTex format
@article{Yavari:2016:10.1016/j.cmet.2016.04.003,
author = {Yavari, A and Stocker, CJ and Ghaffari, S and Wargent, ET and Steeples, V and Czibik, G and Pinter, K and Bellahcene, M and Woods, A and Martínez, de Morentin PB and Cansell, C and Lam, BY and Chuster, A and Petkevicius, K and Nguyen-Tu, MS and Martinez-Sanchez, A and Pullen, TJ and Oliver, PL and Stockenhuber, A and Nguyen, C and Lazdam, M and O'Dowd, JF and Harikumar, P and Tóth, M and Beall, C and Kyriakou, T and Parnis, J and Sarma, D and Katritsis, G and Wortmann, DD and Harper, AR and Brown, LA and Willows, R and Gandra, S and Poncio, V and de, Oliveira Figueiredo MJ and Qi, NR and Peirson, SN and McCrimmon, RJ and Gereben, B and Tretter, L and Fekete, C and Redwood, C and Yeo, GS and Heisler, LK and Rutter, GA and Smith, MA and Withers, DJ and Carling, D and Sternick, EB and Arch, JR and Cawthorne, MA and Watkins, H and Ashrafian, H},
doi = {10.1016/j.cmet.2016.04.003},
journal = {Cell Metabolism},
pages = {821--836},
title = {Chronic activation of γ2 AMPK induces obesity and reduces β cell function},
url = {http://dx.doi.org/10.1016/j.cmet.2016.04.003},
volume = {23},
year = {2016}
}
RIS format (EndNote, RefMan)
TY - JOUR
AB - Despite significant advances in our understanding of the biology determining systemic energy homeostasis, the treatment of obesity remains a medical challenge. Activation of AMP-activated protein kinase (AMPK) has been proposed as an attractive strategy for the treatment of obesity and its complications. AMPK is a conserved, ubiquitously expressed, heterotrimeric serine/threonine kinase whose short-term activation has multiple beneficial metabolic effects. Whether these translate into long-term benefits for obesity and its complications is unknown. Here, we observe that mice with chronic AMPK activation, resulting from mutation of the AMPK γ2 subunit, exhibit ghrelin signaling-dependent hyperphagia, obesity, and impaired pancreatic islet insulin secretion. Humans bearing the homologous mutation manifest a congruent phenotype. Our studies highlight that long-term AMPK activation throughout all tissues can have adverse metabolic consequences, with implications for pharmacological strategies seeking to chronically activate AMPK systemically to treat metabolic disease.
AU - Yavari,A
AU - Stocker,CJ
AU - Ghaffari,S
AU - Wargent,ET
AU - Steeples,V
AU - Czibik,G
AU - Pinter,K
AU - Bellahcene,M
AU - Woods,A
AU - Martínez,de Morentin PB
AU - Cansell,C
AU - Lam,BY
AU - Chuster,A
AU - Petkevicius,K
AU - Nguyen-Tu,MS
AU - Martinez-Sanchez,A
AU - Pullen,TJ
AU - Oliver,PL
AU - Stockenhuber,A
AU - Nguyen,C
AU - Lazdam,M
AU - O'Dowd,JF
AU - Harikumar,P
AU - Tóth,M
AU - Beall,C
AU - Kyriakou,T
AU - Parnis,J
AU - Sarma,D
AU - Katritsis,G
AU - Wortmann,DD
AU - Harper,AR
AU - Brown,LA
AU - Willows,R
AU - Gandra,S
AU - Poncio,V
AU - de,Oliveira Figueiredo MJ
AU - Qi,NR
AU - Peirson,SN
AU - McCrimmon,RJ
AU - Gereben,B
AU - Tretter,L
AU - Fekete,C
AU - Redwood,C
AU - Yeo,GS
AU - Heisler,LK
AU - Rutter,GA
AU - Smith,MA
AU - Withers,DJ
AU - Carling,D
AU - Sternick,EB
AU - Arch,JR
AU - Cawthorne,MA
AU - Watkins,H
AU - Ashrafian,H
DO - 10.1016/j.cmet.2016.04.003
EP - 836
PY - 2016///
SN - 1932-7420
SP - 821
TI - Chronic activation of γ2 AMPK induces obesity and reduces β cell function
T2 - Cell Metabolism
UR - http://dx.doi.org/10.1016/j.cmet.2016.04.003
UR - https://www.sciencedirect.com/science/article/pii/S1550413116301231?via%3Dihub
UR - http://hdl.handle.net/10044/1/32944
VL - 23
ER -
